<?xml version="1.0" encoding="UTF-8"?><xml><records><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">Lacorte, Doriana</style></author><author><style face="normal" font="default" size="100%">Lucafò, Marianna</style></author><author><style face="normal" font="default" size="100%">Cifù, Adriana</style></author><author><style face="normal" font="default" size="100%">Favretto, Diego</style></author><author><style face="normal" font="default" size="100%">Cuzzoni, Eva</style></author><author><style face="normal" font="default" size="100%">Silvestri, Tania</style></author><author><style face="normal" font="default" size="100%">Pozzi Mucelli, Martina</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Fabris, Martina</style></author><author><style face="normal" font="default" size="100%">Bramuzzo, Matteo</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Alvisi, Patrizia</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Causes of Treatment Failure in Children With Inflammatory Bowel Disease Treated With Infliximab: A Pharmacokinetic Study.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Gastroenterol Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Gastroenterol. Nutr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">37-44</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;Anti-tumor necrosis factor antibodies have led to a revolution in the treatment of inflammatory bowel diseases (IBD); however, a sizable proportion of patients does not respond to therapy. There is increasing evidence suggesting that treatment failure may be classified as mechanistic (pharmacodynamic), pharmacokinetic, or immune-mediated. Data regarding the contribution of these factors in children with IBD treated with infliximab (IFX) are still incomplete. The aim was to assess the causes of treatment failure in a prospective cohort of pediatric patients treated with IFX.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This observational study considered 49 pediatric (median age 14.4) IBD patients (34 Crohn disease, 15 ulcerative colitis) treated with IFX. Serum samples were collected at 6, 14, 22 and 54 weeks, before IFX infusions. IFX and anti-infliximab antibodies (AIA) were measured using enzyme linked immunosorbent assays. Disease activity was determined by Pediatric Crohn's Disease Activity Index or Pediatric Ulcerative Colitis Activity Index.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Clinical remission, defined as a clinical score &lt;10, was obtained by 76.3% of patients at week 14 and by 73.9% at week 54. Median trough IFX concentration was higher at all time points in patients achieving sustained clinical remission. IFX levels during maintenance correlated also with C-reactive protein, albumin, and fecal calprotectin. After multivariate analysis, IFX concentration at week 14 &gt;3.11 μg/mL emerged as the strongest predictor of sustained clinical remission. AIA concentrations were correlated inversely with IFX concentrations and directly with adverse reactions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Most cases of therapeutic failure were associated with low serum drug levels. IFX trough levels at the end of induction are associated with sustained long-term response.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30211845?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Skerk, Kristina</style></author><author><style face="normal" font="default" size="100%">Luppi, Stefania</style></author><author><style face="normal" font="default" size="100%">Martinelli, Monica</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cervico-vaginal secretion cytokine profile: A non-invasive approach to study the endometrial receptivity in IVF cycles.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Reprod Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Reprod. Immunol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">81</style></volume><pages><style face="normal" font="default" size="100%">e13064</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;PROBLEM: &lt;/b&gt;Cytokines have a significant role in the process of embryo implantation, trophoblast growth, and differentiation by modulating the immune and endocrine system. The aim of this study was to investigate the profile of a large set of cytokines in the cervico-vaginal washing of women undergoing IVF, to explore the association of these proteins with a good receptive endometrium.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHOD OF STUDY: &lt;/b&gt;A cohort of 155 women scheduled for IVF cycle was recruited. All patients were asymptomatic for genitourinary infections and had been screened for chlamydia, mycoplasma, and other bacterial infections. All IVF subjects were treated according to standard clinical and laboratory protocols. A panel of 48 immune factors was analyzed on cervico-vaginal washing, using magnetic bead-based multiplex immunoassays (Bio-Plex, BIO-RAD Laboratories, Milano, Italy).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;A total of 99 patients reached embryo transfer, of which 31 had a clinical pregnancy. A pattern of four pro-inflammatory immune molecules, IL-12p40, IFN-a, MIF, and MCP3 (P &lt; 0.001), was found significantly up-regulated in the cervico-vaginal fluid of women with clinical pregnancy. A significantly increased expression of IL-9, Gro , and SDF-1 (P &lt; 0.05) was observed in the presence of endometriosis, while high levels of IL-13 and L-15 were associated with ovulatory infertility factor (P &lt; 0.05).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;In this pilot study, we demonstrated that the expression of specific cytokines in the cervico-vaginal washing on the day of oocyte retrieval might have a positive correlation with the potential clinical pregnancy. Therefore, cervico-vaginal secretion cytokine profiling might be a new, non-invasive approach to study the endometrial receptivity in IVF management.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30475413?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Benelli, Elisa</style></author><author><style face="normal" font="default" size="100%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">De Leo, Luigina</style></author><author><style face="normal" font="default" size="100%">Stera, Giacomo</style></author><author><style face="normal" font="default" size="100%">Giangreco, Manuela</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Villanacci, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Changing Epidemiology of Liver Involvement in Children With Celiac Disease.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Gastroenterol Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Gastroenterol. Nutr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2019</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2019 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">68</style></volume><pages><style face="normal" font="default" size="100%">547-551</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;Available data indicate that liver involvement is present in a significant proportion of children with celiac disease (CD) at the diagnosis (elevated transaminases 15%-57%, autoimmune liver disease 1%-2%). We sought to evaluate prevalence, clinical course, and risk factors for liver involvement in a large cohort of children with CD.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Children (age 0-18 years) diagnosed with CD from March 2010 to April 2016 were enrolled. Liver involvement was considered to be present when alanine transaminase (ALT) levels were &gt;40 U/L (hypertransaminasemia [HTS]). Patients with HTS were re-evaluated after at least 12 months of a gluten-free diet.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;CD was diagnosed in 806 patients during the study period; of these, ALT levels were available for 700 patients (86.9%), and were elevated in 27 (3.9%, HTS group); median ALT and aspartate transaminase levels in the HTS group were 57 U/L (interquartile range 49-80 U/L) and 67 U/L (interquartile range 53-85 U/L), respectively. Younger age, malabsorption symptoms, and low hemoglobin or ferritin were significantly more common in the HTS group at univariate analysis. At multivariate analysis, only age ≤4.27 years correlated with risk of liver involvement (odds ratio 3.73; 95% confidence interval: 1.61-8.66). When retested on a gluten-free diet, all but 3 patients normalized ALT levels; of these, 1 was diagnosed with sclerosing cholangitis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Liver involvement in celiac children is now less frequent than previously reported, possibly due to changing CD epidemiology. Younger age is the only risk factor. Associated autoimmune liver disease is rare.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30499881?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bellazzo, Arianna</style></author><author><style face="normal" font="default" size="100%">Di Minin, Giulio</style></author><author><style face="normal" font="default" size="100%">Valentino, Elena</style></author><author><style face="normal" font="default" size="100%">Sicari, Daria</style></author><author><style face="normal" font="default" size="100%">Torre, Denis</style></author><author><style face="normal" font="default" size="100%">Marchionni, Luigi</style></author><author><style face="normal" font="default" size="100%">Serpi, Federica</style></author><author><style face="normal" font="default" size="100%">Stadler, Michael B</style></author><author><style face="normal" font="default" size="100%">Taverna, Daniela</style></author><author><style face="normal" font="default" size="100%">Zuccolotto, Gaia</style></author><author><style face="normal" font="default" size="100%">Montagner, Isabella Monia</style></author><author><style face="normal" font="default" size="100%">Rosato, Antonio</style></author><author><style face="normal" font="default" size="100%">Tonon, Federica</style></author><author><style face="normal" font="default" size="100%">Zennaro, Cristina</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Mano, Miguel</style></author><author><style face="normal" font="default" size="100%">Del Sal, Giannino</style></author><author><style face="normal" font="default" size="100%">Collavin, Licio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cell-autonomous and cell non-autonomous downregulation of tumor suppressor DAB2IP by microRNA-149-3p promotes aggressiveness of cancer cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell Death Differ</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell Death Differ.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">1224-1238</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The tumor suppressor DAB2IP contributes to modulate the network of information established between cancer cells and tumor microenvironment. Epigenetic and post-transcriptional inactivation of this protein is commonly observed in multiple human malignancies, and can potentially favor progression of tumors driven by a variety of genetic mutations. Performing a high-throughput screening of a large collection of human microRNA mimics, we identified miR-149-3p as a negative post-transcriptional modulator of DAB2IP. By efficiently downregulating DAB2IP, this miRNA enhances cancer cell motility and invasiveness, facilitating activation of NF-kB signaling and promoting expression of pro-inflammatory and pro-angiogenic factors. In addition, we found that miR-149-3p secreted by prostate cancer cells induces DAB2IP downregulation in recipient vascular endothelial cells, stimulating their proliferation and motility, thus potentially remodeling the tumor microenvironment. Finally, we found that inhibition of endogenous miR-149-3p restores DAB2IP activity and efficiently reduces tumor growth and dissemination of malignant cells. These observations suggest that miR-149-3p can promote cancer progression via coordinated inhibition of DAB2IP in tumor cells and in stromal cells.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29568059?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bonin, Serena</style></author><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Sartori, Arianna</style></author><author><style face="normal" font="default" size="100%">Bratina, Alessio</style></author><author><style face="normal" font="default" size="100%">Manganotti, Paolo</style></author><author><style face="normal" font="default" size="100%">Trevisan, Giusto</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cerebrospinal Fluid Cytokine Expression Profile in Multiple Sclerosis and Chronic Inflammatory Demyelinating Polyneuropathy.</style></title><secondary-title><style face="normal" font="default" size="100%">Immunol Invest</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Immunol. Invest.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomarkers</style></keyword><keyword><style  face="normal" font="default" size="100%">Central Nervous System</style></keyword><keyword><style  face="normal" font="default" size="100%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Cell Growth Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-12</style></keyword><keyword><style  face="normal" font="default" size="100%">Lectins, C-Type</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Multiple Sclerosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Peripheral Nervous System</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyradiculoneuropathy, Chronic Inflammatory Demyelinating</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteins</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">135-145</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Cerebrospinal fluid (CSF) analysis in patients with particular neurologic disorders is a powerful tool to evaluate specific central nervous system inflammatory markers for diagnostic needs, because CSF represents the specific immune micro-environment to the central nervous system.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;CSF samples from 49 patients with multiple sclerosis (MS), chronic inflammatory demyelinating polyneuropathy (CIDP), and non-inflammatory neurologic disorders (NIND) as controls were submitted to protein expression profiles of 47 inflammatory biomarkers by multiplex Luminex bead assay to investigate possible differences in the inflammatory process for MS and CIDP.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Our results showed differences in CSF cytokine levels in MS and CIDP; in particular, IL12 (p40) was significantly highly expressed in MS in comparison with CIDP and NIND, while SDF-1α and SCGF-β were significantly highly expressed in CIDP cohort when compared to MS and NIND. IL-9, IL-13, and IL-17 had higher expression levels in NIND if compared with the other groups.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our study showed that, despite some common pathogenic mechanisms, central and peripheral nervous system demyelinating diseases, such as MS and CIDP, differ in some specific inflammatory soluble proteins in CSF, underlining differences in the immune response involved in those autoimmune diseases.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29182448?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fichera, A</style></author><author><style face="normal" font="default" size="100%">Pagani, G</style></author><author><style face="normal" font="default" size="100%">Stagnati, V</style></author><author><style face="normal" font="default" size="100%">Cascella, S</style></author><author><style face="normal" font="default" size="100%">Faiola, S</style></author><author><style face="normal" font="default" size="100%">Gaini, C</style></author><author><style face="normal" font="default" size="100%">Lanna, M</style></author><author><style face="normal" font="default" size="100%">Pasquini, L</style></author><author><style face="normal" font="default" size="100%">Raffaelli, R</style></author><author><style face="normal" font="default" size="100%">Stampalija, T</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Prefumo, F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cervical-length measurement in mid-gestation to predict spontaneous preterm birth in asymptomatic triplet pregnancy.</style></title><secondary-title><style face="normal" font="default" size="100%">Ultrasound Obstet Gynecol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ultrasound Obstet Gynecol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervical Length Measurement</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Logistic Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy, Triplet</style></keyword><keyword><style  face="normal" font="default" size="100%">Premature Birth</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">51</style></volume><pages><style face="normal" font="default" size="100%">614-620</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To assess the predictive value of sonographic cervical-length (CL) measurement in mid-gestation for spontaneous preterm birth (PTB) in asymptomatic triplet pregnancy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This was a retrospective study of asymptomatic triplet pregnancies followed at five Italian tertiary referral centers, between 2002 and 2015. CL was measured transvaginally between 18 and 24 weeks' gestation. Pregnancies with medically indicated PTB were excluded. Demographic and pregnancy characteristics of pregnancies complicated by PTB were analyzed and the distributions of CL measurements in these patients were calculated. Logistic regression analysis was performed to assess the association between CL and PTB, adjusted for confounders. Performance of CL measurement in prediction of PTB &lt; 28, &lt; 30 and &lt; 32 weeks of gestation was assessed.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;A total of 120 triplet pregnancies were included in the final analysis. Median CL was 35 (interquartile range (IQR), 29-40) mm measured at a median gestational age of 20 + 2 (IQR, 20 + 0 to 23 + 4) weeks. Overall, 23 (19.2%), 17 (14.2%) and eight (6.7%) patients had a CL &lt; 25, &lt; 20 and &lt; 15 mm, respectively. Spontaneous PTB &lt; 32 weeks occurred in 41 (34.2%) cases, &lt; 30 weeks in 23 (19.2%) and &lt; 28 weeks in 12 (10%) cases. CL &lt; 15 mm was significantly more frequent in the group of patients who delivered &lt; 28 (P = 0.03) and &lt; 30 (P = 0.01) weeks' gestation, compared with those who delivered after 28 and after 30 weeks, respectively, while CL &lt; 20 mm was more common in triplet pregnancies with delivery &lt; 32 weeks compared with those delivered ≥ 32 weeks (P = 0.03). Logistic regression analysis was possible only for PTB &lt; 32 weeks due to the small number of cases that delivered &lt; 30 and &lt; 28 weeks. After adjustment for confounders, CL was not significantly associated with PTB &lt; 32 weeks (adjusted odds ratio, 0.97; 95% CI, 0.94-1.01). CL measurement had an area under the receiver-operating characteristics curve of 0.41 (95% CI, 0.20-0.62), 0.41 (95% CI, 0.26-0.56) and 0.42 (95% CI, 0.31-0.54) for the prediction of spontaneous PTB &lt; 28, &lt; 30 and &lt; 32 weeks, respectively.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;CL assessed in mid-gestation is a poor predictor of PTB &lt; 28, &lt; 30 and &lt; 32 weeks' gestation in asymptomatic triplet pregnancy. Copyright © 2017 ISUOG. Published by John Wiley &amp; Sons Ltd.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28295801?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fontana, L</style></author><author><style face="normal" font="default" size="100%">Bedeschi, M F</style></author><author><style face="normal" font="default" size="100%">Maitz, S</style></author><author><style face="normal" font="default" size="100%">Cereda, A</style></author><author><style face="normal" font="default" size="100%">Faré, C</style></author><author><style face="normal" font="default" size="100%">Motta, S</style></author><author><style face="normal" font="default" size="100%">Seresini, A</style></author><author><style face="normal" font="default" size="100%">D'Ursi, P</style></author><author><style face="normal" font="default" size="100%">Orro, A</style></author><author><style face="normal" font="default" size="100%">Pecile, V</style></author><author><style face="normal" font="default" size="100%">Calvello, M</style></author><author><style face="normal" font="default" size="100%">Selicorni, A</style></author><author><style face="normal" font="default" size="100%">Lalatta, F</style></author><author><style face="normal" font="default" size="100%">Milani, D</style></author><author><style face="normal" font="default" size="100%">Sirchia, S M</style></author><author><style face="normal" font="default" size="100%">Miozzo, M</style></author><author><style face="normal" font="default" size="100%">Tabano, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Characterization of multi-locus imprinting disturbances and underlying genetic defects in patients with chromosome 11p15.5 related imprinting disorders.</style></title><secondary-title><style face="normal" font="default" size="100%">Epigenetics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Epigenetics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adaptor Proteins, Signal Transducing</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Beckwith-Wiedemann Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 15</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Methylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genomic Imprinting</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Kruppel-Like Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Silver-Russell Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">897-909</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The identification of multilocus imprinting disturbances (MLID) appears fundamental to uncover molecular pathways underlying imprinting disorders (IDs) and to complete clinical diagnosis of patients. However, MLID genetic associated mechanisms remain largely unknown. To characterize MLID in Beckwith-Wiedemann (BWS) and Silver-Russell (SRS) syndromes, we profiled by MassARRAY the methylation of 12 imprinted differentially methylated regions (iDMRs) in 21 BWS and 7 SRS patients with chromosome 11p15.5 epimutations. MLID was identified in 50% of BWS and 29% of SRS patients as a maternal hypomethylation syndrome. By next-generation sequencing, we searched for putative MLID-causative mutations in genes involved in methylation establishment/maintenance and found two novel missense mutations possibly causative of MLID: one in NLRP2, affecting ADP binding and protein activity, and one in ZFP42, likely leading to loss of DNA binding specificity. Both variants were paternally inherited. In silico protein modelling allowed to define the functional effect of these mutations. We found that MLID is very frequent in BWS/SRS. In addition, since MLID-BWS patients in our cohort show a peculiar pattern of BWS-associated clinical signs, MLID test could be important for a comprehensive clinical assessment. Finally, we highlighted the possible involvement of ZFP42 variants in MLID development and confirmed NLRP2 as causative locus in BWS-MLID.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30221575?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tamaro, Gianluca</style></author><author><style face="normal" font="default" size="100%">Pederiva, Federica</style></author><author><style face="normal" font="default" size="100%">Dibello, Daniela</style></author><author><style face="normal" font="default" size="100%">Gregori, Massimo</style></author><author><style face="normal" font="default" size="100%">Carbone, Marco</style></author><author><style face="normal" font="default" size="100%">Pantaleoni, Francesca</style></author><author><style face="normal" font="default" size="100%">Dentici, Maria Lisa</style></author><author><style face="normal" font="default" size="100%">Niceta, Marcello</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Child with Diminished Linear Growth and Waddling Gait.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Multiple</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Dwarfism</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gait</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteochondrodysplasias</style></keyword><keyword><style  face="normal" font="default" size="100%">Radiography</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 10</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">201</style></volume><pages><style face="normal" font="default" size="100%">297-297.e1</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29752176?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Grasso, Antonio G</style></author><author><style face="normal" font="default" size="100%">Granzotto, Marilena</style></author><author><style face="normal" font="default" size="100%">Zanon, Davide</style></author><author><style face="normal" font="default" size="100%">Maestro, Alessandra</style></author><author><style face="normal" font="default" size="100%">Loiacono, Stefano</style></author><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Complete Remission of a Refractory Acute Myeloid Leukemia with Myelodysplastic- and Monosomy 7-Related Changes after a Combined Conditioning Regimen of Plerixafor, Cytarabine and Melphalan in a 4-Year-Old Boy: A Case Report and Review of Literature.</style></title><secondary-title><style face="normal" font="default" size="100%">Cancers (Basel)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cancers (Basel)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Aug 27</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Acute myeloid leukemia with myelodysplastic changes and monosomy 7 is a rare form of pediatric leukemia associated with very poor disease-free survival. The refractoriness of the disease is due to the protection offered by the bone marrow niche, making leukemic stem cells impervious to whatever chemotherapy or myeloablative regimen is chosen. Using a mobilizing agent for haematopoietic stem cells, Plerixafor, could sensitise leukemic cells to the myeloablative therapy. This approach was not previously used in a pediatric population, and in adult populations, was used in combination with busulphan with no difference in overall survival. We describe the case of a 4-year-old boy affected by refractory acute myeloid leukemia with myelodysplastic changes and monosomy 7. The child had never achieved a remission. We proposed a combined time-scheduled scheme of therapy with plerixafor and melphalan. Combining pharmacokinetics of plerixafor with pharmacokinetics and rapid and elevated myeloablative potential of melphalan in high dosage (200 mg/m²), we succeeded in mobilizing more than 85% of stem blasts immediately before infusion of Melphalan. The count of residual blasts after 8 h from melphalan infusion was only 1.3 cells/μL. The child achieved an engraftment at day +32 with full donor chimerism. Sixteen months after haematopoietic stem cell transplantation (HSCT), he is well and in complete remission. Our case suggests that the use of plerixafor before a conditioning therapy with melphalan could induce remission in acute myeloid leukemia refractory to the usual conditioning therapy in pediatric patients. This work adds strength to the body of knowledge regarding the &quot;personalized&quot; conditioning regimen for high-risk leukemic patients.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30150522?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bernardi, Stella</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The Complex Interplay between Lipids, Immune System and Interleukins in Cardio-Metabolic Diseases.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int J Mol Sci</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiovascular Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypolipidemic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Immune System</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukins</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipid Metabolism</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipids</style></keyword><keyword><style  face="normal" font="default" size="100%">Metabolic Diseases</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Dec 14</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">19</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Lipids and inflammation regulate each other. Early studies on this topic focused on the systemic effects that the acute inflammatory response-and interleukins-had on lipid metabolism. Today, in the era of the obesity epidemic, whose primary complications are cardio-metabolic diseases, attention has moved to the effects that the nutritional environment and lipid derangements have on peripheral tissues, where lipotoxicity leads to organ damage through an imbalance of chronic inflammatory responses. After an overview of the effects that acute inflammation has on the systemic lipid metabolism, this review will describe the lipid-induced immune responses that take place in peripheral tissues and lead to chronic cardio-metabolic diseases. Moreover, the anti-inflammatory effects of lipid lowering drugs, as well as the possibility of using anti-inflammatory agents against cardio-metabolic diseases, will be discussed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30558209?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Miceli Sopo, S</style></author><author><style face="normal" font="default" size="100%">Romano, A</style></author><author><style face="normal" font="default" size="100%">Bersani, G</style></author><author><style face="normal" font="default" size="100%">Fantacci, C</style></author><author><style face="normal" font="default" size="100%">Badina, L</style></author><author><style face="normal" font="default" size="100%">Longo, G</style></author><author><style face="normal" font="default" size="100%">Monti, G</style></author><author><style face="normal" font="default" size="100%">Viola, S</style></author><author><style face="normal" font="default" size="100%">Tripodi, S</style></author><author><style face="normal" font="default" size="100%">Barilaro, G</style></author><author><style face="normal" font="default" size="100%">Iacono, I D</style></author><author><style face="normal" font="default" size="100%">Caffarelli, C</style></author><author><style face="normal" font="default" size="100%">Mastrorilli, C</style></author><author><style face="normal" font="default" size="100%">Barni, S</style></author><author><style face="normal" font="default" size="100%">Mori, F</style></author><author><style face="normal" font="default" size="100%">Liotti, L</style></author><author><style face="normal" font="default" size="100%">Cuomo, B</style></author><author><style face="normal" font="default" size="100%">Franceschini, F</style></author><author><style face="normal" font="default" size="100%">Viggiano, D</style></author><author><style face="normal" font="default" size="100%">Monaco, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cooking influence in tolerance acquisition in egg-induced acute food protein enterocolitis syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">Allergol Immunopathol (Madr)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Allergol Immunopathol (Madr)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Oct 10</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Few studies on the age of resolution of Food Protein Induced Enterocolitis Syndrome (FPIES) induced by solid foods are available. In particular, for FPIES induced by egg, the mean age of tolerance acquisition reported in the literature ranges from 42 to 63 months.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;We have assessed whether the age of tolerance acquisition in acute egg FPIES varies depending on whether the egg is cooked or raw.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We conducted a retrospective and multicentric study of children with diagnosis of acute egg FPIES seen in 10 Italian allergy units between July 2003 and October 2017. The collected data regarded sex, presence of other allergic diseases, age of onset of symptoms, kind and severity of symptoms, cooking technique of the ingested egg, outcome of the allergy test, age of tolerance acquisition.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Sixty-one children with acute egg FPIES were enrolled, 34 (56%) males and 27 (44%) females. Tolerance to cooked egg has been demonstrated by 47/61 (77%) children at a mean age of 30.2 months. For 32 of them, tolerance to raw egg has been demonstrated at a mean age of 43.9 months. No episodes of severe adverse reaction after baked egg ingestion have been recorded.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;It is possible to perform an OFC with baked egg, to verify the possible acquisition of tolerance, at about 30 months of life in children with acute egg FPIES.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30316559?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fetoni, Anna Rita</style></author><author><style face="normal" font="default" size="100%">Zorzi, Veronica</style></author><author><style face="normal" font="default" size="100%">Paciello, Fabiola</style></author><author><style face="normal" font="default" size="100%">Ziraldo, Gaia</style></author><author><style face="normal" font="default" size="100%">Peres, Chiara</style></author><author><style face="normal" font="default" size="100%">Raspa, Marcello</style></author><author><style face="normal" font="default" size="100%">Scavizzi, Ferdinando</style></author><author><style face="normal" font="default" size="100%">Salvatore, Anna Maria</style></author><author><style face="normal" font="default" size="100%">Crispino, Giulia</style></author><author><style face="normal" font="default" size="100%">Tognola, Gabriella</style></author><author><style face="normal" font="default" size="100%">Gentile, Giulia</style></author><author><style face="normal" font="default" size="100%">Spampinato, Antonio Gianmaria</style></author><author><style face="normal" font="default" size="100%">Cuccaro, Denis</style></author><author><style face="normal" font="default" size="100%">Guarnaccia, Maria</style></author><author><style face="normal" font="default" size="100%">Morello, Giovanna</style></author><author><style face="normal" font="default" size="100%">Van Camp, Guy</style></author><author><style face="normal" font="default" size="100%">Fransen, Erik</style></author><author><style face="normal" font="default" size="100%">Brumat, Marco</style></author><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author><author><style face="normal" font="default" size="100%">Paludetti, Gaetano</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Cavallaro, Sebastiano</style></author><author><style face="normal" font="default" size="100%">Mammano, Fabio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cx26 partial loss causes accelerated presbycusis by redox imbalance and dysregulation of Nfr2 pathway.</style></title><secondary-title><style face="normal" font="default" size="100%">Redox Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Redox Biol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Connexin 26</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Deletion</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">NF-E2-Related Factor 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Presbycusis</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 10</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">301-317</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Mutations in GJB2, the gene that encodes connexin 26 (Cx26), are the most common cause of sensorineural hearing impairment. The truncating variant 35delG, which determines a complete loss of Cx26 protein function, is the prevalent GJB2 mutation in several populations. Here, we generated and analyzed Gjb2 mice as a model of heterozygous human carriers of 35delG. Compared to control mice, auditory brainstem responses (ABRs) and distortion product otoacoustic emissions (DPOAEs) worsened over time more rapidly in Gjb2 mice, indicating they were affected by accelerated age-related hearing loss (ARHL), or presbycusis. We linked causally the auditory phenotype of Gjb2 mice to apoptosis and oxidative damage in the cochlear duct, reduced release of glutathione from connexin hemichannels, decreased nutrient delivery to the sensory epithelium via cochlear gap junctions and deregulated expression of genes that are under transcriptional control of the nuclear factor erythroid 2-related factor 2 (Nrf2), a pivotal regulator of tolerance to redox stress. Moreover, a statistically significant genome-wide association with two genes (PRKCE and TGFB1) related to the Nrf2 pathway (p-value &lt; 4 × 10) was detected in a very large cohort of 4091 individuals, originating from Europe, Caucasus and Central Asia, with hearing phenotype (including 1076 presbycusis patients and 1290 healthy matched controls). We conclude that (i) elements of the Nrf2 pathway are essential for hearing maintenance and (ii) their dysfunction may play an important role in the etiopathogenesis of human presbycusis.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30199819?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Campisciano, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Scrimin, Federica</style></author><author><style face="normal" font="default" size="100%">Blendi, Ura</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Vincenti, Ezio</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cytokine profiles of women with vulvodynia: Identification of a panel of pro-inflammatory molecular targets.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Obstet Gynecol Reprod Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Obstet. Gynecol. Reprod. Biol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Vaginal Smears</style></keyword><keyword><style  face="normal" font="default" size="100%">Vulva</style></keyword><keyword><style  face="normal" font="default" size="100%">Vulvodynia</style></keyword><keyword><style  face="normal" font="default" size="100%">Women's Health</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">226</style></volume><pages><style face="normal" font="default" size="100%">66-70</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;The vulvar pain syndrome (VPS) is a multifactorial disease severely influencing the lifestyle of affected women. Among possible etiological factors, local injury, peripheral and/or central sensitization of the nervous system, and a chronic inflammatory status have been positively associated with the development of VPS. The identification of a constitutive altered local inflammatory profile in VPS women may represent an important point in the characterization of patients' phenotype as a useful marker influencing the vulvar micro-environment. The aim of this study was to investigative the possible role of the local cytokines production in women with VPS in comparison to healthy women.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;In this study were collected vaginal swabs from 57 healthy women (HC) who never suffered from VPS and from 30 patients diagnosed with vulvodynia (VPS) by at least 3 years and currently symptomatic. All patients included in this study showed the absence of Sexually Transmitted (STD) diseases and Reproductive Tract Infection. Real-time PCR was performed to assess the genomic sequences of ST pathogens. The Luminex Bio-Plex platform was used for the analysis of a panel of 48 immune factors.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Eleven molecules, specifically involved in the pro-inflammatory pathway were significantly modulated in VPS patients in comparison to healthy women, suggesting a persistent inflammatory process.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Therefore, these inflammatory factors could be possible biological markers involved in this disease. Nevertheless, other studies are needed to consider this specific immune profile as a valid marker of the vulvodynia.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29852336?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Paviotti, G</style></author><author><style face="normal" font="default" size="100%">Todero, S</style></author><author><style face="normal" font="default" size="100%">Demarini, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cardiac output decreases and systemic vascular resistance increases in newborns placed in the left-lateral position.</style></title><secondary-title><style face="normal" font="default" size="100%">J Perinatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Perinatol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Blood Pressure</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiac Output</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Rate</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Low Birth Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Premature</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Posture</style></keyword><keyword><style  face="normal" font="default" size="100%">Stroke Volume</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Resistance</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">37</style></volume><pages><style face="normal" font="default" size="100%">563-565</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;The objective of the study was to study the effect of short-term left-lateral position on cardiovascular parameters in hemodynamically stable newborns.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;Cardiac output (CO), stroke volume (SV), systemic vascular resistance index (SVRI) and heart rate (HR) were measured by electric velocimetry in hemodynamically stable newborns without respiratory support in the supine, left-lateral and back-to-supine positions, each kept for 10 min.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Thirty-two newborns were enrolled, birth weight 2134 (1818 to 2460) g, gestational age 34.5±2.4 weeks. CO and SV decreased significantly from supine to left-lateral position (CO supine: 193.4 (168.0 to 229.6) ml kgmin; CO left-lateral: 172.0 (154.9 to 201.6) ml kgmin, P&lt;0.0001; SV supine: 3.0 (2.7 to 4.0) ml; SV left-lateral: 2.7 (2.4 to 3.2) ml, P&lt;0.0004). Conversely, SVRI increased in left-lateral position: SVRI supine: 18865±9244 dyns cm m; SVRI left-lateral: 21203±10059 dyns cm m, P&lt;0.0001). All variables returned to the initial value when infants were back in the supine position. HR and blood pressure did not change.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;In stable infants, CO and SV decrease and SVRI increases, in left-lateral position.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28079876?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Toson, Bruno</style></author><author><style face="normal" font="default" size="100%">Dos Santos, Eduardo José</style></author><author><style face="normal" font="default" size="100%">Adelino, José Eduardo</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, Paula</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Louzada-Júnior, Paulo</style></author><author><style face="normal" font="default" size="100%">Oliveira, Renê Donizete Ribeiro</style></author><author><style face="normal" font="default" size="100%">Pedroza, Larysse Santa Rosa Aquino</style></author><author><style face="normal" font="default" size="100%">de Fátima Lobato Cunha Sauma, Maria</style></author><author><style face="normal" font="default" size="100%">de Lima, Clayton Pereira Silva</style></author><author><style face="normal" font="default" size="100%">Barbosa, Fabiola Brasil</style></author><author><style face="normal" font="default" size="100%">Brenol, Claiton Viegas</style></author><author><style face="normal" font="default" size="100%">Xavier, Ricardo Machado</style></author><author><style face="normal" font="default" size="100%">Chies, José Artur Bogo</style></author><author><style face="normal" font="default" size="100%">Veit, Tiago Degani</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CCR5Δ32 and the genetic susceptibility to rheumatoid arthritis in admixed populations: a multicentre study.</style></title><secondary-title><style face="normal" font="default" size="100%">Rheumatology (Oxford)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Rheumatology (Oxford)</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arthritis, Rheumatoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Consanguinity</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, CCR5</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 03 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">56</style></volume><pages><style face="normal" font="default" size="100%">495-497</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28082621?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Alfirevic, Zarko</style></author><author><style face="normal" font="default" size="100%">Stampalija, Tamara</style></author><author><style face="normal" font="default" size="100%">Medley, Nancy</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cervical stitch (cerclage) for preventing preterm birth in singleton pregnancy.</style></title><secondary-title><style face="normal" font="default" size="100%">Cochrane Database Syst Rev</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cochrane Database Syst Rev</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Administration, Intravaginal</style></keyword><keyword><style  face="normal" font="default" size="100%">Cerclage, Cervical</style></keyword><keyword><style  face="normal" font="default" size="100%">Cesarean Section</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Injections, Intramuscular</style></keyword><keyword><style  face="normal" font="default" size="100%">Perinatal Death</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Premature Birth</style></keyword><keyword><style  face="normal" font="default" size="100%">Progesterone</style></keyword><keyword><style  face="normal" font="default" size="100%">Randomized Controlled Trials as Topic</style></keyword><keyword><style  face="normal" font="default" size="100%">Stillbirth</style></keyword><keyword><style  face="normal" font="default" size="100%">Suture Techniques</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 06 06</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">CD008991</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Cervical cerclage is a well-known surgical procedure carried out during pregnancy. It involves positioning of a suture (stitch) around the neck of the womb (cervix), aiming to give mechanical support to the cervix and thereby reduce risk of preterm birth. The effectiveness and safety of this procedure remains controversial. This is an update of a review last published in 2012.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;To assess whether the use of cervical stitch in singleton pregnancy at high risk of pregnancy loss based on woman's history and/or ultrasound finding of 'short cervix' and/or physical exam improves subsequent obstetric care and fetal outcome.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SEARCH METHODS: &lt;/b&gt;We searched Cochrane Pregnancy and Childbirth's Trials Register (30 June 2016) and reference lists of identified studies.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SELECTION CRITERIA: &lt;/b&gt;We included all randomised trials of cervical suturing in singleton pregnancies. Cervical stitch was carried out when the pregnancy was considered to be of sufficiently high risk due to a woman's history, a finding of short cervix on ultrasound or other indication determined by physical exam. We included any study that compared cerclage with either no treatment or any alternative intervention. We planned to include cluster-randomised studies but not cross-over trials. We excluded quasi-randomised studies. We included studies reported in abstract form only.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DATA COLLECTION AND ANALYSIS: &lt;/b&gt;Three review authors independently assessed trials for inclusion. Two review authors independently assessed risk of bias and extracted data. We resolved discrepancies by discussion. Data were checked for accuracy. The quality of the evidence was assessed using the GRADE approach.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MAIN RESULTS: &lt;/b&gt;This updated review includes a total of 15 trials (3490 women); three trials were added for this update (152 women). Cerclage versus no cerclageOverall, cerclage probably leads to a reduced risk of perinatal death when compared with no cerclage, although the confidence interval (CI) crosses the line of no effect (RR 0.82, 95% CI 0.65 to 1.04; 10 studies, 2927 women; moderate quality evidence). Considering stillbirths and neonatal deaths separately reduced the numbers of events and sample size. Although the relative effect of cerclage is similar, estimates were less reliable with fewer data and assessed as of low quality (stillbirths RR 0.89, 95% CI 0.45 to 1.75; 5 studies, 1803 women; low quality evidence; neonatal deaths before discharge RR 0.85, 95% CI 0.53 to 1.39; 6 studies, 1714 women; low quality evidence). Serious neonatal morbidity was similar with and without cerclage (RR 0.80, 95% CI 0.55 to 1.18; 6 studies, 883 women; low-quality evidence). Pregnant women with and without cerclage were equally likely to have a baby discharged home healthy (RR 1.02, 95% CI 0.97 to 1.06; 4 studies, 657 women; moderate quality evidence).Pregnant women with cerclage were less likely to have preterm births compared to controls before 37, 34 (average RR 0.77, 95% CI 0.66 to 0.89; 9 studies, 2415 women; high quality evidence) and 28 completed weeks of gestation.Five subgroups based on clinical indication provided data for analysis (history-indicated; short cervix based on one-off ultrasound in high risk women; short cervix found by serial scans in high risk women; physical exam-indicated; and short cervix found on scan in low risk or mixed populations). There were too few trials in these clinical subgroups to make meaningful conclusions and no evidence of differential effects. Cerclage versus progesteroneTwo trials (129 women) compared cerclage to prevention with vaginal progesterone in high risk women with short cervix on ultrasound; these trials were too small to detect reliable, clinically important differences for any review outcome. One included trial compared cerclage with intramuscular progesterone (75 women) which lacked power to detect group differences. History indicated cerclage versus ultrasound indicated cerclageEvidence from two trials (344 women) was too limited to establish differences for clinically important outcomes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;AUTHORS' CONCLUSIONS: &lt;/b&gt;Cervical cerclage reduces the risk of preterm birth in women at high-risk of preterm birth and probably reduces risk of perinatal deaths. There was no evidence of any differential effect of cerclage based on previous obstetric history or short cervix indications, but data were limited for all clinical groups. The question of whether cerclage is more or less effective than other preventative treatments, particularly vaginal progesterone, remains unanswered.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28586127?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Kassebaum, Nicholas</style></author><author><style face="normal" font="default" size="100%">Kyu, Hmwe Hmwe</style></author><author><style face="normal" font="default" size="100%">Zoeckler, Leo</style></author><author><style face="normal" font="default" size="100%">Olsen, Helen Elizabeth</style></author><author><style face="normal" font="default" size="100%">Thomas, Katie</style></author><author><style face="normal" font="default" size="100%">Pinho, Christine</style></author><author><style face="normal" font="default" size="100%">Bhutta, Zulfiqar A</style></author><author><style face="normal" font="default" size="100%">Dandona, Lalit</style></author><author><style face="normal" font="default" size="100%">Ferrari, Alize</style></author><author><style face="normal" font="default" size="100%">Ghiwot, Tsegaye Tewelde</style></author><author><style face="normal" font="default" size="100%">Hay, Simon I</style></author><author><style face="normal" font="default" size="100%">Kinfu, Yohannes</style></author><author><style face="normal" font="default" size="100%">Liang, Xiaofeng</style></author><author><style face="normal" font="default" size="100%">Lopez, Alan</style></author><author><style face="normal" font="default" size="100%">Malta, Deborah Carvalho</style></author><author><style face="normal" font="default" size="100%">Mokdad, Ali H</style></author><author><style face="normal" font="default" size="100%">Naghavi, Mohsen</style></author><author><style face="normal" font="default" size="100%">Patton, George C</style></author><author><style face="normal" font="default" size="100%">Salomon, Joshua</style></author><author><style face="normal" font="default" size="100%">Sartorius, Benn</style></author><author><style face="normal" font="default" size="100%">Topor-Madry, Roman</style></author><author><style face="normal" font="default" size="100%">Vollset, Stein Emil</style></author><author><style face="normal" font="default" size="100%">Werdecker, Andrea</style></author><author><style face="normal" font="default" size="100%">Whiteford, Harvey A</style></author><author><style face="normal" font="default" size="100%">Abate, Kalkidan Hasen</style></author><author><style face="normal" font="default" size="100%">Abbas, Kaja</style></author><author><style face="normal" font="default" size="100%">Damtew, Solomon Abrha</style></author><author><style face="normal" font="default" size="100%">Ahmed, Muktar Beshir</style></author><author><style face="normal" font="default" size="100%">Akseer, Nadia</style></author><author><style face="normal" font="default" size="100%">Al-Raddadi, Rajaa</style></author><author><style face="normal" font="default" size="100%">Alemayohu, Mulubirhan Assefa</style></author><author><style face="normal" font="default" size="100%">Altirkawi, Khalid</style></author><author><style face="normal" font="default" size="100%">Abajobir, Amanuel Alemu</style></author><author><style face="normal" font="default" size="100%">Amare, Azmeraw T</style></author><author><style face="normal" font="default" size="100%">Antonio, Carl A T</style></author><author><style face="normal" font="default" size="100%">Arnlöv, Johan</style></author><author><style face="normal" font="default" size="100%">Artaman, Al</style></author><author><style face="normal" font="default" size="100%">Asayesh, Hamid</style></author><author><style face="normal" font="default" size="100%">Avokpaho, Euripide Frinel G Arthur</style></author><author><style face="normal" font="default" size="100%">Awasthi, Ashish</style></author><author><style face="normal" font="default" size="100%">Ayala Quintanilla, Beatriz Paulina</style></author><author><style face="normal" font="default" size="100%">Bacha, Umar</style></author><author><style face="normal" font="default" size="100%">Betsu, Balem Demtsu</style></author><author><style face="normal" font="default" size="100%">Barac, Aleksandra</style></author><author><style face="normal" font="default" size="100%">Bärnighausen, Till Winfried</style></author><author><style face="normal" font="default" size="100%">Baye, Estifanos</style></author><author><style face="normal" font="default" size="100%">Bedi, Neeraj</style></author><author><style face="normal" font="default" size="100%">Bensenor, Isabela M</style></author><author><style face="normal" font="default" size="100%">Berhane, Adugnaw</style></author><author><style face="normal" font="default" size="100%">Bernabe, Eduardo</style></author><author><style face="normal" font="default" size="100%">Bernal, Oscar Alberto</style></author><author><style face="normal" font="default" size="100%">Beyene, Addisu Shunu</style></author><author><style face="normal" font="default" size="100%">Biadgilign, Sibhatu</style></author><author><style face="normal" font="default" size="100%">Bikbov, Boris</style></author><author><style face="normal" font="default" size="100%">Boyce, Cheryl Anne</style></author><author><style face="normal" font="default" size="100%">Brazinova, Alexandra</style></author><author><style face="normal" font="default" size="100%">Hailu, Gessessew Bugssa</style></author><author><style face="normal" font="default" size="100%">Carter, Austin</style></author><author><style face="normal" font="default" size="100%">Castañeda-Orjuela, Carlos A</style></author><author><style face="normal" font="default" size="100%">Catalá-López, Ferrán</style></author><author><style face="normal" font="default" size="100%">Charlson, Fiona J</style></author><author><style face="normal" font="default" size="100%">Chitheer, Abdulaal A</style></author><author><style face="normal" font="default" size="100%">Choi, Jee-Young Jasmine</style></author><author><style face="normal" font="default" size="100%">Ciobanu, Liliana G</style></author><author><style face="normal" font="default" size="100%">Crump, John</style></author><author><style face="normal" font="default" size="100%">Dandona, Rakhi</style></author><author><style face="normal" font="default" size="100%">Dellavalle, Robert P</style></author><author><style face="normal" font="default" size="100%">Deribew, Amare</style></author><author><style face="normal" font="default" size="100%">deVeber, Gabrielle</style></author><author><style face="normal" font="default" size="100%">Dicker, Daniel</style></author><author><style face="normal" font="default" size="100%">Ding, Eric L</style></author><author><style face="normal" font="default" size="100%">Dubey, Manisha</style></author><author><style face="normal" font="default" size="100%">Endries, Amanuel Yesuf</style></author><author><style face="normal" font="default" size="100%">Erskine, Holly E</style></author><author><style face="normal" font="default" size="100%">Faraon, Emerito Jose Aquino</style></author><author><style face="normal" font="default" size="100%">Faro, Andre</style></author><author><style face="normal" font="default" size="100%">Farzadfar, Farshad</style></author><author><style face="normal" font="default" size="100%">Fernandes, Joao C</style></author><author><style face="normal" font="default" size="100%">Fijabi, Daniel Obadare</style></author><author><style face="normal" font="default" size="100%">Fitzmaurice, Christina</style></author><author><style face="normal" font="default" size="100%">Fleming, Thomas D</style></author><author><style face="normal" font="default" size="100%">Flor, Luisa Sorio</style></author><author><style face="normal" font="default" size="100%">Foreman, Kyle J</style></author><author><style face="normal" font="default" size="100%">Franklin, Richard C</style></author><author><style face="normal" font="default" size="100%">Fraser, Maya S</style></author><author><style face="normal" font="default" size="100%">Frostad, Joseph J</style></author><author><style face="normal" font="default" size="100%">Fullman, Nancy</style></author><author><style face="normal" font="default" size="100%">Gebregergs, Gebremedhin Berhe</style></author><author><style face="normal" font="default" size="100%">Gebru, Alemseged Aregay</style></author><author><style face="normal" font="default" size="100%">Geleijnse, Johanna M</style></author><author><style face="normal" font="default" size="100%">Gibney, Katherine B</style></author><author><style face="normal" font="default" size="100%">Gidey Yihdego, Mahari</style></author><author><style face="normal" font="default" size="100%">Ginawi, Ibrahim Abdelmageem Mohamed</style></author><author><style face="normal" font="default" size="100%">Gishu, Melkamu Dedefo</style></author><author><style face="normal" font="default" size="100%">Gizachew, Tessema Assefa</style></author><author><style face="normal" font="default" size="100%">Glaser, Elizabeth</style></author><author><style face="normal" font="default" size="100%">Gold, Audra L</style></author><author><style face="normal" font="default" size="100%">Goldberg, Ellen</style></author><author><style face="normal" font="default" size="100%">Gona, Philimon</style></author><author><style face="normal" font="default" size="100%">Goto, Atsushi</style></author><author><style face="normal" font="default" size="100%">Gugnani, Harish Chander</style></author><author><style face="normal" font="default" size="100%">Jiang, Guohong</style></author><author><style face="normal" font="default" size="100%">Gupta, Rajeev</style></author><author><style face="normal" font="default" size="100%">Tesfay, Fisaha Haile</style></author><author><style face="normal" font="default" size="100%">Hankey, Graeme J</style></author><author><style face="normal" font="default" size="100%">Havmoeller, Rasmus</style></author><author><style face="normal" font="default" size="100%">Hijar, Martha</style></author><author><style face="normal" font="default" size="100%">Horino, Masako</style></author><author><style face="normal" font="default" size="100%">Hosgood, H Dean</style></author><author><style face="normal" font="default" size="100%">Hu, Guoqing</style></author><author><style face="normal" font="default" size="100%">Jacobsen, Kathryn H</style></author><author><style face="normal" font="default" size="100%">Jakovljevic, Mihajlo B</style></author><author><style face="normal" font="default" size="100%">Jayaraman, Sudha P</style></author><author><style face="normal" font="default" size="100%">Jha, Vivekanand</style></author><author><style face="normal" font="default" size="100%">Jibat, Tariku</style></author><author><style face="normal" font="default" size="100%">Johnson, Catherine O</style></author><author><style face="normal" font="default" size="100%">Jonas, Jost</style></author><author><style face="normal" font="default" size="100%">Kasaeian, Amir</style></author><author><style face="normal" font="default" size="100%">Kawakami, Norito</style></author><author><style face="normal" font="default" size="100%">Keiyoro, Peter N</style></author><author><style face="normal" font="default" size="100%">Khalil, Ibrahim</style></author><author><style face="normal" font="default" size="100%">Khang, Young-Ho</style></author><author><style face="normal" font="default" size="100%">Khubchandani, Jagdish</style></author><author><style face="normal" font="default" size="100%">Ahmad Kiadaliri, Aliasghar A</style></author><author><style face="normal" font="default" size="100%">Kieling, Christian</style></author><author><style face="normal" font="default" size="100%">Kim, Daniel</style></author><author><style face="normal" font="default" size="100%">Kissoon, Niranjan</style></author><author><style face="normal" font="default" size="100%">Knibbs, Luke D</style></author><author><style face="normal" font="default" size="100%">Koyanagi, Ai</style></author><author><style face="normal" font="default" size="100%">Krohn, Kristopher J</style></author><author><style face="normal" font="default" size="100%">Kuate Defo, Barthelemy</style></author><author><style face="normal" font="default" size="100%">Kucuk Bicer, Burcu</style></author><author><style face="normal" font="default" size="100%">Kulikoff, Rachel</style></author><author><style face="normal" font="default" size="100%">Kumar, G Anil</style></author><author><style face="normal" font="default" size="100%">Lal, Dharmesh Kumar</style></author><author><style face="normal" font="default" size="100%">Lam, Hilton Y</style></author><author><style face="normal" font="default" size="100%">Larson, Heidi J</style></author><author><style face="normal" font="default" size="100%">Larsson, Anders</style></author><author><style face="normal" font="default" size="100%">Laryea, Dennis Odai</style></author><author><style face="normal" font="default" size="100%">Leung, Janni</style></author><author><style face="normal" font="default" size="100%">Lim, Stephen S</style></author><author><style face="normal" font="default" size="100%">Lo, Loon-Tzian</style></author><author><style face="normal" font="default" size="100%">Lo, Warren D</style></author><author><style face="normal" font="default" size="100%">Looker, Katharine J</style></author><author><style face="normal" font="default" size="100%">Lotufo, Paulo A</style></author><author><style face="normal" font="default" size="100%">Magdy Abd El Razek, Hassan</style></author><author><style face="normal" font="default" size="100%">Malekzadeh, Reza</style></author><author><style face="normal" font="default" size="100%">Markos Shifti, Desalegn</style></author><author><style face="normal" font="default" size="100%">Mazidi, Mohsen</style></author><author><style face="normal" font="default" size="100%">Meaney, Peter A</style></author><author><style face="normal" font="default" size="100%">Meles, Kidanu Gebremariam</style></author><author><style face="normal" font="default" size="100%">Memiah, Peter</style></author><author><style face="normal" font="default" size="100%">Mendoza, Walter</style></author><author><style face="normal" font="default" size="100%">Abera Mengistie, Mubarek</style></author><author><style face="normal" font="default" size="100%">Mengistu, Gebremichael Welday</style></author><author><style face="normal" font="default" size="100%">Mensah, George A</style></author><author><style face="normal" font="default" size="100%">Miller, Ted R</style></author><author><style face="normal" font="default" size="100%">Mock, Charles</style></author><author><style face="normal" font="default" size="100%">Mohammadi, Alireza</style></author><author><style face="normal" font="default" size="100%">Mohammed, Shafiu</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Mueller, Ulrich</style></author><author><style face="normal" font="default" size="100%">Nagata, Chie</style></author><author><style face="normal" font="default" size="100%">Naheed, Aliya</style></author><author><style face="normal" font="default" size="100%">Nguyen, Grant</style></author><author><style face="normal" font="default" size="100%">Nguyen, Quyen Le</style></author><author><style face="normal" font="default" size="100%">Nsoesie, Elaine</style></author><author><style face="normal" font="default" size="100%">Oh, In-Hwan</style></author><author><style face="normal" font="default" size="100%">Okoro, Anselm</style></author><author><style face="normal" font="default" size="100%">Olusanya, Jacob Olusegun</style></author><author><style face="normal" font="default" size="100%">Olusanya, Bolajoko O</style></author><author><style face="normal" font="default" size="100%">Ortiz, Alberto</style></author><author><style face="normal" font="default" size="100%">Paudel, Deepak</style></author><author><style face="normal" font="default" size="100%">Pereira, David M</style></author><author><style face="normal" font="default" size="100%">Perico, Norberto</style></author><author><style face="normal" font="default" size="100%">Petzold, Max</style></author><author><style face="normal" font="default" size="100%">Phillips, Michael Robert</style></author><author><style face="normal" font="default" size="100%">Polanczyk, Guilherme V</style></author><author><style face="normal" font="default" size="100%">Pourmalek, Farshad</style></author><author><style face="normal" font="default" size="100%">Qorbani, Mostafa</style></author><author><style face="normal" font="default" size="100%">Rafay, Anwar</style></author><author><style face="normal" font="default" size="100%">Rahimi-Movaghar, Vafa</style></author><author><style face="normal" font="default" size="100%">Rahman, Mahfuzar</style></author><author><style face="normal" font="default" size="100%">Rai, Rajesh Kumar</style></author><author><style face="normal" font="default" size="100%">Ram, Usha</style></author><author><style face="normal" font="default" size="100%">Rankin, Zane</style></author><author><style face="normal" font="default" size="100%">Remuzzi, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Renzaho, Andre M N</style></author><author><style face="normal" font="default" size="100%">Roba, Hirbo Shore</style></author><author><style face="normal" font="default" size="100%">Rojas-Rueda, David</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Sagar, Rajesh</style></author><author><style face="normal" font="default" size="100%">Sanabria, Juan Ramon</style></author><author><style face="normal" font="default" size="100%">Kedir Mohammed, Muktar Sano</style></author><author><style face="normal" font="default" size="100%">Santos, Itamar S</style></author><author><style face="normal" font="default" size="100%">Satpathy, Maheswar</style></author><author><style face="normal" font="default" size="100%">Sawhney, Monika</style></author><author><style face="normal" font="default" size="100%">Schöttker, Ben</style></author><author><style face="normal" font="default" size="100%">Schwebel, David C</style></author><author><style face="normal" font="default" size="100%">Scott, James G</style></author><author><style face="normal" font="default" size="100%">Sepanlou, Sadaf G</style></author><author><style face="normal" font="default" size="100%">Shaheen, Amira</style></author><author><style face="normal" font="default" size="100%">Shaikh, Masood Ali</style></author><author><style face="normal" font="default" size="100%">She, June</style></author><author><style face="normal" font="default" size="100%">Shiri, Rahman</style></author><author><style face="normal" font="default" size="100%">Shiue, Ivy</style></author><author><style face="normal" font="default" size="100%">Sigfusdottir, Inga Dora</style></author><author><style face="normal" font="default" size="100%">Singh, Jasvinder</style></author><author><style face="normal" font="default" size="100%">Silpakit, Naris</style></author><author><style face="normal" font="default" size="100%">Smith, Alison</style></author><author><style face="normal" font="default" size="100%">Sreeramareddy, Chandrashekhar</style></author><author><style face="normal" font="default" size="100%">Stanaway, Jeffrey D</style></author><author><style face="normal" font="default" size="100%">Stein, Dan J</style></author><author><style face="normal" font="default" size="100%">Steiner, Caitlyn</style></author><author><style face="normal" font="default" size="100%">Sufiyan, Muawiyyah Babale</style></author><author><style face="normal" font="default" size="100%">Swaminathan, Soumya</style></author><author><style face="normal" font="default" size="100%">Tabarés-Seisdedos, Rafael</style></author><author><style face="normal" font="default" size="100%">Tabb, Karen M</style></author><author><style face="normal" font="default" size="100%">Tadese, Fentaw</style></author><author><style face="normal" font="default" size="100%">Tavakkoli, Mohammad</style></author><author><style face="normal" font="default" size="100%">Taye, Bineyam</style></author><author><style face="normal" font="default" size="100%">Teeple, Stephanie</style></author><author><style face="normal" font="default" size="100%">Tegegne, Teketo Kassaw</style></author><author><style face="normal" font="default" size="100%">Temam Shifa, Girma</style></author><author><style face="normal" font="default" size="100%">Terkawi, Abdullah Sulieman</style></author><author><style face="normal" font="default" size="100%">Thomas, Bernadette</style></author><author><style face="normal" font="default" size="100%">Thomson, Alan J</style></author><author><style face="normal" font="default" size="100%">Tobe-Gai, Ruoyan</style></author><author><style face="normal" font="default" size="100%">Tonelli, Marcello</style></author><author><style face="normal" font="default" size="100%">Tran, Bach Xuan</style></author><author><style face="normal" font="default" size="100%">Troeger, Christopher</style></author><author><style face="normal" font="default" size="100%">Ukwaja, Kingsley N</style></author><author><style face="normal" font="default" size="100%">Uthman, Olalekan</style></author><author><style face="normal" font="default" size="100%">Vasankari, Tommi</style></author><author><style face="normal" font="default" size="100%">Venketasubramanian, Narayanaswamy</style></author><author><style face="normal" font="default" size="100%">Vlassov, Vasiliy Victorovich</style></author><author><style face="normal" font="default" size="100%">Weiderpass, Elisabete</style></author><author><style face="normal" font="default" size="100%">Weintraub, Robert</style></author><author><style face="normal" font="default" size="100%">Gebrehiwot, Solomon Weldemariam</style></author><author><style face="normal" font="default" size="100%">Westerman, Ronny</style></author><author><style face="normal" font="default" size="100%">Williams, Hywel C</style></author><author><style face="normal" font="default" size="100%">Wolfe, Charles D A</style></author><author><style face="normal" font="default" size="100%">Woodbrook, Rachel</style></author><author><style face="normal" font="default" size="100%">Yano, Yuichiro</style></author><author><style face="normal" font="default" size="100%">Yonemoto, Naohiro</style></author><author><style face="normal" font="default" size="100%">Yoon, Seok-Jun</style></author><author><style face="normal" font="default" size="100%">Younis, Mustafa Z</style></author><author><style face="normal" font="default" size="100%">Yu, Chuanhua</style></author><author><style face="normal" font="default" size="100%">Zaki, Maysaa El Sayed</style></author><author><style face="normal" font="default" size="100%">Zegeye, Elias Asfaw</style></author><author><style face="normal" font="default" size="100%">Zuhlke, Liesl Joanna</style></author><author><style face="normal" font="default" size="100%">Murray, Christopher J L</style></author><author><style face="normal" font="default" size="100%">Vos, Theo</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Global Burden of Disease Child and Adolescent Health Collaboration</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Child and Adolescent Health From 1990 to 2015: Findings From the Global Burden of Diseases, Injuries, and Risk Factors 2015 Study.</style></title><secondary-title><style face="normal" font="default" size="100%">JAMA Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">JAMA Pediatr</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent Health</style></keyword><keyword><style  face="normal" font="default" size="100%">Age Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Cause of Death</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child Health</style></keyword><keyword><style  face="normal" font="default" size="100%">Child Mortality</style></keyword><keyword><style  face="normal" font="default" size="100%">Disabled Children</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Global Burden of Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Global Health</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Complications</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Sex Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Wounds and Injuries</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jun 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">171</style></volume><pages><style face="normal" font="default" size="100%">573-592</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;Importance: &lt;/b&gt;Comprehensive and timely monitoring of disease burden in all age groups, including children and adolescents, is essential for improving population health.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Objective: &lt;/b&gt;To quantify and describe levels and trends of mortality and nonfatal health outcomes among children and adolescents from 1990 to 2015 to provide a framework for policy discussion.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Evidence Review: &lt;/b&gt;Cause-specific mortality and nonfatal health outcomes were analyzed for 195 countries and territories by age group, sex, and year from 1990 to 2015 using standardized approaches for data processing and statistical modeling, with subsequent analysis of the findings to describe levels and trends across geography and time among children and adolescents 19 years or younger. A composite indicator of income, education, and fertility was developed (Socio-demographic Index [SDI]) for each geographic unit and year, which evaluates the historical association between SDI and health loss.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Findings: &lt;/b&gt;Global child and adolescent mortality decreased from 14.18 million (95% uncertainty interval [UI], 14.09 million to 14.28 million) deaths in 1990 to 7.26 million (95% UI, 7.14 million to 7.39 million) deaths in 2015, but progress has been unevenly distributed. Countries with a lower SDI had a larger proportion of mortality burden (75%) in 2015 than was the case in 1990 (61%). Most deaths in 2015 occurred in South Asia and sub-Saharan Africa. Global trends were driven by reductions in mortality owing to infectious, nutritional, and neonatal disorders, which in the aggregate led to a relative increase in the importance of noncommunicable diseases and injuries in explaining global disease burden. The absolute burden of disability in children and adolescents increased 4.3% (95% UI, 3.1%-5.6%) from 1990 to 2015, with much of the increase owing to population growth and improved survival for children and adolescents to older ages. Other than infectious conditions, many top causes of disability are associated with long-term sequelae of conditions present at birth (eg, neonatal disorders, congenital birth defects, and hemoglobinopathies) and complications of a variety of infections and nutritional deficiencies. Anemia, developmental intellectual disability, hearing loss, epilepsy, and vision loss are important contributors to childhood disability that can arise from multiple causes. Maternal and reproductive health remains a key cause of disease burden in adolescent females, especially in lower-SDI countries. In low-SDI countries, mortality is the primary driver of health loss for children and adolescents, whereas disability predominates in higher-SDI locations; the specific pattern of epidemiological transition varies across diseases and injuries.&lt;/p&gt;&lt;p&gt;&lt;b&gt;Conclusions and Relevance: &lt;/b&gt;Consistent international attention and investment have led to sustained improvements in causes of health loss among children and adolescents in many countries, although progress has been uneven. The persistence of infectious diseases in some countries, coupled with ongoing epidemiologic transition to injuries and noncommunicable diseases, require all countries to carefully evaluate and implement appropriate strategies to maximize the health of their children and adolescents and for the international community to carefully consider which elements of child and adolescent health should be monitored.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28384795?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Minute, Marta</style></author><author><style face="normal" font="default" size="100%">Cozzi, Giorgio</style></author><author><style face="normal" font="default" size="100%">Plotti, Chiara</style></author><author><style face="normal" font="default" size="100%">Montanari, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Pecile, Paolo</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio Andrea</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Children with cancer: a survey on the experience of Italian primary care pediatricians.</style></title><secondary-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Cross-Sectional Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease-Free Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Needs Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Outcome Assessment (Health Care)</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatricians</style></keyword><keyword><style  face="normal" font="default" size="100%">Practice Patterns, Physicians'</style></keyword><keyword><style  face="normal" font="default" size="100%">Prevalence</style></keyword><keyword><style  face="normal" font="default" size="100%">Primary Health Care</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">Survival Analysis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 May 25</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">43</style></volume><pages><style face="normal" font="default" size="100%">48</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Cancer is the second cause of death in children and its diagnosis can be difficult, due to the presence of vague and non-specific symptoms. The primary care pediatrician is often involved in the diagnostic process, but no longer in child care once the treatment started. Care models involving both primary care pediatricians and oncologic referral centre highlighted a higher family satisfaction when they worked together. We conducted a survey on primary care pediatricians involved in childhood cancer in order to describe the actual situation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We conducted a retrospective survey enrolling primary care pediatricians from a north-eastern area of Italy. They received a questionnaire that consisted in two parts: the first one aimed to assess the physician's seniority and experience and the second one pertained to each case of cancer and explored the relationship between the pediatrician, the family and the referral centre, and pediatricians degree of satisfaction and emotional impact.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We obtained data from 79 pediatricians who described 150 cancer cases. In 99 cases the primary care pediatrician had visited the child at the onset of symptoms and had referred him to the hospital. In 89 cases, he understood the severity of the disease. In 53.3% of cases the pediatrician was informed by the referral centre. The relationship between the pediatrician and child's family improved in 38% of cases and this was related with their participation to the multidisciplinary meetings on child health.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Primary pediatricians' sharing in the management of their patients with cancer was not satisfactory. Development of specific protocols targeted to an integrated care is needed to increase primary pediatricians' involvement and families' satisfactions.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28545557?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bernardi, Stella</style></author><author><style face="normal" font="default" size="100%">Toffoli, Barbara</style></author><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Stenner, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Carretta, Renzo</style></author><author><style face="normal" font="default" size="100%">Barbone, Fabio</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Circulating osteoprotegerin is associated with chronic kidney disease in hypertensive patients.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Nephrol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Nephrol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomarkers</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Follow-Up Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypertension</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoprotegerin</style></keyword><keyword><style  face="normal" font="default" size="100%">Random Allocation</style></keyword><keyword><style  face="normal" font="default" size="100%">Renal Insufficiency, Chronic</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jul 06</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">219</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Osteoprotegerin (OPG) is a glycoprotein that plays an important regulatory role in the skeletal, vascular, and immune system. It has been shown that OPG predicts chronic kidney disease (CKD) in diabetic patients. We hypothesized that OPG could be a risk marker of CKD development also in non-diabetic hypertensive patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A case-control study was carried out to measure circulating OPG levels in 42 hypertensive patients with CKD and in 141 hypertensive patients without CKD. A potential relationship between OPG and the presence of CKD was investigated and a receiver-operating characteristic (ROC) curve was designed thereafter to identify a cut-off value of OPG that best explained the presence of CKD. Secondly, to evaluate whether OPG increase could affect the kidney, 18 C57BL/6J mice were randomized to be treated with saline or recombinant OPG every 3 weeks for 12 weeks.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Circulating OPG levels were significantly higher in hypertensive patients with CKD, and there was a significant inverse association between OPG and renal function, that was independent from other variables. ROC analysis showed that OPG levels had a high statistically predictive value on CKD in hypertensive patients, which was greater than that of hypertension. The OPG best cut-off value associated with CKD was 1109.19 ng/L. In the experimental study, OPG delivery significantly increased the gene expression of pro-inflammatory and pro-fibrotic mediators, as well as the glomerular nitrosylation of proteins.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;This study shows that OPG is associated with CKD in hypertensive patients, where it might have a higher predictive value than that of hypertension for CKD development. Secondly, we found that OPG delivery significantly increased the expression of molecular pathways involved in kidney damage. Further longitudinal studies are needed not only to evaluate whether OPG predicts CKD development but also to clarify whether OPG should be considered a risk factor for CKD.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28683789?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cegolon, L</style></author><author><style face="normal" font="default" size="100%">Heymann, W C</style></author><author><style face="normal" font="default" size="100%">Lange, J H</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Climate change, emerging infections and blood donations.</style></title><secondary-title><style face="normal" font="default" size="100%">J Travel Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Travel Med</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Blood Transfusion</style></keyword><keyword><style  face="normal" font="default" size="100%">Climate Change</style></keyword><keyword><style  face="normal" font="default" size="100%">Communicable Diseases, Emerging</style></keyword><keyword><style  face="normal" font="default" size="100%">Global Health</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Travel</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 05 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">24</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28355622?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Callea, Michele</style></author><author><style face="normal" font="default" size="100%">Cammarata-Scalisi, Francisco</style></author><author><style face="normal" font="default" size="100%">Willoughby, Colin E</style></author><author><style face="normal" font="default" size="100%">Giglio, Sabrina R</style></author><author><style face="normal" font="default" size="100%">Sani, Ilaria</style></author><author><style face="normal" font="default" size="100%">Bargiacchi, Sara</style></author><author><style face="normal" font="default" size="100%">Traficante, Giovanna</style></author><author><style face="normal" font="default" size="100%">Bellacchio, Emanuele</style></author><author><style face="normal" font="default" size="100%">Tadini, Gianluca</style></author><author><style face="normal" font="default" size="100%">Yavuz, Izzet</style></author><author><style face="normal" font="default" size="100%">Galeotti, Angela</style></author><author><style face="normal" font="default" size="100%">Clarich, Gabriella</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">[Clinical and molecular study in a family with autosomal dominant hypohidrotic ectodermal dysplasia].</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Argent Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch Argent Pediatr</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Ectodermal Dysplasia 1, Anhidrotic</style></keyword><keyword><style  face="normal" font="default" size="100%">Edar Receptor</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 02 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">115</style></volume><pages><style face="normal" font="default" size="100%">e34-e38</style></pages><language><style face="normal" font="default" size="100%">spa</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hypohidrotic ectodermal dysplasia (HED) is a rare disease characterized by deficiency in development of structure derived from the ectoderm and is caused by mutations in the genes EDA, EDAR, or EDARADD. Phenotypes caused by mutations in these three may exhibit similar clinical features, explained by a common signaling pathway. Mutations in EDA gene cause X linked HED, which is the most common form. Mutations in EDAR and EDARADD genes cause autosomal dominant and recessive form of HED. The most striking clinical findings in HED are hypodontia, hypotrichosis and hypohidrosis that can lead to episodes of hyperthermia. We report on clinical findings in a child with HED with autosomal dominant inheritance pattern with a heterozygous mutation c.1072C&gt;T (p.Arg358X) in the EDAR gene. A review of the literature with regard to other cases presenting the same mutation has been carried out and discussed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28097853?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gianoncelli, Alessandra</style></author><author><style face="normal" font="default" size="100%">Kourousias, George</style></author><author><style face="normal" font="default" size="100%">Cammisuli, Francesca</style></author><author><style face="normal" font="default" size="100%">Cassese, Damiano</style></author><author><style face="normal" font="default" size="100%">Rizzardi, Clara</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Lazzarino, Marco</style></author><author><style face="normal" font="default" size="100%">Pascolo, Lorella</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Combined use of AFM and soft X-ray microscopy to reveal fibres' internalization in mesothelial cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Analyst</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Analyst</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Asbestos</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelium</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Microscopy, Atomic Force</style></keyword><keyword><style  face="normal" font="default" size="100%">X-Rays</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 May 30</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">142</style></volume><pages><style face="normal" font="default" size="100%">1982-1992</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Nanotoxicology and nanomedicine investigations often require the probing of nano-objects such as fibres and particles in biological samples and cells, whilst internalization and intracellular destiny are the main issues for in vitro cellular studies. Various high resolution microscopy techniques are well suited for providing this highly sought-after information. However, sample preparation, nanomaterial composition and sectioning challenges make it often difficult to establish whether the fibres or particles have been internalized or they are simply overlaying or underlying the biological matter. In this paper we suggest a novel suitable combination of two different microscopic techniques to reveal in intact cells the uptake of asbestos fibres by mesothelial cells. After exposure to asbestos fibres and fixation, cells were first analysed under the AFM instrument and then imaged under the TwinMic soft X-ray microscope at Elettra Sincrotrone. The suggested approach combines standard soft X-ray microscopy imaging and AFM microscopy, with a common non-invasive sample preparation protocol which drastically reduces the experimental uncertainty and provides a quick and definitive answer to the nanoparticle cellular and tissue uptake.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28509933?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Corre, Tanguy</style></author><author><style face="normal" font="default" size="100%">Olinger, Eric</style></author><author><style face="normal" font="default" size="100%">Harris, Sarah E</style></author><author><style face="normal" font="default" size="100%">Traglia, Michela</style></author><author><style face="normal" font="default" size="100%">Ulivi, Sheila</style></author><author><style face="normal" font="default" size="100%">Lenarduzzi, Stefania</style></author><author><style face="normal" font="default" size="100%">Belge, Hendrica</style></author><author><style face="normal" font="default" size="100%">Youhanna, Sonia</style></author><author><style face="normal" font="default" size="100%">Tokonami, Natsuko</style></author><author><style face="normal" font="default" size="100%">Bonny, Olivier</style></author><author><style face="normal" font="default" size="100%">Houillier, Pascal</style></author><author><style face="normal" font="default" size="100%">Polasek, Ozren</style></author><author><style face="normal" font="default" size="100%">Deary, Ian J</style></author><author><style face="normal" font="default" size="100%">Starr, John M</style></author><author><style face="normal" font="default" size="100%">Toniolo, Daniela</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Vollenweider, Peter</style></author><author><style face="normal" font="default" size="100%">Hayward, Caroline</style></author><author><style face="normal" font="default" size="100%">Bochud, Murielle</style></author><author><style face="normal" font="default" size="100%">Devuyst, Olivier</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Common variants in CLDN14 are associated with differential excretion of magnesium over calcium in urine.</style></title><secondary-title><style face="normal" font="default" size="100%">Pflugers Arch</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pflugers Arch.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Calcium</style></keyword><keyword><style  face="normal" font="default" size="100%">Claudins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Kidney Tubules</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnesium</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Urine</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 01</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">469</style></volume><pages><style face="normal" font="default" size="100%">91-103</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The nature and importance of genetic factors regulating the differential handling of Ca and Mg by the renal tubule in the general population are poorly defined. We conducted a genome-wide meta-analysis of urinary magnesium-to-calcium ratio to identify associated common genetic variants. We included 9320 adults of European descent from four genetic isolates and three urban cohorts. Urinary magnesium and calcium concentrations were measured centrally in spot urine, and each study conducted linear regression analysis of urinary magnesium-to-calcium ratio on ~2.5 million single-nucleotide polymorphisms (SNPs) using an additive model. We investigated, in mouse, the renal expression profile of the top candidate gene and its variation upon changes in dietary magnesium. The genome-wide analysis evidenced a top locus (rs172639, p = 1.7 × 10), encompassing CLDN14, the gene coding for claudin-14, that was genome-wide significant when using urinary magnesium-to-calcium ratio, but not either one taken separately. In mouse, claudin-14 is expressed in the distal nephron segments specifically handling magnesium, and its expression is regulated by chronic changes in dietary magnesium content. A genome-wide approach identified common variants in the CLDN14 gene exerting a robust influence on the differential excretion of Mg over Ca in urine. These data highlight the power of urinary electrolyte ratios to unravel genetic determinants of renal tubular function. Coupled with mouse experiments, these results support a major role for claudin-14, a gene associated with kidney stones, in the differential paracellular handling of divalent cations by the renal tubule.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27915449?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author><author><style face="normal" font="default" size="100%">Schillani, Giulia</style></author><author><style face="normal" font="default" size="100%">Simeone, Roberto</style></author><author><style face="normal" font="default" size="100%">Maestro, Alessandra</style></author><author><style face="normal" font="default" size="100%">Zanon, Davide</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparison of Efficacy and Safety of Caspofungin Versus Micafungin in Pediatric Allogeneic Stem Cell Transplant Recipients: A Retrospective Analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">Adv Ther</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Adv Ther</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antifungal Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspofungin</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Echinocandins</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipopeptides</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Micafungin</style></keyword><keyword><style  face="normal" font="default" size="100%">Mycoses</style></keyword><keyword><style  face="normal" font="default" size="100%">Neutropenia</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 05</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">1184-1199</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;INTRODUCTION: &lt;/b&gt;The high morbidity and mortality associated with invasive fungal infections (IFIs) provide the rationale for antifungal prophylaxis in immuno-compromised pediatric patients undergoing hematopoietic stem cell transplantation (HSCT). Caspofungin and micafungin are antifungal agents of interest for prophylaxis of IFIs because of their potency against Candida and minimal toxicity or interactions with other drugs. Few studies have demonstrated the safety and efficacy of such echinocandins as prophylaxis for IFIs in patients undergoing HSCT.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This retrospective cohort study compared caspofungin and micafungin for prevention of IFIs in 93 pediatric patients undergoing HSCT for oncological or non-oncological disease. The observation began with the first dose of antifungal agent and ended 3 months after transplantation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Patients in the micafungin group had a higher overall treatment success rate of 87.2 versus 84.8% in the caspofungin group, but the difference was not significant. There were no statistically significant differences in the incidence or type of proven/probable IFIs between the 2 groups. The low incidence of death did not differ statistically between the groups. Patients in the caspofungin group presented more frequently with fever, during and after neutropenia. In both groups, we observed an expected worsening of blood chemistry parameters. There were no adverse events definitely attributable to the two antifungal agents.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;These results demonstrate good efficacy and tolerability for caspofungin and micafungin. However, better results with respect to the incidence and resolution of fever in the micafungin group may suggest its use in preference to that of caspofungin.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28429246?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Vidergar, Romana</style></author><author><style face="normal" font="default" size="100%">Belmonte, Beatrice</style></author><author><style face="normal" font="default" size="100%">Mangogna, Alessandro</style></author><author><style face="normal" font="default" size="100%">Amadio, Leonardo</style></author><author><style face="normal" font="default" size="100%">Geri, Pietro</style></author><author><style face="normal" font="default" size="100%">Borelli, Violetta</style></author><author><style face="normal" font="default" size="100%">Zanconati, Fabrizio</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author><author><style face="normal" font="default" size="100%">Confalonieri, Marco</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Kishore, Uday</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Complement Protein C1q Binds to Hyaluronic Acid in the Malignant Pleural Mesothelioma Microenvironment and Promotes Tumor Growth.</style></title><secondary-title><style face="normal" font="default" size="100%">Front Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Front Immunol</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">1559</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;C1q is the first recognition subcomponent of the complement classical pathway, which acts toward the clearance of pathogens and apoptotic cells. C1q is also known to modulate a range of functions of immune and non-immune cells, and has been shown to be involved in placental development and sensorial synaptic pruning. We have recently shown that C1q can promote tumor by encouraging their adhesion, migration, and proliferation in addition to angiogenesis and metastasis. In this study, we have examined the role of human C1q in the microenvironment of malignant pleural mesothelioma (MPM), a rare form of cancer commonly associated with exposure to asbestos. We found that C1q was highly expressed in all MPM histotypes, particularly in epithelioid rather than in sarcomatoid histotype. C1q avidly bound high and low molecular weight hyaluronic acid (HA)  its globular domain. C1q bound to HA was able to induce adhesion and proliferation of mesothelioma cells (MES)  enhancement of ERK1/2, SAPK/JNK, and p38 phosphorylation; however, it did not activate the complement cascade. Consistent with the modular organization of the globular domain, we demonstrated that C1q may bind to HA through ghA module, whereas it may interact with human MES through the ghC. In conclusion, C1q highly expressed in MPM binds to HA and enhances the tumor growth promoting cell adhesion and proliferation. These data can help develop novel diagnostic markers and molecular targets for MPM.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29209316?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Villa, N</style></author><author><style face="normal" font="default" size="100%">Conconi, D</style></author><author><style face="normal" font="default" size="100%">Benussi, D Gambel</style></author><author><style face="normal" font="default" size="100%">Tornese, G</style></author><author><style face="normal" font="default" size="100%">Crosti, F</style></author><author><style face="normal" font="default" size="100%">Sala, E</style></author><author><style face="normal" font="default" size="100%">Dalprà, L</style></author><author><style face="normal" font="default" size="100%">Pecile, V</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A complete duplication of X chromosome resulting in a tricentric isochromosome originated by centromere repositioning.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Cytogenet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol Cytogenet</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">22</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Neocentromeres are rare and considered chromosomal aberrations, because a non-centromeric region evolves in an active centromere by mutation. The literature reported several structural anomalies of X chromosome and they influence the female reproductive capacity or are associated to Turner syndrome in the presence of monosomy X cell line.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CASE PRESENTATION: &lt;/b&gt;We report a case of chromosome X complex rearrangement found in a prenatal diagnosis. The fetal karyotype showed a mosaicism with a 45,X cell line and a 46 chromosomes second line with a big marker, instead of a sex chromosome. The marker morphology and fluorescence in situ hybridization (FISH) characterization allowed us to identify a tricentric X chromosome constituted by two complete X chromosome fused at the p arms telomere and an active neocentromere in the middle, at the union of the two Xp arms, where usually are the telomeric regions. FISH also showed the presence of a paracentric inversion of both Xp arms. Furthermore, fragility figures were found in 56% of metaphases from peripheral blood lymphocytes culture at birth: a shorter marker chromosome and an apparently acentric fragment frequently lost.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;At our knowledge, this is the first isochromosome of an entire non-acrocentric chromosome. The neocentromere is constituted by canonical sequences but localized in an unusual position and the original centromeres are inactivated. We speculated that marker chromosome was the result of a double rearrangement: firstly, a paracentric inversion which involved the Xp arm, shifting a part of the centromere at the p end and subsequently a duplication of the entire X chromosome, which gave rise to an isochromosome. It is possible to suppose that the first event could be a result of a non-allelic homologous recombination mediated by inverted low-copy repeats. As expected, our case shows a Turner phenotype with mild facial features and no major skeletal deformity, normal psychomotor development and a spontaneous development of puberty and menarche, although with irregular menses since the last follow-up.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28630649?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Matarazzo, L</style></author><author><style face="normal" font="default" size="100%">Delise, A</style></author><author><style face="normal" font="default" size="100%">Zennaro, F</style></author><author><style face="normal" font="default" size="100%">Bussani, R</style></author><author><style face="normal" font="default" size="100%">Demarini, S</style></author><author><style face="normal" font="default" size="100%">Berti, I</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A congenital purplish tumour.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child Educ Pract Ed</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch Dis Child Educ Pract Ed</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Congenital Abnormalities</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">India</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Knee</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Neonatology</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">102</style></volume><pages><style face="normal" font="default" size="100%">79-81</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26908941?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Biffi, Stefania</style></author><author><style face="normal" font="default" size="100%">Andolfi, Laura</style></author><author><style face="normal" font="default" size="100%">Caltagirone, Claudia</style></author><author><style face="normal" font="default" size="100%">Garrovo, Chiara</style></author><author><style face="normal" font="default" size="100%">Falchi, Angela M</style></author><author><style face="normal" font="default" size="100%">Lippolis, Vito</style></author><author><style face="normal" font="default" size="100%">Lorenzon, Andrea</style></author><author><style face="normal" font="default" size="100%">Macor, Paolo</style></author><author><style face="normal" font="default" size="100%">Meli, Valeria</style></author><author><style face="normal" font="default" size="100%">Monduzzi, Maura</style></author><author><style face="normal" font="default" size="100%">Obiols-Rabasa, Marc</style></author><author><style face="normal" font="default" size="100%">Petrizza, Luca</style></author><author><style face="normal" font="default" size="100%">Prodi, Luca</style></author><author><style face="normal" font="default" size="100%">Rosa, Antonella</style></author><author><style face="normal" font="default" size="100%">Schmidt, Judith</style></author><author><style face="normal" font="default" size="100%">Talmon, Yeshayahu</style></author><author><style face="normal" font="default" size="100%">Murgia, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cubosomes for in vivo fluorescence lifetime imaging.</style></title><secondary-title><style face="normal" font="default" size="100%">Nanotechnology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nanotechnology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Carbocyanines</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug Compounding</style></keyword><keyword><style  face="normal" font="default" size="100%">Erythrocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fluorescent Dyes</style></keyword><keyword><style  face="normal" font="default" size="100%">Glycerides</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Injections, Intravenous</style></keyword><keyword><style  face="normal" font="default" size="100%">Liposomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Liver</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred BALB C</style></keyword><keyword><style  face="normal" font="default" size="100%">Nanoparticles</style></keyword><keyword><style  face="normal" font="default" size="100%">NIH 3T3 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Optical Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Particle Size</style></keyword><keyword><style  face="normal" font="default" size="100%">Spectroscopy, Near-Infrared</style></keyword><keyword><style  face="normal" font="default" size="100%">Time-Lapse Imaging</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Feb 03</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">28</style></volume><pages><style face="normal" font="default" size="100%">055102</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Herein we provided the first proof of principle for in vivo fluorescence optical imaging application using monoolein-based cubosomes in a healthy mouse animal model. This formulation, administered at a non-cytotoxic concentration, was capable of providing both exogenous contrast for NIR fluorescence imaging with very high efficiency and chemospecific information upon lifetime analysis. Time-resolved measurements of fluorescence after the intravenous injection of cubosomes revealed that the dye rapidly accumulated mainly in the liver, while lifetimes profiles obtained in vivo allowed for discriminating between free dye or dye embedded within the cubosome nanostructure after injection.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28032617?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Loganes, Claudia</style></author><author><style face="normal" font="default" size="100%">Lega, Sara</style></author><author><style face="normal" font="default" size="100%">Bramuzzo, Matteo</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Curcumin Anti-Apoptotic Action in a Model of Intestinal Epithelial Inflammatory Damage.</style></title><secondary-title><style face="normal" font="default" size="100%">Nutrients</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nutrients</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents, Non-Steroidal</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Curcuma</style></keyword><keyword><style  face="normal" font="default" size="100%">Curcumin</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">HT29 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Interferon-gamma</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-7</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Mucosa</style></keyword><keyword><style  face="normal" font="default" size="100%">NF-kappa B</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 Jun 06</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The purpose of this study is to determine if a preventive treatment with curcumin can protect intestinal epithelial cells from inflammatory damage induced by IFNγ. To achieve this goal we have used a human intestinal epithelial cell line (HT29) treated with IFNγ to undergo apoptotic changes that can reproduce the damage of intestinal epithelia exposed to inflammatory cytokines. In this model, we measured the effect of curcumin (curcuminoid from ) added as a pre-treatment at different time intervals before stimulation with IFNγ. Curcumin administration to HT29 culture before the inflammatory stimulus IFNγ reduced the cell apoptosis rate. This effect gradually declined with the reduction of the curcumin pre-incubation time. This anti-apoptotic action by curcumin pre-treatment was paralleled by a reduction of secreted IL7 in the HT29 culture media, while there was no relevant change in the other cytokine levels. Even though curcumin pre-administration did not impact the activation of the NF-κB pathway, a slight effect on the phosphorylation of proteins in this inflammatory signaling pathway was observed. In conclusion, curcumin pre-treatment can protect intestinal cells from inflammatory damage. These results can be the basis for studying the preventive role of curcumin in inflammatory bowel diseases.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28587282?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Llop, Sabrina</style></author><author><style face="normal" font="default" size="100%">Tran, Van</style></author><author><style face="normal" font="default" size="100%">Ballester, Ferran</style></author><author><style face="normal" font="default" size="100%">Barbone, Fabio</style></author><author><style face="normal" font="default" size="100%">Sofianou-Katsoulis, Aikaterini</style></author><author><style face="normal" font="default" size="100%">Sunyer, Jordi</style></author><author><style face="normal" font="default" size="100%">Engström, Karin</style></author><author><style face="normal" font="default" size="100%">Alhamdow, Ayman</style></author><author><style face="normal" font="default" size="100%">Love, Tanzy M</style></author><author><style face="normal" font="default" size="100%">Watson, Gene E</style></author><author><style face="normal" font="default" size="100%">Bustamante, Mariona</style></author><author><style face="normal" font="default" size="100%">Murcia, Mario</style></author><author><style face="normal" font="default" size="100%">Iñiguez, Carmen</style></author><author><style face="normal" font="default" size="100%">Shamlaye, Conrad F</style></author><author><style face="normal" font="default" size="100%">Rosolen, Valentina</style></author><author><style face="normal" font="default" size="100%">Mariuz, Marika</style></author><author><style face="normal" font="default" size="100%">Horvat, Milena</style></author><author><style face="normal" font="default" size="100%">Tratnik, Janja S</style></author><author><style face="normal" font="default" size="100%">Mazej, Darja</style></author><author><style face="normal" font="default" size="100%">van Wijngaarden, Edwin</style></author><author><style face="normal" font="default" size="100%">Davidson, Philip W</style></author><author><style face="normal" font="default" size="100%">Myers, Gary J</style></author><author><style face="normal" font="default" size="100%">Rand, Matthew D</style></author><author><style face="normal" font="default" size="100%">Broberg, Karin</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CYP3A genes and the association between prenatal methylmercury exposure and neurodevelopment.</style></title><secondary-title><style face="normal" font="default" size="100%">Environ Int</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Environ Int</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Child Development</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytochrome P-450 CYP3A</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Blood</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Greece</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mercury</style></keyword><keyword><style  face="normal" font="default" size="100%">Methylmercury Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Neurodevelopmental Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Neuropsychological Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Prenatal Exposure Delayed Effects</style></keyword><keyword><style  face="normal" font="default" size="100%">Seychelles</style></keyword><keyword><style  face="normal" font="default" size="100%">Spain</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 08</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">105</style></volume><pages><style face="normal" font="default" size="100%">34-42</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Results on the association between prenatal exposure to methylmercury (MeHg) and child neuropsychological development are heterogeneous. Underlying genetic differences across study populations could contribute to this varied response to MeHg. Studies in Drosophila have identified the cytochrome p450 3A (CYP3A) family as candidate MeHg susceptibility genes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;We evaluated whether genetic variation in CYP3A genes influences the association between prenatal exposure to MeHg and child neuropsychological development.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The study population included 2639 children from three birth cohort studies: two subcohorts in Seychelles (SCDS) (n=1160, 20 and 30months of age, studied during the years 2001-2012), two subcohorts from Spain (INMA) (n=625, 14months of age, 2003-2009), and two subcohorts from Italy and Greece (PHIME) (n=854, 18months of age, 2006-2011). Total mercury, as a surrogate of MeHg, was analyzed in maternal hair and/or cord blood samples. Neuropsychological development was evaluated using Bayley Scales of Infant Development (BSID). Three functional polymorphisms in the CYP3A family were analyzed: rs2257401 (CYP3A7), rs776746 (CYP3A5), and rs2740574 (CYP3A4).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;There was no association between CYP3A polymorphisms and cord mercury concentrations. The scores for the BSID mental scale improved with increasing cord blood mercury concentrations for carriers of the most active alleles (β[95% CI]:=2.9[1.53,4.27] for CYP3A7 rs2257401 GG+GC, 2.51[1.04,3.98] for CYP3A5 rs776746 AA+AG and 2.31[0.12,4.50] for CYP3A4 rs2740574 GG+AG). This association was near the null for CYP3A7 CC, CYP3A5 GG and CYP3A4 AA genotypes. The interaction between the CYP3A genes and total mercury was significant (p&lt;0.05) in European cohorts only.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our results suggest that the polymorphisms in CYP3A genes may modify the response to dietary MeHg exposure during early life development.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28500872?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Rami, Damiano</style></author><author><style face="normal" font="default" size="100%">Ling, Guang Sheng</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Guarnotta, Carla</style></author><author><style face="normal" font="default" size="100%">Zorzet, Sonia</style></author><author><style face="normal" font="default" size="100%">Durigutto, Paolo</style></author><author><style face="normal" font="default" size="100%">Botto, Marina</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">C1q acts in the tumour microenvironment as a cancer-promoting factor independently of complement activation.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Commun</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat Commun</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C1q</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C3</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C5</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">10346</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Complement C1q is the activator of the classical pathway. However, it is now recognized that C1q can exert functions unrelated to complement activation. Here we show that C1q, but not C4, is expressed in the stroma and vascular endothelium of several human malignant tumours. Compared with wild-type (WT) or C3- or C5-deficient mice, C1q-deficient (C1qa(-/-)) mice bearing a syngeneic B16 melanoma exhibit a slower tumour growth and prolonged survival. This effect is not attributable to differences in the tumour-infiltrating immune cells. Tumours developing in WT mice display early deposition of C1q, higher vascular density and an increase in the number of lung metastases compared with C1qa(-/-) mice. Bone marrow (BM) chimeras between C1qa(-/-) and WT mice identify non-BM-derived cells as the main local source of C1q that can promote cancer cell adhesion, migration and proliferation. Together these findings support a role for locally synthesized C1q in promoting tumour growth.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26831747?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zanotta, Nunzia</style></author><author><style face="normal" font="default" size="100%">Tornesello, Maria Lina</style></author><author><style face="normal" font="default" size="100%">Annunziata, Clorinda</style></author><author><style face="normal" font="default" size="100%">Stellato, Giovanni</style></author><author><style face="normal" font="default" size="100%">Buonaguro, Franco Maria</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Candidate Soluble Immune Mediators in Young Women with High-Risk Human Papillomavirus Infection: High Expression of Chemokines Promoting Angiogenesis and Cell Proliferation.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS ONE</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervix Uteri</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Pathologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Papillomaviridae</style></keyword><keyword><style  face="normal" font="default" size="100%">Papillomavirus Infections</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">11</style></volume><pages><style face="normal" font="default" size="100%">e0151851</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The causal interpretation of cervical immune response to Human Papillomavirus (HPV) infection is complex and poorly characterized mainly due to the delicate balance that exists between viral infection, increase of inflammatory cytokines and host risk factors. This study aims to explore the significance of cervical immune mediators associated to cell survival, angiogenesis and interaction with immune response, in predicting the risk to develop HPV-related intraepithelial lesions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A panel of 48 cytokines and growth factors were explored in a selected cohort of 168 immunocompetent women including 88 diagnosed with low (LSIL) or high (HSIL) squamous intraepithelial lesions of the cervix and 80 with normal cervical cytology (NIL). HPV genotyping was performed by Linear Array HPV test and the soluble concentration of 48 immune molecules was analyzed using the Bio-Plex platform.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The prevalence of single HR-HPV infection was 30% in NIL and 100% in LSIL and HSIL women. The expression of 13 cytokines, including interleukins IL-6, IL-3, IL-12p40, IL-12p70, IL-16, IL-18, LIF, of chemokines CCL7 (MCP-3), CXCL9 (MIG), CXCL12 (SDF-1α) and of the tropic factors VEGF, G-CSF, M-CSF were significantly associated with the presence of infection, with levels being higher in women with precancerous lesions compared to NIL HPV negative women. Only the growth factor GM-CSF was positively associated with the cytological abnormalities.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The ability of HR-HPV to escape from innate immune recognition and to orchestrate the production of specific inflammatory and growth factors, involved in early inflammatory response and in the cell-proliferating phase of intraepithelial damage, was documented in women before the development of cervical lesions.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26990868?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Abate, Maria Valentina</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Devescovi, Raffaella</style></author><author><style face="normal" font="default" size="100%">Carrozzi, Marco</style></author><author><style face="normal" font="default" size="100%">Pierobon, Chiara</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Lucafò, Marianna</style></author><author><style face="normal" font="default" size="100%">Di Silvestre, Alessia</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Pio</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Carbamazepine-induced thrombocytopenic purpura in a child: Insights from a genomic analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">Blood Cells Mol Dis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Blood Cells Mol. Dis.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">59</style></volume><pages><style face="normal" font="default" size="100%">97-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27282575?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Quadrifoglio, Mariachiara</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Bussani, Rossana</style></author><author><style face="normal" font="default" size="100%">Pecile, Vanna</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Grasso, Alessandra</style></author><author><style face="normal" font="default" size="100%">Zandonà, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Alberico, Salvatore</style></author><author><style face="normal" font="default" size="100%">Stampalija, Tamara</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Case of Prenatal Neurocytoma Associated With ATR-16 Syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">J Ultrasound Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Ultrasound Med</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">35</style></volume><pages><style face="normal" font="default" size="100%">1359-61</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27235459?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Santos, Erinaldo Ubirajara Damasceno Dos</style></author><author><style face="normal" font="default" size="100%">Lima, Géssica Dayane Cordeiro de</style></author><author><style face="normal" font="default" size="100%">Oliveira, Micheline de Lucena</style></author><author><style face="normal" font="default" size="100%">Heráclio, Sandra de Andrade</style></author><author><style face="normal" font="default" size="100%">Silva, Hildson Dornelas Angelo da</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Maia, Maria de Mascena Diniz</style></author><author><style face="normal" font="default" size="100%">Souza, Paulo Roberto Eleutério de</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CCR2 and CCR5 genes polymorphisms in women with cervical lesions from Pernambuco, Northeast Region of Brazil: a case-control study.</style></title><secondary-title><style face="normal" font="default" size="100%">Mem Inst Oswaldo Cruz</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mem. Inst. Oswaldo Cruz</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">174-80</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Polymorphisms in chemokine receptors play an important role in the progression of cervical intraepithelial neoplasia (CIN) to cervical cancer (CC). Our study examined the association of CCR2-64I (rs1799864) andCCR5-Δ32 (rs333) polymorphisms with susceptibility to develop cervical lesion (CIN and CC) in a Brazilian population. The genotyping of 139 women with cervical lesions and 151 women without cervical lesions for the CCR2-64I and CCR5-Δ32 polymorphisms were performed using polymerase chain reaction-restriction fragment length polymorphism. The individuals carrying heterozygous or homozygous genotypes (GA+AA) for CCR2-64I polymorphisms seem to be at lower risk for cervical lesion [odds ratio (OR) = 0.37, p = 0.0008)]. The same was observed for the A allele (OR = 0.39, p = 0.0002), while no association was detected (p &gt; 0.05) with CCR5-Δ32 polymorphism. Regarding the human papillomavirus (HPV) type, patients carrying the CCR2-64Ipolymorphism were protected against infection by HPV type 16 (OR = 0.35, p = 0.0184). In summary, our study showed a protective effect ofCCR2-64I rs1799864 polymorphism against the development of cervical lesions (CIN and CC) and in the susceptibility of HPV 16 infection.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26982176?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zupin, Luisa</style></author><author><style face="normal" font="default" size="100%">Polesello, Vania</style></author><author><style face="normal" font="default" size="100%">Alberi, Giulia</style></author><author><style face="normal" font="default" size="100%">Moratelli, Giulia</style></author><author><style face="normal" font="default" size="100%">Crocè, Saveria Lory</style></author><author><style face="normal" font="default" size="100%">Masutti, Flora</style></author><author><style face="normal" font="default" size="100%">Pozzato, Gabriele</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CD209 promoter polymorphisms associate with HCV infection and pegylated-interferon plus ribavirin treatment response.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol. Immunol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">76</style></volume><pages><style face="normal" font="default" size="100%">49-54</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hepatitis C is a severe liver disease caused by hepatitis C virus that could persist in the host causing progression towards chronic disease in about 80% of the cases. Pegylated-interferon plus ribavirin was the gold standard therapy, however treatment's response was quite variable among individuals and different host/viral factors may play a role in disease outcome. The cluster of differentiation 209 (CD209 antigen) is a component of the innate immune system able to recognize HCV and consequently activating the immune response. We enrolled 203 Italian HCV infected patients and 220 healthy controls investigating if five promoter polymorphisms within CD209 gene (encoding for CD209 antigen) correlated with HCV infection susceptibility, spontaneous viral clearance and interferon treatment response. CD209 -939G&gt;A and -871A&gt;G polymorphisms associated with HCV infection susceptibility, while, CD209 -871A&gt;G and -336A&gt;G polymorphisms associated with response to treatment. In conclusion, CD209 polymorphisms could play a role in the susceptibility to HCV infection as well as interferon treatment response in our study population from North-East of Italy.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27348632?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Comar, M</style></author><author><style face="normal" font="default" size="100%">Zanotta, N</style></author><author><style face="normal" font="default" size="100%">Zanconati, F</style></author><author><style face="normal" font="default" size="100%">Cortale, M</style></author><author><style face="normal" font="default" size="100%">Bonotti, A</style></author><author><style face="normal" font="default" size="100%">Cristaudo, A</style></author><author><style face="normal" font="default" size="100%">Bovenzi, M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chemokines involved in the early inflammatory response and in pro-tumoral activity in asbestos-exposed workers from an Italian coastal area with territorial clusters of pleural malignant mesothelioma.</style></title><secondary-title><style face="normal" font="default" size="100%">Lung Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Lung Cancer</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">94</style></volume><pages><style face="normal" font="default" size="100%">61-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;Immune mediators are likely to be relevant for the biological response to asbestos exposure. The aim of this study was to investigate the association between immune mediators involved in inflammation, cell survival and angiogenesis, and asbestos-related diseases in workers from a coastal area of North-East Italy with a high incidence of pleural malignant mesothelioma (PMM).&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;A selected custom set of 12 soluble mediators was evaluated with a Luminex platform in sera, pleural fluid and mesothelioma biopsies from 123 asbestos-exposed workers (38 free from pleural-pulmonary disorders, 46 with non-malignant asbestos diseases, 39 with PMM) and in sera from 33 healthy controls from the same territorial area.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Increased immune mediator concentrations were observed in the sera of the asbestos-exposed workers compared to controls for human fibroblast growth factor (FGF-b), vascular endothelial growth factor (VEGF), CCL5 (RANTES), CXCL10 (IP-10), CLEC11A (SCGF-b), CCL27 (CTACK), CCL11 (EOTAXIN), IL-5 and IL-6 (p&lt;0.001). The chemokines IP-10 and RANTES were associated with the severity of asbestos-related diseases. In the workers with PMM, the immune proteins secreted by mesothelioma biopsies showed detectable levels of RANTES, VEGF, and IP-10. In the same workers with PMM, a significant relationship between serum and pleural fluid concentrations was found for RANTES alone.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Occupational exposure to asbestos seems to drive the production of specific growth factors dually involved in the early inflammatory response and in pro-tumoral activity before clinical evidence of related disorders, suggesting that their over-expression may precede the onset of asbestos-related diseases. These findings suggest that some chemokines may have a prognostic role in the progression of asbestos-related diseases and could be used for the health surveillance of either workers with an occupational history of asbestos exposure or patients affected by non-malignant asbestos-related diseases.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26973208?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Celerino da Silva, Ronaldo</style></author><author><style face="normal" font="default" size="100%">Victor Campos Coelho, Antonio</style></author><author><style face="normal" font="default" size="100%">Cláudio Arraes, Luiz</style></author><author><style face="normal" font="default" size="100%">André Cavalcanti Brandão, Lucas</style></author><author><style face="normal" font="default" size="100%">Lima Guimarães, Rafael</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chemokines SNPs in HIV-1+ Patients and Healthy Controls from Northeast Brazil: Association with Protection against HIV-1 Infection.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr HIV Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. HIV Res.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">340-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;HIV-1 virus is known to infect the host mainly through CD4+ T-lymphocyte cells, by interactions among the viral envelope proteins, CD4 receptor and HIV-1 coreceptors, such as chemokines receptors. Variations in the genes encoding HIV-1 coreceptors and their natural ligands have been shown to modify HIV-1 infection susceptibility and disease progression.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS AND RESULTS: &lt;/b&gt;We analysed the distribution of SNPs in chemokines (CCL3, CCL4, CCL5, CXCL12) and chemokine receptor (CXCR6) genes, in 268 HIV-1 infected patients (HIV-1+) and 221 healthy controls from Northeast Brazil, and their possible connection with susceptibility to HIV-1 infection. The genotyping were performed through allele specific fluorogenic probes using real time PCR. We observed that the T alleles and AT genotype of rs1719153 CCL4 SNP were more frequent in healthy controls (19.8% and 35.0%, respectively) than in HIV-1+ patients (T allele: 14.1%; OR=0.67; 95%CI=0.47-0.95; p-value=0.020; and AT genotype: 24.4%; OR=0.61; 95%CI=0.40- 0.93; p-value=0.021) after correcting for age and sex. The rs1719134 (CCL3) and rs1719153 (CCL4) SNPs presented linkage disequilibrium (D'=0.83). The AT haplotype frequency was increased in healthy controls (17.3%) in relation to HIV-1+ patients (11.0%; OR=0.62; 95%CI=0.42-0.93; p-value=0.020).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Since our results revealed an increased frequency of alleles and genotypes of CCL3/CCL4 SNPs and haplotype (CCL3-CCL4) among healthy controls, we suggest that these variations might have a potential protective role against HIV-1 infection.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26785888?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rossetto, Elena</style></author><author><style face="normal" font="default" size="100%">Matarazzo, Lorenza</style></author><author><style face="normal" font="default" size="100%">Maschio, Massimo</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Costa, Paola</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Child with Severe Developmental Delay and Growth Retardation.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">175</style></volume><pages><style face="normal" font="default" size="100%">241-241.e1</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27266964?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Orzan, E</style></author><author><style face="normal" font="default" size="100%">Ruta, F</style></author><author><style face="normal" font="default" size="100%">Bolzonello, P</style></author><author><style face="normal" font="default" size="100%">Marchi, R</style></author><author><style face="normal" font="default" size="100%">Ceschin, F</style></author><author><style face="normal" font="default" size="100%">Ciciriello, E</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Childhood hearing surveillance activity in Italy: preliminary recommendations.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Otorhinolaryngol Ital</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Otorhinolaryngol Ital</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">15-20</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Following the positive outcomes of the newborn hearing screening programmes already underway in several Italian regions, it is now necessary to address the identification of childhood hearing impairments that missed the neonatal screening programme or have delayed onset. Within the framework of the Ministry of Health project CCM 2013 &quot;Preventing Communication Disorders: a Regional Program for early Identification, Intervention and Care of Hearing Impaired Children&quot;, a group of professionals identified three main recommendations that can be useful to improve hearing surveillance activity within the regional and state Italian Health System. The family paediatrician is recognised as having a key role in ongoing monitoring of hearing capacity and development of the growing child.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27054386?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Ferrara, Giovanna</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Meini, Antonella</style></author><author><style face="normal" font="default" size="100%">Cattalini, Marco</style></author><author><style face="normal" font="default" size="100%">Martino, Silvana</style></author><author><style face="normal" font="default" size="100%">Alessio, Maria</style></author><author><style face="normal" font="default" size="100%">La Torre, Francesco</style></author><author><style face="normal" font="default" size="100%">Teruzzi, Barbara</style></author><author><style face="normal" font="default" size="100%">Gerloni, Valeria</style></author><author><style face="normal" font="default" size="100%">Breda, Luciana</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chronic nonbacterial osteomyelitis may be associated with renal disease and bisphosphonates are a good option for the majority of patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Paediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Paediatr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">105</style></volume><pages><style face="normal" font="default" size="100%">e328-33</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;The aim of this Italian study was to describe the clinical features, treatment options and outcomes of a cohort of patients with chronic nonbacterial osteomyelitis (CNO).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This was a retrospective cohort study. Laboratory data, diagnostic imaging, histological features and clinical course are reported.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We enrolled 47 patients diagnosed with CNO. Bone pain was the leading symptom, and multifocal disease was present in 87% of the patients. The majority of the bone lesions were located in the appendicular skeleton (58%). Extraosseous manifestations were present in 34% of the patients, and renal involvement was detected in four patients. Inflammatory indices were increased in 80%, and bone x-rays were negative in 15% of the patients. Nonsteroidal anti-inflammatory drugs (NSAIDs) were the first therapy for all patients, achieving clinical remission in 27%. A good response to NSAIDs was significantly associated with a better prognosis. Bisphosphonates were used in 26 patients, with remission in 73%. Only six patients (13%), all with spine involvement, developed sequelae.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;We found a possible association between CNO and renal disease. Bisphosphonates were more likely to lead to clinical remission when NSAIDs and corticosteroids had failed. Vertebral localisation was the only risk factor for potential sequelae.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27059298?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Färkkilä, Anniina</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Haltia, Ulla-Maija</style></author><author><style face="normal" font="default" size="100%">Pihlajoki, Marjut</style></author><author><style face="normal" font="default" size="100%">Unkila-Kallio, Leila</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Heikinheimo, Markku</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Circulating levels of TNF-related apoptosis inducing-ligand are decreased in patients with large adult-type granulosa cell tumors-implications for therapeutic potential.</style></title><secondary-title><style face="normal" font="default" size="100%">Tumour Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tumour Biol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Apr 11</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Targeted treatments are needed for advanced adult-type granulosa cell tumors (AGCTs). We set out to assess tumor tissue and circulating levels of TNF-related apoptosis-inducing ligand (TRAIL), a promising anti-cancer cytokine, in patients affected by AGCT. We analyzed tissue expression of TRAIL in 127 AGCTs using immunohistochemistry or RT-PCR. Soluble TRAIL was measured by means of ELISA from 141 AGCT patient serum samples, as well as the conditioned media of 15 AGCT patient-derived primary cell cultures, and the KGN cell line. Tissue and serum TRAIL levels were analyzed in relationship with clinical parameters, and serum estradiol, FSH, and LH levels. We found that AGCT samples expressed TRAIL mRNA and protein at levels comparable to normal granulosa cells. AGCT cells did not release soluble TRAIL. TRAIL protein levels were decreased in tumors over 10 cm in diameter (p = 0.04). Consistently, circulating TRAIL levels correlated negatively to tumor dimension (p = 0.01). Circulating TRAIL levels negatively associated with serum estradiol levels. In multiple regression analysis, tumor size was an independent factor contributing to the decreased levels of soluble TRAIL in AGCT patients. AGCTs associate with significantly decreased tumor tissue and serum TRAIL levels in patients with a large tumor mass. These findings encourage further study of agonistic TRAIL treatments in patients with advanced or recurrent AGCT.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27067438?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Melazzini, Federica</style></author><author><style face="normal" font="default" size="100%">Palombo, Flavia</style></author><author><style face="normal" font="default" size="100%">Balduini, Alessandra</style></author><author><style face="normal" font="default" size="100%">De Rocco, Daniela</style></author><author><style face="normal" font="default" size="100%">Marconi, Caterina</style></author><author><style face="normal" font="default" size="100%">Noris, Patrizia</style></author><author><style face="normal" font="default" size="100%">Gnan, Chiara</style></author><author><style face="normal" font="default" size="100%">Pippucci, Tommaso</style></author><author><style face="normal" font="default" size="100%">Bozzi, Valeria</style></author><author><style face="normal" font="default" size="100%">Faleschini, Michela</style></author><author><style face="normal" font="default" size="100%">Barozzi, Serena</style></author><author><style face="normal" font="default" size="100%">Doubek, Michael</style></author><author><style face="normal" font="default" size="100%">Di Buduo, Christian A</style></author><author><style face="normal" font="default" size="100%">Stano Kozubik, Katerina</style></author><author><style face="normal" font="default" size="100%">Radova, Lenka</style></author><author><style face="normal" font="default" size="100%">Loffredo, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Pospisilova, Sarka</style></author><author><style face="normal" font="default" size="100%">Alfano, Caterina</style></author><author><style face="normal" font="default" size="100%">Seri, Marco</style></author><author><style face="normal" font="default" size="100%">Balduini, Carlo L</style></author><author><style face="normal" font="default" size="100%">Pecci, Alessandro</style></author><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical and pathogenetic features of ETV6 related thrombocytopenia with predisposition to acute lymphoblastic leukemia.</style></title><secondary-title><style face="normal" font="default" size="100%">Haematologica</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Haematologica</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jun 30</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;ETV6-related thrombocytopenia (ETV6-RT) is an autosomal dominant thrombocytopenia that has been recently identified in a few families and has been suspected to predispose to hematological malignancies. To gain further information on this disorder, we searched for ETV6 mutations in the 130 families with inherited thrombocytopenia of unknown origin from our cohort of 274 consecutive pedigrees with familial thrombocytopenia. We identified 20 ETV6-RT patients from 7 pedigrees. They have 5 different ETV6 variants, including three novel mutations affecting the highly conserved E26 transformation-specific domain. The relative frequency of ETV6-RT resulted 2.6% in the whole case series and 4.6% among the families with known forms of inherited thrombocytopenia. The degree of thrombocytopenia and bleeding tendency of ETV6-RT patients were mild, but 4 subjects developed B-cell acute lymphoblastic leukemia during childhood, resulting in a significantly increased incidence compared to the general population. Clinical and laboratory findings did not identify any peculiar defects that can be used to suspect this disorder by routine diagnostic workup. However, at variance with most inherited thrombocytopenias, platelet size was not enlarged. In vitro studies revealed that patients megakaryocytes have defective maturation and impaired proplatelet formation. Moreover, ETV6-RT platelets have reduced ability to spread on fibrinogen. Since also the dominant thrombocytopenias due to mutations in RUNX1 and ANKRD26 are characterized by normal platelet size and predispose to hematological malignancies, we suggest that mutation screening of ETV6, RUNX1 and ANKRD26 should be performed in all the subjects with autosomal dominant thrombocytopenia and normal platelet size.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27365488?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Naselli, Aldo</style></author><author><style face="normal" font="default" size="100%">Penco, Federica</style></author><author><style face="normal" font="default" size="100%">Cantarini, Luca</style></author><author><style face="normal" font="default" size="100%">Insalaco, Antonella</style></author><author><style face="normal" font="default" size="100%">Alessio, Mariolina</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Maggio, Cristina</style></author><author><style face="normal" font="default" size="100%">Obici, Laura</style></author><author><style face="normal" font="default" size="100%">Gallizi, Romina</style></author><author><style face="normal" font="default" size="100%">Cimmino, Marco</style></author><author><style face="normal" font="default" size="100%">Signa, Sara</style></author><author><style face="normal" font="default" size="100%">Lucherini, Orso Maria</style></author><author><style face="normal" font="default" size="100%">Carta, Sonia</style></author><author><style face="normal" font="default" size="100%">Caroli, Francesco</style></author><author><style face="normal" font="default" size="100%">Martini, Alberto</style></author><author><style face="normal" font="default" size="100%">Rubartelli, Anna</style></author><author><style face="normal" font="default" size="100%">Ceccherini, Isabella</style></author><author><style face="normal" font="default" size="100%">Gattorno, Marco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical Characteristics of Patients Carrying the Q703K Variant of the NLRP3 Gene: A 10-year Multicentric National Study.</style></title><secondary-title><style face="normal" font="default" size="100%">J Rheumatol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Rheumatol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">43</style></volume><pages><style face="normal" font="default" size="100%">1093-100</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;The aim of our study was to analyze the clinical and functional effect of the p.Q703K (p. Q705K, c. 2107C&gt;A) variant of the NLRP3 gene in a population of patients screened for suspected cryopyrin-associated periodic syndrome (CAPS).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Since 2002, 580 patients underwent molecular analysis for NLRP3. Data on clinical presentation, response to treatment, and longterm followup were collected using a uniform questionnaire. The pattern of cytokine secretion after lipopolysaccharide stimulation from isolated monocytes was analyzed in 3 patients carrying the p.Q703K variant and 1 patient with a chronic infantile neurologic, cutaneous, articular syndrome phenotype carrying both the p.M406I and p.Q703K, and compared with 7 patients with CAPS with sure pathogenic variants and 6 healthy controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The p.Q703K variant was found in 57 screened patients with an overall allelic frequency of 5%. The frequency in normal controls was 5.5%. Clinical data at the moment of molecular analysis and at followup were available in 36 patients. Two patients displayed additional mutations of NLRP3. The mean followup was 2.5 years. Thirteen patients (39%) had a final diagnosis different from the original suspicion of CAPS. The remaining 21 patients displayed a mild phenotype mainly characterized by recurrent episodes of urticarial rash and arthralgia. Only 8 patients were treated with anti-interleukin (IL)-1 treatment, with a complete response in 5 patients. The pattern of secretion of IL-1β and other cytokines (IL-6 and IL-1 receptor antagonist) in patients did not display the aberrancies observed in patients with CAPS and was similar to that observed in healthy controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The present study confirms the weak clinical and functional effect of the p.Q703K variant.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27036377?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Porto, Andrea Giuseppe</style></author><author><style face="normal" font="default" size="100%">Brun, Francesca</style></author><author><style face="normal" font="default" size="100%">Severini, Giovanni Maria</style></author><author><style face="normal" font="default" size="100%">Losurdo, Pasquale</style></author><author><style face="normal" font="default" size="100%">Fabris, Enrico</style></author><author><style face="normal" font="default" size="100%">Taylor, Matthew R G</style></author><author><style face="normal" font="default" size="100%">Mestroni, Luisa</style></author><author><style face="normal" font="default" size="100%">Sinagra, Gianfranco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical Spectrum of PRKAG2 Syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">Circ Arrhythm Electrophysiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Circ Arrhythm Electrophysiol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">AMP-Activated Protein Kinases</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Conduction System</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Wolff-Parkinson-White Syndrome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">e003121</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26729852?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">von Lowtzow, Catharina</style></author><author><style face="normal" font="default" size="100%">Hofmann, Andrea</style></author><author><style face="normal" font="default" size="100%">Zhang, Rong</style></author><author><style face="normal" font="default" size="100%">Marsch, Florian</style></author><author><style face="normal" font="default" size="100%">Ebert, Anne-Karoline</style></author><author><style face="normal" font="default" size="100%">Rösch, Wolfgang</style></author><author><style face="normal" font="default" size="100%">Stein, Raimund</style></author><author><style face="normal" font="default" size="100%">Boemers, Thomas M</style></author><author><style face="normal" font="default" size="100%">Hirsch, Karin</style></author><author><style face="normal" font="default" size="100%">Marcelis, Carlo</style></author><author><style face="normal" font="default" size="100%">Feitz, Wouter F J</style></author><author><style face="normal" font="default" size="100%">Brusco, Alfredo</style></author><author><style face="normal" font="default" size="100%">Migone, Nicola</style></author><author><style face="normal" font="default" size="100%">Di Grazia, Massimo</style></author><author><style face="normal" font="default" size="100%">Moebus, Susanne</style></author><author><style face="normal" font="default" size="100%">Nöthen, Markus M</style></author><author><style face="normal" font="default" size="100%">Reutter, Heiko</style></author><author><style face="normal" font="default" size="100%">Ludwig, Michael</style></author><author><style face="normal" font="default" size="100%">Draaken, Markus</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CNV analysis in 169 patients with bladder exstrophy-epispadias complex.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Med Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Med. Genet.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">17</style></volume><pages><style face="normal" font="default" size="100%">35</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The bladder exstrophy-epispadias complex (BEEC) represents the severe end of the congenital uro-rectal malformation spectrum. Initial studies have implicated rare copy number variations (CNVs), including recurrent duplications of chromosomal region 22q11.21, in BEEC etiology.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;To detect further CNVs, array analysis was performed in 169 BEEC patients. Prior to inclusion, 22q11.21 duplications were excluded using multiplex ligation-dependent probe amplification.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Following the application of stringent filter criteria, seven rare CNVs were identified: n = 4, not present in 1307 in-house controls; n = 3, frequency of &lt;0.002 in controls. These CNVs ranged from 1 to 6.08 Mb in size. To identify smaller CNVs, relaxed filter criteria used in the detection of previously reported BEEC associated chromosomal regions were applied. This resulted in the identification of six additional rare CNVs: n = 4, not present in 1307 in-house controls; n = 2, frequency &lt;0.0008 in controls. These CNVs ranged from 0.03-0.08 Mb in size. For 10 of these 13 CNVs, confirmation and segregation analyses were performed (5 of maternal origin; 5 of paternal origin). Interestingly, one female with classic bladder extrophy carried a 1.18 Mb duplication of 22q11.1, a chromosomal region that is associated with cat eye syndrome.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;A number of rare CNVs were identified in BEEC patients, and these represent candidates for further evaluation. Rare inherited CNVs may constitute modifiers of, or contributors to, multifactorial BEEC phenotypes.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27138190?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Galli, Elena</style></author><author><style face="normal" font="default" size="100%">Neri, Iria</style></author><author><style face="normal" font="default" size="100%">Ricci, Giampaolo</style></author><author><style face="normal" font="default" size="100%">Baldo, Ermanno</style></author><author><style face="normal" font="default" size="100%">Barone, Maurizio</style></author><author><style face="normal" font="default" size="100%">Belloni Fortina, Anna</style></author><author><style face="normal" font="default" size="100%">Bernardini, Roberto</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author><author><style face="normal" font="default" size="100%">Caffarelli, Carlo</style></author><author><style face="normal" font="default" size="100%">Calamelli, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Capra, Lucetta</style></author><author><style face="normal" font="default" size="100%">Carello, Rossella</style></author><author><style face="normal" font="default" size="100%">Cipriani, Francesca</style></author><author><style face="normal" font="default" size="100%">Comberiati, Pasquale</style></author><author><style face="normal" font="default" size="100%">Diociaiuti, Andrea</style></author><author><style face="normal" font="default" size="100%">El Hachem, Maya</style></author><author><style face="normal" font="default" size="100%">Fontana, Elena</style></author><author><style face="normal" font="default" size="100%">Gruber, Michaela</style></author><author><style face="normal" font="default" size="100%">Haddock, Ellen</style></author><author><style face="normal" font="default" size="100%">Maiello, Nunzia</style></author><author><style face="normal" font="default" size="100%">Meglio, Paolo</style></author><author><style face="normal" font="default" size="100%">Patrizi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Peroni, Diego</style></author><author><style face="normal" font="default" size="100%">Scarponi, Dorella</style></author><author><style face="normal" font="default" size="100%">Wielander, Ingrid</style></author><author><style face="normal" font="default" size="100%">Eichenfield, Lawrence F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Consensus Conference on Clinical Management of pediatric Atopic Dermatitis.</style></title><secondary-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">26</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The Italian Consensus Conference on clinical management of atopic dermatitis in children reflects the best and most recent scientific evidence, with the aim to provide specialists with a useful tool for managing this common, but complex clinical condition. Thanks to the contribution of experts in the field and members of the Italian Society of Pediatric Allergology and Immunology (SIAIP) and the Italian Society of Pediatric Dermatology (SIDerP), this Consensus statement integrates the basic principles of the most recent guidelines for the management of atopic dermatitis to facilitate a practical approach to the disease. The therapeutical approach should be adapted to the clinical severity and requires a tailored strategy to ensure good compliance by children and their parents. In this Consensus, levels and models of intervention are also enriched by the Italian experience to facilitate a practical approach to the disease.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26936273?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bembich, Stefano</style></author><author><style face="normal" font="default" size="100%">Marrazzo, Francesca</style></author><author><style face="normal" font="default" size="100%">Barini, Alice</style></author><author><style face="normal" font="default" size="100%">Ravalico, Paola</style></author><author><style face="normal" font="default" size="100%">Cont, Gabriele</style></author><author><style face="normal" font="default" size="100%">Demarini, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The cortical response to a noxious procedure changes over time in preterm infants.</style></title><secondary-title><style face="normal" font="default" size="100%">Pain</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pain</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">157</style></volume><pages><style face="normal" font="default" size="100%">1979-87</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The aim of the study was to investigate whether cortical response to a repeated noxious procedure may change over time in preterm infants. Possible reasons for change are: (1) advancing maturation of central nervous system; and (2) increasing experience with noxious procedures during hospital stay. Sixteen preterm infants were recruited, with a postmenstrual age (PMA) ranging between 29 and 36 weeks. Newborns were assessed during a heel-prick procedure, once a week for at least 3 consecutive times. Multichannel near-infrared spectroscopy was used to detect cortical activation, by measuring increase in cortical oxy-haemoglobin (HbO2). Parietal, temporal, and posterior frontal areas were monitored bilaterally. By regression analysis, we studied the effect of (1) increasing PMA and (2) increasing number of heel pricks, on the magnitude of cortical activation. We observed a bilateral nociceptive event-related activation of the posterior frontal cortex, mainly contralateral to the side pricked. Additionally, we found a significant positive effect of PMA, as HbO2 progressively increased in the posterior frontal cortex (P &lt; 0.001), bilaterally, over time. Conversely, the degree of cortical activation decreased as the number of noxious events increased (P &lt; 0.002). We conclude the following: (1) Preterm newborns showed a significant activation of the posterior frontal cortex in association with noxious stimuli; (2) Cortical activation was progressively greater with increasing PMA; (3) There was an inverse relationship between cortical activation and the number of heel pricks. We speculate that such findings may be due to both endogenous cortical maturation and experience-dependent neuroplasticity of the developing brain (eg, synaptogenesis, synaptic pruning).&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27152689?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zanella, Sara</style></author><author><style face="normal" font="default" size="100%">De Leo, Luigina</style></author><author><style face="normal" font="default" size="100%">Nguyen-Ngoc-Quynh, Le</style></author><author><style face="normal" font="default" size="100%">Nguyen-Duy, Bo</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Tran-Thi-Chi, Mai</style></author><author><style face="normal" font="default" size="100%">Phung-Duc, Son</style></author><author><style face="normal" font="default" size="100%">Le-Thanh, Hai</style></author><author><style face="normal" font="default" size="100%">Malaventura, Cristina</style></author><author><style face="normal" font="default" size="100%">Vatta, Serena</style></author><author><style face="normal" font="default" size="100%">Ziberna, Fabiana</style></author><author><style face="normal" font="default" size="100%">Mazzocco, Martina</style></author><author><style face="normal" font="default" size="100%">Volpato, Stefano</style></author><author><style face="normal" font="default" size="100%">Phung-Tuyet, Lan</style></author><author><style face="normal" font="default" size="100%">Le-Thi-Minh, Huong</style></author><author><style face="normal" font="default" size="100%">Borgna-Pignatti, Caterina</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cross-sectional study of coeliac autoimmunity in a population of Vietnamese children.</style></title><secondary-title><style face="normal" font="default" size="100%">BMJ Open</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMJ Open</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">e011173</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;The prevalence of coeliac disease (CD) in Vietnam is unknown. To fill this void, we assessed the prevalence of serological markers of CD autoimmunity in a population of children in Hanoi.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SETTING: &lt;/b&gt;The outpatient blood drawing laboratory of the largest paediatric hospital in North Vietnam was used for the study, which was part of an international project of collaboration between Italy and Vietnam.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PARTICIPANTS: &lt;/b&gt;Children having blood drawn for any reason were included. Exclusion criteria were age younger than 2 years, acquired or congenital immune deficiency and inadequate sample. A total of 1961 children (96%) were enrolled (838 females, 1123 males, median age 5.3 years).&lt;/p&gt;&lt;p&gt;&lt;b&gt;OUTCOMES: &lt;/b&gt;Primary outcome was the prevalence of positive autoimmunity to both IgA antitransglutaminase antibodies (anti-tTG) assessed with an ELISA test and antiendomysial antibodies (EMA). Secondary outcome was the prevalence of CD predisposing human leucocyte antigens (HLA) (HLA DQ2/8) in the positive children and in a random group of samples negative for IgA anti-tTG.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The IgA anti-tTG test was positive in 21/1961 (1%; 95% CI 0.61% to 1.53%); however, EMA antibodies were negative in all. HLA DQ2/8 was present in 7/21 (33%; 95% CI 14.5% to 56.9%) of the anti-tTG-positive children and in 72/275 (26%; 95% CI 21% to 32%) of those who were negative.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Coeliac autoimmunity is rare in Vietnam, although prevalence of HLA DQ2/8 is similar to that of other countries. We hypothesise that the scarce exposure to gluten could be responsible for these findings.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27329441?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Krauss, Baruch S</style></author><author><style face="normal" font="default" size="100%">Calligaris, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Green, Steven M</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Current concepts in management of pain in children in the emergency department.</style></title><secondary-title><style face="normal" font="default" size="100%">Lancet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Lancet</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acute Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Analgesics, Opioid</style></keyword><keyword><style  face="normal" font="default" size="100%">Anesthetics, Local</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents, Non-Steroidal</style></keyword><keyword><style  face="normal" font="default" size="100%">Anxiety</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Emergency Medicine</style></keyword><keyword><style  face="normal" font="default" size="100%">Emergency Service, Hospital</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain Management</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</style></keyword><keyword><style  face="normal" font="default" size="100%">Stress, Psychological</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jan 2</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">387</style></volume><pages><style face="normal" font="default" size="100%">83-92</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Pain is common in children presenting to emergency departments with episodic illnesses, acute injuries, and exacerbation of chronic disorders. We review recognition and assessment of pain in infants and children and discuss the manifestations of pain in children with chronic illness, recurrent pain syndromes, and cognitive impairment, including the difficulties of pain management in these patients. Non-pharmacological interventions, as adjuncts to pharmacological management for acute anxiety and pain, are described by age and development. We discuss the pharmacological management of acute pain and anxiety, reviewing invasive and non-invasive routes of administration, pharmacology, and adverse effects.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10013</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26095580?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Tornese, Gianluca</style></author><author><style face="normal" font="default" size="100%">Marzuillo, Pierluigi</style></author><author><style face="normal" font="default" size="100%">Pellegrin, Maria Chiara</style></author><author><style face="normal" font="default" size="100%">Germani, Claudio</style></author><author><style face="normal" font="default" size="100%">Faleschini, Elena</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Grandone, Anna</style></author><author><style face="normal" font="default" size="100%">Miraglia Del Giudice, Emanuele</style></author><author><style face="normal" font="default" size="100%">Perrone, Laura</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A case of Rubinstein-Taybi syndrome associated with growth hormone deficiency in childhood.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Endocrinol (Oxf)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Endocrinol. (Oxf)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">83</style></volume><pages><style face="normal" font="default" size="100%">437-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25683362?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Crocoli, Alessandro</style></author><author><style face="normal" font="default" size="100%">Tornesello, Assunta</style></author><author><style face="normal" font="default" size="100%">Pittiruti, Mauro</style></author><author><style face="normal" font="default" size="100%">Barone, Angelica</style></author><author><style face="normal" font="default" size="100%">Muggeo, Paola</style></author><author><style face="normal" font="default" size="100%">Inserra, Alessandro</style></author><author><style face="normal" font="default" size="100%">Molinari, Angelo Claudio</style></author><author><style face="normal" font="default" size="100%">Grillenzoni, Valeria</style></author><author><style face="normal" font="default" size="100%">Durante, Viviana</style></author><author><style face="normal" font="default" size="100%">Cicalese, Maria Pia</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio Andrea</style></author><author><style face="normal" font="default" size="100%">Cesaro, Simone</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Central venous access devices in pediatric malignancies: a position paper of Italian Association of Pediatric Hematology and Oncology.</style></title><secondary-title><style face="normal" font="default" size="100%">J Vasc Access</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Vasc Access</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Mar-Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">130-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;INTRODUCTION: &lt;/b&gt;Treatment of pediatric malignancies is becoming progressively more complex, implying the adoption of multimodal therapies. A reliable, long-lasting venous access represents one of the critical requirements for the success of those treatments. Recent technical innovations-such as minimally invasive procedures for placement, new devices and novel materials-have rapidly spread for clinical use in adult patients, but are still not consistently used in the pediatric population.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The Supportive Therapy Working Group of Italian Association of Hematology and Oncology (AIEOP) reviewed medical literature focusing on new aspects of central venous access devices (VADs) in pediatric patients affected by oncohematological diseases.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Appropriate recommendations for clinical use in these patients have been discussed and formulated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The importance of the correct choice, management and use of VADs in pediatric oncohematological patients is a necessary prerequisite for an adequate standard of care, also considering the increased chances of cure and the longer life expectancy of those patients with modern therapies.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25362978?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bembich, Stefano</style></author><author><style face="normal" font="default" size="100%">Travan, Laura</style></author><author><style face="normal" font="default" size="100%">Cont, Gabriele</style></author><author><style face="normal" font="default" size="100%">Bua, Jenny</style></author><author><style face="normal" font="default" size="100%">Strajn, Tamara</style></author><author><style face="normal" font="default" size="100%">Demarini, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cerebral oxygenation with different nasal continuous positive airway pressure levels in preterm infants.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child Fetal Neonatal Ed</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Dis. Child. Fetal Neonatal Ed.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cerebrovascular Circulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Continuous Positive Airway Pressure</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemoglobins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Premature</style></keyword><keyword><style  face="normal" font="default" size="100%">Intensive Care, Neonatal</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Nasal Cavity</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxygen Consumption</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxyhemoglobins</style></keyword><keyword><style  face="normal" font="default" size="100%">Spectroscopy, Near-Infrared</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">100</style></volume><pages><style face="normal" font="default" size="100%">F165-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;This study evaluates the effect of varying nasal continuous positive airway pressure (NCPAP) level on cerebral blood flow (CBF) and oxygenation in preterm infants.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Oxy-haemoglobin (HbO2) and total haemoglobin (HbTot), as CBF estimates, and the ratio between HbO2 and HbTot (HbO2/HbTot), as cerebral oxygenation estimate, were assessed by near-infrared spectroscopy in 26 stable preterm newborns at a postmenstrual age between 26 and 33 weeks. Baseline HbO2, HbTot and HbO2/HbTot values were initially collected with NCPAP at 5 cm H2O and then compared with values obtained with NCPAP levels at both 3 and 8 cm H2O.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Compared with 5 cm H2O, cerebral HbO2, HbTot and HbO2/HbTot remained unchanged both after increasing (to 8 cm H2O) and decreasing (to 3 cm H2O) the NCPAP level. This result was observed both in regional areas (24 sites) and in the overall monitored area (frontal and parietal cortex). Compared with 8 cm H2O, peripheral oxygen saturation significantly decreased at 3 cm H2O (p=0.021). Heart rate did not change.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;No differences in CBF and cerebral oxygenation were observed with NCPAP levels in the range 3-8 cm H2O despite a decrease in peripheral oxygenation with 3 cm H2O.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25336677?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rusconi, Daniela</style></author><author><style face="normal" font="default" size="100%">Negri, Gloria</style></author><author><style face="normal" font="default" size="100%">Colapietro, Patrizia</style></author><author><style face="normal" font="default" size="100%">Picinelli, Chiara</style></author><author><style face="normal" font="default" size="100%">Milani, Donatella</style></author><author><style face="normal" font="default" size="100%">Spena, Silvia</style></author><author><style face="normal" font="default" size="100%">Magnani, Cinzia</style></author><author><style face="normal" font="default" size="100%">Silengo, Margherita Cirillo</style></author><author><style face="normal" font="default" size="100%">Sorasio, Lorena</style></author><author><style face="normal" font="default" size="100%">Curtisova, Vaclava</style></author><author><style face="normal" font="default" size="100%">Cavaliere, Maria Luigia</style></author><author><style face="normal" font="default" size="100%">Prontera, Paolo</style></author><author><style face="normal" font="default" size="100%">Stangoni, Gabriela</style></author><author><style face="normal" font="default" size="100%">Ferrero, Giovanni Battista</style></author><author><style face="normal" font="default" size="100%">Biamino, Elisa</style></author><author><style face="normal" font="default" size="100%">Fischetto, Rita</style></author><author><style face="normal" font="default" size="100%">Piccione, Maria</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Salviati, Leonardo</style></author><author><style face="normal" font="default" size="100%">Selicorni, Angelo</style></author><author><style face="normal" font="default" size="100%">Finelli, Palma</style></author><author><style face="normal" font="default" size="100%">Larizza, Lidia</style></author><author><style face="normal" font="default" size="100%">Gervasini, Cristina</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Characterization of 14 novel deletions underlying Rubinstein-Taybi syndrome: an update of the CREBBP deletion repertoire.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum. Genet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Cohort Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">CREB-Binding Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Point Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Rubinstein-Taybi Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Deletion</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">134</style></volume><pages><style face="normal" font="default" size="100%">613-26</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Rubinstein-Taybi syndrome (RSTS) is a rare, clinically heterogeneous disorder characterized by cognitive impairment and several multiple congenital anomalies. The syndrome is caused by almost private point mutations in the CREBBP (~55% of cases) and EP300 (~8%) genes. The CREBBP mutational spectrum is variegated and characterized by point mutations (30-50 %) and deletions (~10%). The latter are diverse in size and genomic position and remove either the whole CREBBP gene and its flanking regions or only an intragenic portion. Here, we report 14 novel CREBBP deletions ranging from single exons to the whole gene and flanking regions which were identified by applying complementary cytomolecular techniques: fluorescence in situ hybridization, multiplex ligation-dependent probe amplification and array comparative genome hybridization, to a large cohort of RSTS patients. Deletions involving CREBBP account for 23% of our detected CREBBP mutations, making an important contribution to the mutational spectrum. Genotype-phenotype correlations revealed that patients with CREBBP deletions extending beyond this gene did not always have a more severe phenotype than patients harboring CREBBP point mutations, suggesting that neighboring genes play only a limited role in the etiopathogenesis of CREBBP-centerd contiguous gene syndrome. Accordingly, the extent of the deletion is not predictive of the severity of the clinical phenotype.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25805166?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Callea, Michele</style></author><author><style face="normal" font="default" size="100%">Yavuz, Izzet</style></author><author><style face="normal" font="default" size="100%">Clarich, Gabriella</style></author><author><style face="normal" font="default" size="100%">Cammarata-Scalisi, Francisco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">[Clinical and molecular study in a child with X-linked hypohidrotic ectodermal dysplasia].</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Argent Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch Argent Pediatr</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Dec 1</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">113</style></volume><pages><style face="normal" font="default" size="100%">e341-4</style></pages><language><style face="normal" font="default" size="100%">spa</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Ectodermal dysplasia encompasses more than 200 clinically distinct entities, which affect at least two structures derived from the ectoderm, including the skin, hair, nails, teeth, sweat glands, and sebaceous glands. X-linked hypohidrotic ectodermal dysplasia is the most common type and is caused by mutation of the EDA gene that encodes Ectodysplasin-A. It occurs in less than 1 in 100 000 individuals and is clinically characterized by hypodontia, hypohidrosis, hypotrichosis, and eye dis orders. We present a child evaluated in a multidisciplinary manner with clinical and molecular diagnosis of X-linked hypohidrotic ectodermal dysplasia with type missense mutation c.1133C&gt; T; p.T378M in EDA gene.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26593813?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Nicchia, Elena</style></author><author><style face="normal" font="default" size="100%">Benedicenti, Francesco</style></author><author><style face="normal" font="default" size="100%">Rocco, Daniela De</style></author><author><style face="normal" font="default" size="100%">Greco, Chiara</style></author><author><style face="normal" font="default" size="100%">Bottega, Roberta</style></author><author><style face="normal" font="default" size="100%">Inzana, Francesca</style></author><author><style face="normal" font="default" size="100%">Faleschini, Michela</style></author><author><style face="normal" font="default" size="100%">Bonin, Serena</style></author><author><style face="normal" font="default" size="100%">Cappelli, Enrico</style></author><author><style face="normal" font="default" size="100%">Mogni, Massimo</style></author><author><style face="normal" font="default" size="100%">Stanzial, Franco</style></author><author><style face="normal" font="default" size="100%">Svahn, Johanna</style></author><author><style face="normal" font="default" size="100%">Dufour, Carlo</style></author><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical aspects of Fanconi anemia individuals with the same mutation of FANCF identified by next generation sequencing.</style></title><secondary-title><style face="normal" font="default" size="100%">Birth Defects Res A Clin Mol Teratol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Birth Defects Res. Part A Clin. Mol. Teratol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">1003-1010</style></pages><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Fanconi anemia (FA) is a rare genetic disease characterized by congenital malformations, aplastic anemia and increased risk of developing malignancies. FA is genetically heterogeneous as it is caused by at least 17 different genes. Among these, FANCA, FANCC, and FANCG account for approximately 85% of the patients whereas the remaining genes are mutated in only a small percentage of cases. For this reason, the molecular diagnostic process is complex and not always extended to all the FA genes, preventing the characterization of individuals belonging to rare groups.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The FA genes were analyzed using a next generation sequencing approach in two unrelated families.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The analysis identified the same, c.484_485del, homozygous mutation of FANCF in both families. A careful examination of three electively aborted fetuses in one family and one affected girl in the other indicated an association of the FANCF loss-of-function mutation with a severe phenotype characterized by multiple malformations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The systematic use of next generation sequencing will allow the recognition of individuals from rare complementation groups, a better definition of their clinical phenotypes, and consequently, an appropriate genetic counseling. Birth Defects Research (Part A) 103:1003-1010, 2015. © 2015 Wiley Periodicals, Inc.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26033879?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Benelli, Elisa</style></author><author><style face="normal" font="default" size="100%">Carrato, Valentina</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Coeliac disease in the ERA of the new ESPGHAN and BSPGHAN guidelines: a prospective cohort study.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Dis. Child.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Nov 17</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To evaluate the consequences of the last European Society of Paediatric Gastroenterology, Hepatology and Nutrition (ESPGHAN) and British Society of Paediatric Gastroenterology, Hepatology and Nutrition (BSPGHAN) guidelines for the diagnosis of coeliac disease (CD) by means of a prospective study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;Prospective cohort study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SETTING: &lt;/b&gt;Institute for Maternal and Child Health IRCCS Burlo Garofolo (Trieste, Italy).&lt;/p&gt;&lt;p&gt;&lt;b&gt;PATIENTS: &lt;/b&gt;Children diagnosed with CD without a duodenal biopsy (group 1), following the last ESPGHAN and BSPGHAN guidelines, and children diagnosed with a duodenal biopsy, matched for sex, age and year of diagnosis (group 2), were prospectively enrolled over a 3-year period. All patients were put on a gluten-free diet (GFD) and were followed up for clinical conditions and laboratory testing at 6 months every year since diagnosis (median follow up: 1.9 years).&lt;/p&gt;&lt;p&gt;&lt;b&gt;OUTCOME MEASURES: &lt;/b&gt;Resolution of symptoms, body mass index, laboratory testing (haemoglobin, anti-transglutaminase IgA), adherence to a GFD, quality of life, and supplementary post-diagnosis medical consultations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;51 out of 468 (11%) patients were diagnosed without a duodenal biopsy (group 1; median age 2.1 years) and matched to 92 patients diagnosed with a biopsy (group 2; median age 2.4 years). At the end of follow-up the two groups were statistically comparable in terms of clinical and nutritional status, anti-transglutaminase IgA antibody titres, quality of life, adherence to a GFD, and number of supplementary medical consultations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;On the basis of this prospective study, diagnosis of CD can be reliably performed without a duodenal biopsy in approximately 11% of cases. At least during a medium-term follow-up, this approach has no negative consequences relating to clinical remission, adherence to diet, and quality of life of children with CD.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26578746?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Agostinis, C</style></author><author><style face="normal" font="default" size="100%">Zorzet, S</style></author><author><style face="normal" font="default" size="100%">De Leo, R</style></author><author><style face="normal" font="default" size="100%">Zauli, G</style></author><author><style face="normal" font="default" size="100%">De Seta, F</style></author><author><style face="normal" font="default" size="100%">Bulla, R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The combination of N-acetyl cysteine, alpha-lipoic acid, and bromelain shows high anti-inflammatory properties in novel in vivo and in vitro models of endometriosis.</style></title><secondary-title><style face="normal" font="default" size="100%">Mediators Inflamm</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mediators Inflamm.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">2015</style></volume><pages><style face="normal" font="default" size="100%">918089</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;To evaluate the efficacy of an association of N-acetyl cystein, alpha-lipoic acid, and bromelain (NAC/LA/Br) in the treatment of endometriosis we set up a new in vivo murine model. We explored the anti-inflammatory and proapoptotic effect of this combination on human endometriotic endothelial cells (EECs) and on endothelial cells isolated from normal uterus (UtMECs). We implanted fragments of human endometriotic cysts intraperitoneally into SCID mice to evaluate the efficacy of NAC/LA/Br treatment. UtMECs and EECs, untreated or treated with NAC/LA/Br, were activated with the proinflammatory stimulus TNF-α and their response in terms of VCAM1 expression was evaluated. The proapoptotic effect of higher doses of NAC/LA/Br on UtMECs and EECs was measured with a fluorogenic substrate for activated caspases 3 and 7. The preincubation of EECs with NAC/LA/Br prior to cell stimulation with TNF-α prevents the upregulation of the expression of the inflammatory &quot;marker&quot; VCAM1. Furthermore NAC/LA/Br were able to induce EEC, but not UtMEC, apoptosis. Finally, the novel mouse model allowed us to demonstrate that mice treated with NAC/LA/Br presented a lower number of cysts, smaller in size, compared to untreated mice. Our findings suggest that these dietary supplements may have potential therapeutic uses in the treatment of chronic inflammatory diseases like endometriosis.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25960622?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Santarelli, Lory</style></author><author><style face="normal" font="default" size="100%">Staffolani, Sara</style></author><author><style face="normal" font="default" size="100%">Strafella, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Nocchi, Linda</style></author><author><style face="normal" font="default" size="100%">Manzella, Nicola</style></author><author><style face="normal" font="default" size="100%">Grossi, Paola</style></author><author><style face="normal" font="default" size="100%">Bracci, Massimo</style></author><author><style face="normal" font="default" size="100%">Pignotti, Elettra</style></author><author><style face="normal" font="default" size="100%">Alleva, Renata</style></author><author><style face="normal" font="default" size="100%">Borghi, Battista</style></author><author><style face="normal" font="default" size="100%">Pompili, Cecilia</style></author><author><style face="normal" font="default" size="100%">Sabbatini, Armando</style></author><author><style face="normal" font="default" size="100%">Rubini, Corrado</style></author><author><style face="normal" font="default" size="100%">Zuccatosta, Lina</style></author><author><style face="normal" font="default" size="100%">Bichisecchi, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Valentino, Matteo</style></author><author><style face="normal" font="default" size="100%">Horwood, Keith</style></author><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Bovenzi, Massimo</style></author><author><style face="normal" font="default" size="100%">Dong, Lan-Feng</style></author><author><style face="normal" font="default" size="100%">Neuzil, Jiri</style></author><author><style face="normal" font="default" size="100%">Amati, Monica</style></author><author><style face="normal" font="default" size="100%">Tomasetti, Marco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Combined circulating epigenetic markers to improve mesothelin performance in the diagnosis of malignant mesothelioma.</style></title><secondary-title><style face="normal" font="default" size="100%">Lung Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Lung Cancer</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Sep 25</style></date></pub-dates></dates><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;Malignant mesothelioma (MM) is a highly aggressive tumor with poor prognosis. A major challenge is the development and application of early and highly reliable diagnostic marker(s). Serum biomarkers, such as 'soluble mesothelin-related proteins' (SMRPs), is the most studied and frequently used in MM. However, the low sensitivity of SMRPs for early MM limits its value; therefore, additional biomarkers are required. In this study, two epigenetically regulated markers in MM (microRNA-126, miR-126, and methylated thrombomodulin promoter, Met-TM) were combined with SMRPs and evaluated as a potential strategy to detect MM at an early stage.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;A total of 188 subjects, including 45 MM patients, 99 asbestos-exposed subjects, and 44 healthy controls were prospectively enrolled, serum samples collected, and serum levels of SMRPs, miR-126 and Met-TM evaluated. Logistic regression analysis was performed to evaluate the diagnostic value of the three biomarkers. Using this approach, the performance of the '3-biomarker classifier' was tested by calculating the overall probability score of the MM and control samples, respectively, and the ROC curve was generated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS AND CONCLUSION: &lt;/b&gt;The combination of the three biomarkers was the best predictor to differentiate MM patients from asbestos-exposed subjects and healthy controls. The accuracy and cancer specificity was confirmed in a second validation cohort and lung cancer population. We propose that the combination of the two epigenetic biomarkers with SMRPs as a diagnosis for early MM overcomes the limitations of using SMRPs alone.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26431916?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Knowles, Alessandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comment on: 'Anthropometric parameters in relation to glycaemic status and lipid profile in a multi-ethnic sample in Italy' by Gualdi-Russo et al.</style></title><secondary-title><style face="normal" font="default" size="100%">Public Health Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Public Health Nutr</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Oct 28</style></date></pub-dates></dates><pages><style face="normal" font="default" size="100%">1</style></pages><language><style face="normal" font="default" size="100%">ENG</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26507801?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Santos, Ruda de Luna Almeida</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Celsi, Fulvio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comment to Santos et al., &quot;hyper-IgD and periodic fever syndrome: a new MVK mutation (p.R277G) associated with a severe phenotype&quot;.</style></title><secondary-title><style face="normal" font="default" size="100%">Gene</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Gene</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Fever</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoglobulin D</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphotransferases (Alcohol Group Acceptor)</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Mar 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">559</style></volume><pages><style face="normal" font="default" size="100%">99-101</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We performed molecular modeling analysis onto a novel mutation in the gene MVK, described by Santos et al., found to be causative of a severe form of Hyper-IgD/Mevalonate Kinase Deficiency. The mutation p.R277G, in our analysis, lowers the binding affinity for some enzyme's substrates. Interestingly, we found that p.R277G mutation inhibits binding of Isopentenyl Pyrophosphate (IPP) (binding free energy=0 kcal/mol), one of isoprenoids responsible for feedback-inhibition of MVK. IPP is known to be an activator of a specific class of T-cells and we can hypothesize that increased levels of this metabolite generate an aberrant immune system response. Indeed other experiments are needed to verify this hypothesis; however, this work demonstrates usefulness of molecular modeling in generating novel pathogenic hypothesis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25620160?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author><author><style face="normal" font="default" size="100%">Antonio, Pizzol</style></author><author><style face="normal" font="default" size="100%">Marilena, Granzotto</style></author><author><style face="normal" font="default" size="100%">Rovere, Francesca</style></author><author><style face="normal" font="default" size="100%">Tamaro, Paolo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Complete remission of VZV reactivation treated with valganciclovir in a patient with total lymphocyte depletion and acute kidney injury after allogeneic bone marrow transplantation.</style></title><secondary-title><style face="normal" font="default" size="100%">APMIS</style></secondary-title><alt-title><style face="normal" font="default" size="100%">APMIS</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acute Kidney Injury</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Marrow Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Fatal Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Ganciclovir</style></keyword><keyword><style  face="normal" font="default" size="100%">Herpes Zoster</style></keyword><keyword><style  face="normal" font="default" size="100%">Herpesvirus 3, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Precursor Cell Lymphoblastic Leukemia-Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Load</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">123</style></volume><pages><style face="normal" font="default" size="100%">77-80</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Varicella zoster virus (VZV), a threat for hematopoietic stem cell transplantation (HSCT) recipients, is still one of the most common viral pathogens that affect these patients with a reported incidence ranging between 17% and 50% in the post transplantation period. Valganciclovir (V-GCV), a valine ester pro-drug of GCV orally administrable, has recently shown great activity against CMV infections, but there are no reports of its clinical efficacy against VZV. We here report a case history of a patient with positive serologic test for VZV, who underwent allogeneic HSCT and developed an atypical varicella-like illness. First-line therapy with foscarnet had to be discontinued due rapid development of renal impairment (creatinine: 2.60 mg/dL, urea: 130.6 mg/dL) and therefore was switched to V-GCV. The renal impairment and skin lesions of the patient fully recovered after few days of therapy, even though the patient had complete lymphocyte depletion. This is the first case of a patient with chickenpox-like illness treated successfully with V-GCV.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25131855?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Addobbati, C</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Sotero Fragoso, T</style></author><author><style face="normal" font="default" size="100%">Tavares Dantas, A</style></author><author><style face="normal" font="default" size="100%">de Ataíde Mariz, H</style></author><author><style face="normal" font="default" size="100%">Ferreira da Rocha Junior, L</style></author><author><style face="normal" font="default" size="100%">Branco PintoDuarte, A L</style></author><author><style face="normal" font="default" size="100%">Coelho, A V C</style></author><author><style face="normal" font="default" size="100%">de Moura, R R</style></author><author><style face="normal" font="default" size="100%">Polesello, V</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author><author><style face="normal" font="default" size="100%">Sandrin Garcia, P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comprehensive analysis of polymorphisms in the HLA-G 5' upstream regulatory and 3' untranslated regions in Brazilian patients with systemic lupus erythematosus.</style></title><secondary-title><style face="normal" font="default" size="100%">Tissue Antigens</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Tissue Antigens</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">85</style></volume><pages><style face="normal" font="default" size="100%">458-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;This study aims to comprehensively analyze human leucocyte antigen (HLA)-G polymorphisms association with susceptibility to systemic lupus erythematosus (SLE) development and clinical manifestations. The HLA-G 5' upstream regulatory region (URR), 3' untranslated region (UTR) and a cytosine deletion at exon 3 (ΔC, HLA-G*0105N allele) were analyzed in 114 SLE patients and 128 healthy controls from North East Brazil. The +3003T&gt;C (rs1707) C allele and the HG010101c extended HLA-G allele were significantly more frequent in SLE patients than healthy controls (+3003C allele frequency: 12% in SLE patients vs 6% in controls; odds ratio (OR), 2.10, 95% confidence interval (CI), 1.06-4.28, P = 0.026; HG010101c frequency: 11.8% in SLE patients and 6.3% in controls; OR, 2.14, 95% CI, 1.01-4.51, P = 0.046) and were associated with susceptibility for disease development. Other polymorphisms were associated with different clinical manifestations. Although HLA-G role in SLE disease is far from being elucidated yet, our association study results along with a systematic review and meta-analysis suggest that HLA-G might be able to slightly modulate the complex SLE phenotype (pooled OR, 1.14, 95% CI, 1.02-1.27, P = 0.021).&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25762019?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Vuckovic, Dragana</style></author><author><style face="normal" font="default" size="100%">Dallapiccola, Bruno</style></author><author><style face="normal" font="default" size="100%">Franzè, Annamaria</style></author><author><style face="normal" font="default" size="100%">Mauri, Lucia</style></author><author><style face="normal" font="default" size="100%">Perrone, Maria Dolores</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Connexin 26 variant carriers have a better gastrointestinal health: is this the heterozygote advantage?</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Hum Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Hum. Genet.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">563-4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25099251?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Rizzi, Lucia</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Guarnotta, Carla</style></author><author><style face="normal" font="default" size="100%">Munaut, Carine</style></author><author><style face="normal" font="default" size="100%">Baldassarre, Gustavo</style></author><author><style face="normal" font="default" size="100%">Papa, Giovanni</style></author><author><style face="normal" font="default" size="100%">Zorzet, Sonia</style></author><author><style face="normal" font="default" size="100%">Ghebrehiwet, Berhane</style></author><author><style face="normal" font="default" size="100%">Ling, Guang Sheng</style></author><author><style face="normal" font="default" size="100%">Botto, Marina</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">C1q as a unique player in angiogenesis with therapeutic implication in wound healing.</style></title><secondary-title><style face="normal" font="default" size="100%">Proc Natl Acad Sci U S A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Proc. Natl. Acad. Sci. U.S.A.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Complement C1q</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Primers</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">Human Umbilical Vein Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoblotting</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">In Situ Hybridization</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats, Wistar</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Wound Healing</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Mar 18</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">111</style></volume><pages><style face="normal" font="default" size="100%">4209-14</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We have previously shown that C1q is expressed on endothelial cells (ECs) of newly formed decidual tissue. Here we demonstrate that C1q is deposited in wound-healing skin in the absence of C4 and C3 and that C1q mRNA is locally expressed as revealed by real-time PCR and in situ hybridization. C1q was found to induce permeability of the EC monolayer, to stimulate EC proliferation and migration, and to promote tube formation and sprouting of new vessels in a rat aortic ring assay. Using a murine model of wound healing we observed that vessel formation was defective in C1qa(-/-) mice and was restored to normal after local application of C1q. The mean vessel density of wound-healing tissue and the healed wound area were significantly increased in C1q-treated rats. On the basis of these results we suggest that C1q may represent a valuable therapeutic agent that can be used to treat chronic ulcers or other pathological conditions in which angiogenesis is impaired, such as myocardial ischemia.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24591625?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Cunto, Angela</style></author><author><style face="normal" font="default" size="100%">Paviotti, Giulia</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Travan, Laura</style></author><author><style face="normal" font="default" size="100%">Bua, Jenny</style></author><author><style face="normal" font="default" size="100%">Cont, Gabriele</style></author><author><style face="normal" font="default" size="100%">Demarini, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Can body mass index accurately predict adiposity in newborns?</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child Fetal Neonatal Ed</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Dis. Child. Fetal Neonatal Ed.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adiposity</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Anthropometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Composition</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Mass Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Cross-Sectional Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mothers</style></keyword><keyword><style  face="normal" font="default" size="100%">Plethysmography</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Regression Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword><keyword><style  face="normal" font="default" size="100%">Sex Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">99</style></volume><pages><style face="normal" font="default" size="100%">F238-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Body mass index (BMI) is correlated with body fatness and risk of related diseases in children and adults. Proportionality indexes such as BMI and ponderal index (PI) have been suggested as complementary measures in neonatal growth assessment. Yet, they are still not used in neonates and their correlation with fatness is unknown. The aim of the study was to test the hypothesis that BMI z-score would predict neonatal adiposity. Body composition measurements (ie, fat mass, fat-free mass) by air displacement plethysmography (PEA POD, LMI, Concord-USA), weight and length were obtained in 200 infants ≥36 weeks' gestational age (GA) at birth. Linear regression analysis showed a direct association between BMI z-score and %fat mass (r(2)=0.43, p&lt;0.0001). This association was confirmed independently from sex, GA and maternal prepregnancy BMI. BMI z-score predicted adiposity better than PI. However, both BMI z-score and PI were poor predictors of adiposity at birth.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24302686?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Murina, Filippo</style></author><author><style face="normal" font="default" size="100%">Graziottin, Alessandra</style></author><author><style face="normal" font="default" size="100%">Vicariotto, Franco</style></author><author><style face="normal" font="default" size="100%">De Seta, Francesco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Can Lactobacillus fermentum LF10 and Lactobacillus acidophilus LA02 in a slow-release vaginal product be useful for prevention of recurrent vulvovaginal candidiasis?: A clinical study.</style></title><secondary-title><style face="normal" font="default" size="100%">J Clin Gastroenterol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Clin. Gastroenterol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Administration, Intravaginal</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biofilms</style></keyword><keyword><style  face="normal" font="default" size="100%">Candidiasis, Vulvovaginal</style></keyword><keyword><style  face="normal" font="default" size="100%">Delayed-Action Preparations</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Lactobacillus acidophilus</style></keyword><keyword><style  face="normal" font="default" size="100%">Lactobacillus fermentum</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Probiotics</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Tablets</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Vagina</style></keyword><keyword><style  face="normal" font="default" size="100%">Vulva</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Nov-Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">48 Suppl 1</style></volume><pages><style face="normal" font="default" size="100%">S102-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To assess the effectiveness of the association of 2 specific strains, Lactobacillus fermentum LF10 (DSM 19187) and Lactobacillus acidophilus LA02 (DSM 21717), specifically formulated in slow-release effervescent tablets, in patients with recurrent vulvovaginal candidiasis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;The study was a clinical trial of 58 women diagnosed with recurrent VVC (≥4 culture-confirmed episodes in a 12-mo period). All patients were given 200 mg of fluconazole orally as an induction dose for 3 alternate days during the first treatment week. Afterward, the patients were given a new product formulated in slow-release vaginal tablets containing at least 0.4 billion live cells of each of lactobacillus L. fermentum LF10 and L. acidophilus LA02 (first phase of the prophylactic period), on alternate days for 10 consecutive nights. Patients who were still free of symptoms were given 1 vaginal tablet every week for the next 10 weeks (second phase of the prophylactic period). Patients asymptomatic after the total duration of the observation phase (7 mo) were considered as responders.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;During the second 10-week prophylactic phase, 49 of 57 (86.0%) patients remained free of clinical recurrence, whereas symptomatic VVC occurred in 8 patients (14.0%). During the 7-month follow-up, 42 patients of 49 (85.7%) were symptom free at the end of the protocol, whereas clinical recurrences occurred in 7 women (14.3%). Overall, 42 of 58 women enrolled in the study (72.4%) experienced no clinical recurrence throughout the 7-month observation phase (responders).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;This study strengthens the evidence supporting the use of specific lactobacilli with well-demonstrated activities associated with the creation and maintenance of a vaginal biofilm that hinders the persistence of an infection caused by Candida.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25291115?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Conter, Valentino</style></author><author><style face="normal" font="default" size="100%">Valsecchi, Maria Grazia</style></author><author><style face="normal" font="default" size="100%">Parasole, Rosanna</style></author><author><style face="normal" font="default" size="100%">Putti, Maria Caterina</style></author><author><style face="normal" font="default" size="100%">Locatelli, Franco</style></author><author><style face="normal" font="default" size="100%">Barisone, Elena</style></author><author><style face="normal" font="default" size="100%">Lo Nigro, Luca</style></author><author><style face="normal" font="default" size="100%">Santoro, Nicola</style></author><author><style face="normal" font="default" size="100%">Aricò, Maurizio</style></author><author><style face="normal" font="default" size="100%">Ziino, Ottavio</style></author><author><style face="normal" font="default" size="100%">Pession, Andrea</style></author><author><style face="normal" font="default" size="100%">Testi, Anna Maria</style></author><author><style face="normal" font="default" size="100%">Micalizzi, Concetta</style></author><author><style face="normal" font="default" size="100%">Casale, Fiorina</style></author><author><style face="normal" font="default" size="100%">Zecca, Marco</style></author><author><style face="normal" font="default" size="100%">Casazza, Gabriella</style></author><author><style face="normal" font="default" size="100%">Tamaro, Paolo</style></author><author><style face="normal" font="default" size="100%">La Barba, Gaetano</style></author><author><style face="normal" font="default" size="100%">Notarangelo, Lucia Dora</style></author><author><style face="normal" font="default" size="100%">Silvestri, Daniela</style></author><author><style face="normal" font="default" size="100%">Colombini, Antonella</style></author><author><style face="normal" font="default" size="100%">Rizzari, Carmelo</style></author><author><style face="normal" font="default" size="100%">Biondi, Andrea</style></author><author><style face="normal" font="default" size="100%">Masera, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Basso, Giuseppe</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Childhood high-risk acute lymphoblastic leukemia in first remission: results after chemotherapy or transplant from the AIEOP ALL 2000 study.</style></title><secondary-title><style face="normal" font="default" size="100%">Blood</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Blood</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antineoplastic Combined Chemotherapy Protocols</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Combined Modality Therapy</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm, Residual</style></keyword><keyword><style  face="normal" font="default" size="100%">Precursor Cell Lymphoblastic Leukemia-Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Radiotherapy</style></keyword><keyword><style  face="normal" font="default" size="100%">Remission Induction</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Mar 6</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">123</style></volume><pages><style face="normal" font="default" size="100%">1470-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The outcome of high-risk (HR) acute lymphoblastic leukemia patients enrolled in the AIEOP-BFM ALL 2000 study in Italy is described. HR criteria were minimal residual disease (MRD) levels ≥10(-3) at day 78 (MRD-HR), no complete remission (CR) at day 33, t(4;11) translocation, and prednisone poor response (PPR). Treatment (2 years) included protocol I, 3 polychemotherapy blocks, delayed intensification (protocol IIx2 or IIIx3), cranial radiotherapy, and maintenance. A total of 312 HR patients had a 5-year event-free survival (EFS) of 58.9% (standard error [SE] = 2.8) and an overall survival of 68.9% (SE = 2.6). In hierarchical order, EFS was 45.9% (4.4) in 132 MRD-HR patients, 41.2% (11.9) in 17 patients with no CR at day 33, 36.4% (14.5) in 11 patients with t(4;11), and 74.0% (3.6) in 152 HR patients only for PPR. No statistically significant difference was found for disease-free survival in patients with very HR features [MRD-HR, no CR at day 33, t(4;11) translocation], given hematopoietic stem cell transplantation (HSCT) (n = 66) or chemotherapy only (n = 88), after adjusting for waiting time to HSCT (5.7 months). Patients at HR only for PPR have a favorable outcome. MRD-HR is associated with poor outcome despite intensive treatment and/or HSCT and may qualify for innovative therapies. The study was registered at www.clinicaltrials.gov as #NCT00613457.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24415536?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Chermetz, Maddalena</style></author><author><style face="normal" font="default" size="100%">Gobbo, Margherita</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Ottaviani, Giulia</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio A</style></author><author><style face="normal" font="default" size="100%">Verzegnassi, Federico</style></author><author><style face="normal" font="default" size="100%">Treister, Nathaniel S</style></author><author><style face="normal" font="default" size="100%">Di Lenarda, Roberto</style></author><author><style face="normal" font="default" size="100%">Biasotto, Matteo</style></author><author><style face="normal" font="default" size="100%">Zacchigna, Serena</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Class IV laser therapy as treatment for chemotherapy-induced oral mucositis in onco-haematological paediatric patients: a prospective study.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Paediatr Dent</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int J Paediatr Dent</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">24</style></volume><pages><style face="normal" font="default" size="100%">441-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Oral mucositis is a debilitating side effect of chemotherapy. Laser therapy has recently demonstrated efficacy in the management of oral mucositis (OM).&lt;/p&gt;&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;This prospective study was conducted to evaluate the efficacy of class IV laser therapy in patients affected by OM.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;Eighteen onco-haematological paediatric patients receiving chemotherapy and/or haematopoietic stem cell transplantation, prior to total body irradiation, affected by OM, were enrolled in this study. Patients were treated with class IV laser therapy for four consecutive days; the assessment of OM was performed through WHO Oral Mucositis Grading Objective Scale, and pain was evaluated through visual analogue scale. Patients completed a validated questionnaire, and photographs of lesions were taken during each session. Patients were re-evaluated 11 days after the first day of laser therapy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;All patients demonstrated improvement in pain sensation, and all mucositis was fully resolved at the 11-day follow-up visit, with no apparent side effects. Laser therapy was well tolerated with remarkable reduction in pain associated with oral mucositis after 1-2 days of laser therapy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Given class IV laser therapy appears to be safe, non-invasive, and potentially effective, prospective, randomized, controlled trials are necessary to further assess efficacy and to determine optimal treatment parameters.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24372909?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cancrini, Caterina</style></author><author><style face="normal" font="default" size="100%">Puliafito, Pamela</style></author><author><style face="normal" font="default" size="100%">Digilio, Maria Cristina</style></author><author><style face="normal" font="default" size="100%">Soresina, Annarosa</style></author><author><style face="normal" font="default" size="100%">Martino, Silvana</style></author><author><style face="normal" font="default" size="100%">Rondelli, Roberto</style></author><author><style face="normal" font="default" size="100%">Consolini, Rita</style></author><author><style face="normal" font="default" size="100%">Ruga, Ezia Maria</style></author><author><style face="normal" font="default" size="100%">Cardinale, Fabio</style></author><author><style face="normal" font="default" size="100%">Finocchi, Andrea</style></author><author><style face="normal" font="default" size="100%">Romiti, Maria Luisa</style></author><author><style face="normal" font="default" size="100%">Martire, Baldassarre</style></author><author><style face="normal" font="default" size="100%">Bacchetta, Rosa</style></author><author><style face="normal" font="default" size="100%">Albano, Veronica</style></author><author><style face="normal" font="default" size="100%">Carotti, Adriano</style></author><author><style face="normal" font="default" size="100%">Specchia, Fernando</style></author><author><style face="normal" font="default" size="100%">Montin, Davide</style></author><author><style face="normal" font="default" size="100%">Cirillo, Emilia</style></author><author><style face="normal" font="default" size="100%">Cocchi, Guido</style></author><author><style face="normal" font="default" size="100%">Trizzino, Antonino</style></author><author><style face="normal" font="default" size="100%">Bossi, Grazia</style></author><author><style face="normal" font="default" size="100%">Milanesi, Ornella</style></author><author><style face="normal" font="default" size="100%">Azzari, Chiara</style></author><author><style face="normal" font="default" size="100%">Corsello, Giovanni</style></author><author><style face="normal" font="default" size="100%">Pignata, Claudio</style></author><author><style face="normal" font="default" size="100%">Aiuti, Alessandro</style></author><author><style face="normal" font="default" size="100%">Pietrogrande, Maria Cristina</style></author><author><style face="normal" font="default" size="100%">Marino, Bruno</style></author><author><style face="normal" font="default" size="100%">Ugazio, Alberto Giovanni</style></author><author><style face="normal" font="default" size="100%">Plebani, Alessandro</style></author><author><style face="normal" font="default" size="100%">Rossi, Paolo</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Italian Network for Primary Immunodeficiencies</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical features and follow-up in patients with 22q11.2 deletion syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Multiple</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Age Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 22</style></keyword><keyword><style  face="normal" font="default" size="100%">Delayed Diagnosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Developmental Disabilities</style></keyword><keyword><style  face="normal" font="default" size="100%">DiGeorge Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Progression</style></keyword><keyword><style  face="normal" font="default" size="100%">Early Diagnosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Follow-Up Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Testing</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Monitoring, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">Severity of Illness Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Sex Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">164</style></volume><pages><style face="normal" font="default" size="100%">1475-80.e2</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To investigate the clinical manifestations at diagnosis and during follow-up in patients with 22q11.2 deletion syndrome to better define the natural history of the disease.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;A retrospective and prospective multicenter study was conducted with 228 patients in the context of the Italian Network for Primary Immunodeficiencies. Clinical diagnosis was confirmed by cytogenetic or molecular analysis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The cohort consisted of 112 males and 116 females; median age at diagnosis was 4 months (range 0 to 36 years 10 months). The diagnosis was made before 2 years of age in 71% of patients, predominantly related to the presence of heart anomalies and neonatal hypocalcemia. In patients diagnosed after 2 years of age, clinical features such as speech and language impairment, developmental delay, minor cardiac defects, recurrent infections, and facial features were the main elements leading to diagnosis. During follow-up (available for 172 patients), the frequency of autoimmune manifestations (P = .015) and speech disorders (P = .002) increased. After a median follow-up of 43 months, the survival probability was 0.92 at 15 years from diagnosis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data show a delay in the diagnosis of 22q11.2 deletion syndrome with noncardiac symptoms. This study provides guidelines for pediatricians and specialists for early identification of cases that can be confirmed by genetic testing, which would permit the provision of appropriate clinical management.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24657119?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Copetti, Valentina</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">De Pieri, Carlo</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical significance of hyper-IgA in a paediatric laboratory series.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Dis Child</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Dis. Child.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hospitals, Pediatric</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypergammaglobulinemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoglobulin A</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Tertiary Care Centers</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">99</style></volume><pages><style face="normal" font="default" size="100%">1114-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The causes of extremely elevated IgA, whether isolated or associated with an increase in other classes of immunoglobulin, are poorly defined in paediatrics. We reviewed the diagnostic significance of very high IgA levels (greater than 3 SD above the mean for age) in a cohort of patients referred to a tertiary care children's hospital. Hyper-IgA was found in 91 of 6364 subjects (1.4%) and in 68 cases was not associated with an increased IgG and/or IgM level. Most subjects with hyper-IgA (73.5%) had a severe immune defect, a chronic rheumatic disease or inflammatory bowel disease, while these conditions were very rare in a control group with normal IgA values (8%). Although our results may in part reflect the experience of a tertiary care centre, we suggest that hyper-IgA in children should always arouse suspicion of a serious disease.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25053738?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Olden, Matthias</style></author><author><style face="normal" font="default" size="100%">Corre, Tanguy</style></author><author><style face="normal" font="default" size="100%">Hayward, Caroline</style></author><author><style face="normal" font="default" size="100%">Toniolo, Daniela</style></author><author><style face="normal" font="default" size="100%">Ulivi, Sheila</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Pistis, Giorgio</style></author><author><style face="normal" font="default" size="100%">Hwang, Shih-Jen</style></author><author><style face="normal" font="default" size="100%">Bergmann, Sven</style></author><author><style face="normal" font="default" size="100%">Campbell, Harry</style></author><author><style face="normal" font="default" size="100%">Cocca, Massimiliano</style></author><author><style face="normal" font="default" size="100%">Gandin, Ilaria</style></author><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author><author><style face="normal" font="default" size="100%">Glaudemans, Bob</style></author><author><style face="normal" font="default" size="100%">Hastie, Nicholas D</style></author><author><style face="normal" font="default" size="100%">Loffing, Johannes</style></author><author><style face="normal" font="default" size="100%">Polasek, Ozren</style></author><author><style face="normal" font="default" size="100%">Rampoldi, Luca</style></author><author><style face="normal" font="default" size="100%">Rudan, Igor</style></author><author><style face="normal" font="default" size="100%">Sala, Cinzia</style></author><author><style face="normal" font="default" size="100%">Traglia, Michela</style></author><author><style face="normal" font="default" size="100%">Vollenweider, Peter</style></author><author><style face="normal" font="default" size="100%">Vuckovic, Dragana</style></author><author><style face="normal" font="default" size="100%">Youhanna, Sonia</style></author><author><style face="normal" font="default" size="100%">Weber, Julien</style></author><author><style face="normal" font="default" size="100%">Wright, Alan F</style></author><author><style face="normal" font="default" size="100%">Kutalik, Zoltán</style></author><author><style face="normal" font="default" size="100%">Bochud, Murielle</style></author><author><style face="normal" font="default" size="100%">Fox, Caroline S</style></author><author><style face="normal" font="default" size="100%">Devuyst, Olivier</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Common variants in UMOD associate with urinary uromodulin levels: a meta-analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">J Am Soc Nephrol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Am. Soc. Nephrol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Creatinine</style></keyword><keyword><style  face="normal" font="default" size="100%">European Continental Ancestry Group</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Variation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Uromodulin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">1869-82</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Uromodulin is expressed exclusively in the thick ascending limb and is the most abundant protein excreted in normal urine. Variants in UMOD, which encodes uromodulin, are associated with renal function, and urinary uromodulin levels may be a biomarker for kidney disease. However, the genetic factors regulating uromodulin excretion are unknown. We conducted a meta-analysis of urinary uromodulin levels to identify associated common genetic variants in the general population. We included 10,884 individuals of European descent from three genetic isolates and three urban cohorts. Each study measured uromodulin indexed to creatinine and conducted linear regression analysis of approximately 2.5 million single nucleotide polymorphisms using an additive model. We also tested whether variants in genes expressed in the thick ascending limb associate with uromodulin levels. rs12917707, located near UMOD and previously associated with renal function and CKD, had the strongest association with urinary uromodulin levels (P&lt;0.001). In all cohorts, carriers of a G allele of this variant had higher uromodulin levels than noncarriers did (geometric means 10.24, 14.05, and 17.67 μg/g creatinine for zero, one, or two copies of the G allele). rs12446492 in the adjacent gene PDILT (protein disulfide isomerase-like, testis expressed) also reached genome-wide significance (P&lt;0.001). Regarding genes expressed in the thick ascending limb, variants in KCNJ1, SORL1, and CAB39 associated with urinary uromodulin levels. These data indicate that common variants in the UMOD promoter region may influence urinary uromodulin levels. They also provide insights into uromodulin biology and the association of UMOD variants with renal function.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">8</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24578125?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Massaro, Marta</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Ferrara, Giovanna</style></author><author><style face="normal" font="default" size="100%">Badina, Laura</style></author><author><style face="normal" font="default" size="100%">Giorgi, Rita</style></author><author><style face="normal" font="default" size="100%">D'Osualdo, Flavio</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A comparison of three scales for measuring pain in children with cognitive impairment.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Paediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Paediatr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">e495-500</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;Pain is a neglected problem in children with cognitive impairments, and few studies compare the clinical use of specific pain scales. We compared the Non-Communicating Children's Pain Checklist Postoperative Version (NCCPC-PV), the Echelle Douleur Enfant San Salvador (DESS) and the Children's Hospital of Eastern Ontario Pain Scale (CHEOPS). The first two were developed for children with cognitive impairment, and the third is a more general pain scale.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Two external observers and the child's caregiver assessed 40 children with cognitive impairment for pain levels. We assessed inter-rater agreement, correlation, dependence on knowledge of the child's behaviour, simplicity and adequacy in pain rating according to the caregiver for all three scales.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The correlation between the NCCPC-PV and the DESS was strong (Spearman correlation coefficient = 0.76) and better than between each scale and the CHEOPS. Although the DESS showed better inter-rater agreement, it was more dependent on familiarity with the child and was judged more difficult to use by all observers. The NCCPC-PV was the easiest use and the most appropriate for rating the child's pain.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The NCCPC-PV was the easiest to use for pain assessment in cognitively impaired children and should be adopted in clinical settings.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25040148?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author><author><style face="normal" font="default" size="100%">Mezzavilla, Massimo</style></author><author><style face="normal" font="default" size="100%">Abdulhadi, Khalid</style></author><author><style face="normal" font="default" size="100%">Vuckovic, Dragana</style></author><author><style face="normal" font="default" size="100%">Vozzi, Diego</style></author><author><style face="normal" font="default" size="100%">Khalifa Alkowari, Moza</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Badii, Ramin</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Consanguinity and hereditary hearing loss in Qatar.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Hered</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum. Hered.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Consanguinity</style></keyword><keyword><style  face="normal" font="default" size="100%">Hearing Loss</style></keyword><keyword><style  face="normal" font="default" size="100%">Homozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inheritance Patterns</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Prevalence</style></keyword><keyword><style  face="normal" font="default" size="100%">Principal Component Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Qatar</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factor TFIIIB</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">77</style></volume><pages><style face="normal" font="default" size="100%">175-82</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Qatar is a sovereign state located on the Eastern coast of the Arabian Peninsula in the Persian Gulf. Its native population consists of 3 major subgroups: people of Arabian origin or Bedouins, those from an Eastern or Persian ancestry and individuals with African admixture. Historically, all types of consanguineous marriages have been and still are common in the Qatari population, particularly among first and double-first cousins. Thus, there is a higher risk for most inherited diseases including hereditary hearing loss (HHL). In particular, a hearing loss prevalence of 5.2% has been reported in Qatar, with parental consanguinity being more common among affected individuals as compared with unaffected ones. Our recent molecular results confirm a high homogeneity and level of inbreeding in Qatari HHL patients. Among all HHL genes, GJB2, the major player worldwide, accounts for a minor proportion of cases and at least 3 additional genes have been found to be mutated in Qatari patients. Interestingly, one gene, BDP1, has been described to cause HHL only in this country. These results point towards an unexpected level of genetic heterogeneity despite the high level of inbreeding. This review provides an up-to-date picture of HHL in Qatar and of the impact of consanguinity on this disease.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1-4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25060281?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Calligaris, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Longo, Giorgio</style></author><author><style face="normal" font="default" size="100%">Badina, Laura</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cow's milk allergy in children, from avoidance to tolerance.</style></title><secondary-title><style face="normal" font="default" size="100%">Endocr Metab Immune Disord Drug Targets</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Endocr Metab Immune Disord Drug Targets</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cattle</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Desensitization, Immunologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immune Tolerance</style></keyword><keyword><style  face="normal" font="default" size="100%">Milk Hypersensitivity</style></keyword><keyword><style  face="normal" font="default" size="100%">Milk Substitutes</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">47-53</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Food allergy is the primary cause of anaphylaxis in paediatric age affecting roughly 4% of children and their families worldwide, and requiring changes in dietary habits. The prognosis for food allergy in children has traditionally been regarded as good for the most frequent allergens, however the prognosis for cow's milk allergy in the pediatric age is currently considered to be worse than previously believed. There is now enough evidence that measures of avoidance for children at risk did not have any preventive effect whatsoever, but they still came to be counterproductive by avoiding the physiological interaction between food allergens and gastrointestinal mucosal immune system. Programs of specific oral tolerance induction (SOTI) have obtained interesting results in the treatment of food allergy supporting the idea that antigen exposure through gastrointestinal section is important to allow the development of tolerance. Nevertheless this approach is not yet considered &quot;ready&quot; for community recommendations. In this paper we describe our experience in the field of SOTI in children with cow's milk allergy.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24450451?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Tricarico, Paola Maura</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Bianco, Anna Monica</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Curcumin and inflammatory bowel disease: potential and limits of innovative treatments.</style></title><secondary-title><style face="normal" font="default" size="100%">Molecules</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Molecules</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents, Non-Steroidal</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemistry, Pharmaceutical</style></keyword><keyword><style  face="normal" font="default" size="100%">Clinical Trials as Topic</style></keyword><keyword><style  face="normal" font="default" size="100%">Curcumin</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Targeted Therapy</style></keyword><keyword><style  face="normal" font="default" size="100%">Nanotechnology</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">19</style></volume><pages><style face="normal" font="default" size="100%">21127-53</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Curcumin belongs to the family of natural compounds collectively called curcuminoids and it possesses remarkable beneficial anti-oxidant, anti-inflammatory, anti-cancer, and neuroprotective properties. Moreover it is commonly assumed that curcumin has also been suggested as a remedy for digestive diseases such as inflammatory bowel diseases (IBD), a chronic immune disorder affecting the gastrointestinal tract and that can be divided in two major subgroups: Crohn's disease (CD) and Ulcerative Colitis (UC), depending mainly on the intestine tract affected by the inflammatory events. The chronic and intermittent nature of IBD imposes, where applicable, long-term treatments conducted in most of the cases combining different types of drugs. In more severe cases and where there has been no good response to the drugs, a surgery therapy is carried out. Currently, IBD-pharmacological treatments are generally not curative and often present serious side effects; for this reason, being known the relationship between nutrition and IBD, it is worthy of interesting the study and the development of new dietary strategy. The curcumin principal mechanism is the suppression of IBD inflammatory compounds (NF-κB) modulating immune response. This review summarizes literature data of curcumin as anti-inflammatory and anti-oxidant in IBD, trying to understand the different effects in CD e UC.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25521115?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Girardelli, M</style></author><author><style face="normal" font="default" size="100%">Bianco, A M</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, A</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A comparative analysis of serologic parameters and oxidative stress in osteoarthritis and rheumatoid arthritis: reply to Mishra and colleagues.</style></title><secondary-title><style face="normal" font="default" size="100%">Rheumatol Int</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Rheumatol. Int.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arthritis, Rheumatoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipids</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoarthritis</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">33</style></volume><pages><style face="normal" font="default" size="100%">2445-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;In chronic diseases such as rheumatoid arthritis and osteoarthritis, the progression of the disease is characterized by stress oxidative, inflammation, and elevated levels of cholesterol. In mevalonate kinase deficiency, an auto-inflammatory disease, the correlation between inflammation and cholesterol levels is opposite. The metabolic pathway that underlies the production of cholesterol is the mevalonate pathway; it is also essential for the biosynthesis of isoprenoids involved in the control of several cell functions. This divergence of cholesterol levels, associated with these two inflammatory disorders, is probably due to a different etiology, pathogenesis, and progression.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22562750?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Cunto, Angela</style></author><author><style face="normal" font="default" size="100%">Bensa, Marco</style></author><author><style face="normal" font="default" size="100%">Tonelli, Alessandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A case of familial hemiplegic migraine associated with a novel ATP1A2 gene mutation.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Neurol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr. Neurol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Migraine with Aura</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Sodium-Potassium-Exchanging ATPase</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">133-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hemiplegic migraine constitutes an unusual form, characterized by periodic attacks of migraine with a motor component (hemiplegia). Familial forms are dominantly inherited, and are attributable to mutations in genes encoding proteins involved in ion transportation, including ATP1A2, which codes for the α-2 isoform of the sodium-potassium adenosine triphosphatase, a P-type cation transport adenosine triphosphatase, and responsible for the so-called familial hemiplegic migraine type 2. We describe a 9-year-old boy affected by familial hemiplegic migraine, with a novel ATP1A2 gene mutation (c.1799T&gt;C p.V600A) in exon 13. Long-term treatment with flunarizine resulted in a good clinical response and the prevention of further attacks.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22759692?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Catamo, E</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Lenarduzzi, S</style></author><author><style face="normal" font="default" size="100%">Petix, V</style></author><author><style face="normal" font="default" size="100%">Morgutti, M</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">CD14 polymorphisms correlate with an augmented risk for celiac disease in Italian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Genes Immun</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genes Immun.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD14</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">European Continental Ancestry Group</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">HLA Antigens</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Linkage Disequilibrium</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">489-95</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Celiac disease (CD) is a T-cell-mediated chronic inflammatory disease characterized by autoimmune, immunological and environmental components, where genetic factors in addition to the main known risk factors (gliadin and human leukocyte antigen (HLA)-DQ haplotypes) are supposed to be involved. CD14 is a multifunctional receptor involved in the bacterial lipopolysaccharides-dependent signal transduction. The CD14 gene maps on the long arm of chromosome 5 (5q22-q32), a 'hotbed' region for CD; promoter polymorphisms are known to influence its expression. In this study we analyzed three CD14 promoter polymorphisms (c.-1359G&gt;T, c.-1145A&gt;G and c.-159C&gt;T, ) in 938 CD Italian patients and 533 healthy controls, with known HLA-DQ haplotypes, with the aim of evaluating their possible association with the disease. The c.-1145A&gt;G G and c.-159C&gt;T T alleles (as well as the combination of the two alleles in the GT haplotype), were identified as susceptibility factors for CD development, being significantly more frequent in CD patients than in healthy controls. This association was also confirmed when the analysis was restricted to only those subjects characterized by HLA-DQ risk haplotypes. Our results indicate the involvement of CD14 gene polymorphisms in the susceptibility to CD.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22648004?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Carlino, Claudia</style></author><author><style face="normal" font="default" size="100%">Trotta, Eleonora</style></author><author><style face="normal" font="default" size="100%">Stabile, Helena</style></author><author><style face="normal" font="default" size="100%">Morrone, Stefania</style></author><author><style face="normal" font="default" size="100%">Bulla, Roberta</style></author><author><style face="normal" font="default" size="100%">Soriani, Alessandra</style></author><author><style face="normal" font="default" size="100%">Iannitto, Maria Luisa</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Mocci, Carlo</style></author><author><style face="normal" font="default" size="100%">Minozzi, Massimo</style></author><author><style face="normal" font="default" size="100%">Aragona, Cesare</style></author><author><style face="normal" font="default" size="100%">Perniola, Giorgia</style></author><author><style face="normal" font="default" size="100%">Tedesco, Francesco</style></author><author><style face="normal" font="default" size="100%">Sozzani, Silvano</style></author><author><style face="normal" font="default" size="100%">Santoni, Angela</style></author><author><style face="normal" font="default" size="100%">Gismondi, Angela</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Chemerin regulates NK cell accumulation and endothelial cell morphogenesis in the decidua during early pregnancy.</style></title><secondary-title><style face="normal" font="default" size="100%">J Clin Endocrinol Metab</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Clin. Endocrinol. Metab.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Capillaries</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Decidua</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Killer Cells, Natural</style></keyword><keyword><style  face="normal" font="default" size="100%">MAP Kinase Signaling System</style></keyword><keyword><style  face="normal" font="default" size="100%">Neovascularization, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Trimester, First</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Chemokine</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Stromal Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Trophoblasts</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">97</style></volume><pages><style face="normal" font="default" size="100%">3603-12</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;CONTEXT: &lt;/b&gt;Although decidual natural killer (NK) cell accumulation and vascular remodeling are critical steps to ensure successful pregnancy, the molecular mechanisms controlling these events are poorly defined.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;Herein we analyzed whether chemerin, a recently identified chemoattractant involved in many pathophysiological processes, could be expressed in the uterine compartment and could regulate events relevant for the good outcome of pregnancy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;Chemerin expression in human primary culture of stromal (ST) cells, extravillous trophoblast cells, and decidual endothelial cells (DEC) was analyzed by RT-PCR, ELISA, and Western blot. Migration through ST or DEC of peripheral blood and decidual (d) NK cells from pregnant women was performed using a transwell assay. A DEC capillary-like tube formation assay was used to evaluate endothelial morphogenesis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Chemerin is differentially expressed by decidual cells during early pregnancy being present at high levels in ST and extravillous trophoblast cells but not in DEC. Notably, ST cells from pregnant women exhibit and release higher levels of chemerin as compared with ST cells from menopausal or fertile nonpregnant women. Chemerin can support peripheral blood NK cell migration through both DEC and ST cells. Although dNK cells exhibit lower chemerin receptor (CMKLR1) expression than their blood counterpart, CMKLR1 engagement on dNK cells resulted in both ERK activation and migration through decidual ST cells. Interestingly, DEC also express CMKLR1 and undergo ERK activation and capillary-like tube structure formation upon exposure to chemerin.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our data indicate that chemerin is up-regulated during decidualization and might contribute to NK cell accumulation and vascular remodeling during early pregnancy.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22791765?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Gortani, Giulia</style></author><author><style face="normal" font="default" size="100%">Maschio, Massimo</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A child with edema, lower limb deformity, and recurrent diarrhea.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Bone Retroversion</style></keyword><keyword><style  face="normal" font="default" size="100%">Capsule Endoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Diarrhea</style></keyword><keyword><style  face="normal" font="default" size="100%">Edema</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Knee Joint</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphangiectasis, Intestinal</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphedema</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">161</style></volume><pages><style face="normal" font="default" size="100%">1177</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">6</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22835881?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Copertino, Marco</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author><author><style face="normal" font="default" size="100%">Poli, Furio</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Ferrari, Maurizio</style></author><author><style face="normal" font="default" size="100%">Carrera, Paola</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A child with severe pneumomediastinum and ABCA3 gene mutation: a puzzling connection.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Bronconeumol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Bronconeumol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Anemia</style></keyword><keyword><style  face="normal" font="default" size="100%">ATP-Binding Cassette Transporters</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Dyspnea</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intensive Care</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mediastinal Emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Point Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pulmonary Emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">Respiratory Tract Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Subcutaneous Emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">Tomography, X-Ray Computed</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">48</style></volume><pages><style face="normal" font="default" size="100%">139-40</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22304854?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bianco, Anna Monica</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clarification of the pleiotropic effects of statins on mevalonate pathway and the feedback regulation of isoprenoids requires more comprehensive investigation.</style></title><secondary-title><style face="normal" font="default" size="100%">Cell Biochem Funct</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cell Biochem. Funct.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Carcinoma, Hepatocellular</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydroxymethylglutaryl-CoA Reductase Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Liver Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Simvastatin</style></keyword><keyword><style  face="normal" font="default" size="100%">Terpenes</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">30</style></volume><pages><style face="normal" font="default" size="100%">176</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22275121?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Noris, Patrizia</style></author><author><style face="normal" font="default" size="100%">Perrotta, Silverio</style></author><author><style face="normal" font="default" size="100%">Bottega, Roberta</style></author><author><style face="normal" font="default" size="100%">Pecci, Alessandro</style></author><author><style face="normal" font="default" size="100%">Melazzini, Federica</style></author><author><style face="normal" font="default" size="100%">Civaschi, Elisa</style></author><author><style face="normal" font="default" size="100%">Russo, Sabina</style></author><author><style face="normal" font="default" size="100%">Magrin, Silvana</style></author><author><style face="normal" font="default" size="100%">Loffredo, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Di Salvo, Veronica</style></author><author><style face="normal" font="default" size="100%">Russo, Giovanna</style></author><author><style face="normal" font="default" size="100%">Casale, Maddalena</style></author><author><style face="normal" font="default" size="100%">De Rocco, Daniela</style></author><author><style face="normal" font="default" size="100%">Grignani, Claudio</style></author><author><style face="normal" font="default" size="100%">Cattaneo, Marco</style></author><author><style face="normal" font="default" size="100%">Baronci, Carlo</style></author><author><style face="normal" font="default" size="100%">Dragani, Alfredo</style></author><author><style face="normal" font="default" size="100%">Albano, Veronica</style></author><author><style face="normal" font="default" size="100%">Jankovic, Momcilo</style></author><author><style face="normal" font="default" size="100%">Scianguetta, Saverio</style></author><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author><author><style face="normal" font="default" size="100%">Balduini, Carlo L</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical and laboratory features of 103 patients from 42 Italian families with inherited thrombocytopenia derived from the monoallelic Ala156Val mutation of GPIbα (Bolzano mutation).</style></title><secondary-title><style face="normal" font="default" size="100%">Haematologica</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Haematologica</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Aged, 80 and over</style></keyword><keyword><style  face="normal" font="default" size="100%">Bernard-Soulier Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Family Health</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Membrane Glycoproteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Aggregation</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Glycoprotein GPIb-IX Complex</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombocytopenia</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombopoietin</style></keyword><keyword><style  face="normal" font="default" size="100%">Tubulin</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">97</style></volume><pages><style face="normal" font="default" size="100%">82-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Bernard-Soulier syndrome is a very rare form of inherited thrombocytopenia that derives from mutations in GPIbα, GPIbβ, or GPIX and is typically inherited as a recessive disease. However, some years ago it was shown that the monoallelic c.515C&gt;T transition in the GPIBA gene (Bolzano mutation) was responsible for macrothrombocytopenia in a few Italian patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN AND METHODS: &lt;/b&gt;Over the past 10 years, we have searched for the Bolzano mutation in all subjects referred to our institutions because of an autosomal, dominant form of thrombocytopenia of unknown origin.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We identified 42 new Italian families (103 cases) with a thrombocytopenia induced by monoallelic Bolzano mutation. Analyses of the geographic origin of affected pedigrees and haplotypes indicated that this mutation originated in southern Italy. Although the clinical expression was variable, patients with this mutation typically had a mild form of Bernard-Soulier syndrome with mild thrombocytopenia and bleeding tendency. The most indicative laboratory findings were enlarged platelets and reduced GPIb/IX/V platelet expression; in vitro platelet aggregation was normal in nearly all of the cases.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our study indicates that monoallelic Bolzano mutation is the most frequent cause of inherited thrombocytopenia in Italy, affecting 20% of patients recruited at our institutions during the last 10 years. Because many people from southern Italy have emigrated during the last century, this mutation may have spread to other countries.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21933849?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Maso, Gianpaolo</style></author><author><style face="normal" font="default" size="100%">Businelli, Caterina</style></author><author><style face="normal" font="default" size="100%">Piccoli, Monica</style></author><author><style face="normal" font="default" size="100%">Montico, Marcella</style></author><author><style face="normal" font="default" size="100%">De Seta, Francesco</style></author><author><style face="normal" font="default" size="100%">Sartore, Andrea</style></author><author><style face="normal" font="default" size="100%">Alberico, Salvatore</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">The clinical interpretation and significance of electronic fetal heart rate patterns 2 h before delivery: an institutional observational study.</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Gynecol Obstet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Gynecol. Obstet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acidosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Bradycardia</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Blood</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Heart Rate, Fetal</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen-Ion Concentration</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Labor, Obstetric</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Single-Blind Method</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistics, Nonparametric</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">286</style></volume><pages><style face="normal" font="default" size="100%">1153-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;PURPOSE: &lt;/b&gt;To evaluate the clinical significance of intrapartum fetal heart rate (FHR) monitoring in low-risk pregnancies according to guidelines and specific patterns.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;An obstetrician, blinded to neonatal outcome, retrospectively reviewed 198 low-risk cases that underwent continuous electronic fetal monitoring (EFM) during the last 2 h before delivery. The tracings were interpreted as normal, suspicious or pathological, according to specific guidelines of EFM and by grouping the different FHR patterns considering baseline, variability, presence of decelerations and bradycardia. The EFM groups and the different FHR-subgroups were associated with neonatal acid base status at birth, as well as the short-term neonatal composite outcome. Comparisons between groups were performed with Kruskal-Wallis test. Differences among categorical variables were evaluated using Fisher's exact test. Significance was set at p &lt; 0.05 level.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Significant differences were found for mean pH values in the three EFM groups, with a significant trend from &quot;normal&quot; [pH 7.25, 95 % confidence interval (CI) 7.28-7.32] to &quot;pathological&quot; tracings (pH 7.20, 95 % CI 7.17-7.13). Also the rates of adverse composite neonatal outcome were statistically different between the two groups (p &lt; 0.005). Among the different FHR patterns, tracings with atypical variable decelerations and severe bradycardia were more frequently associated with adverse neonatal composite outcome (11.1 and 26.7 %, respectively). However, statistically significant differences were only observed between the subgroups with normal tracings and bradycardia.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;In low-risk pregnancies, there is a significant association between neonatal outcome and EFM classification. However, within abnormal tracings, neonatal outcome might differ according to specific FHR pattern.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22791414?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Ribes-Koninckx, C</style></author><author><style face="normal" font="default" size="100%">Mearin, M L</style></author><author><style face="normal" font="default" size="100%">Korponay-Szabó, I R</style></author><author><style face="normal" font="default" size="100%">Shamir, R</style></author><author><style face="normal" font="default" size="100%">Husby, S</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author><author><style face="normal" font="default" size="100%">Branski, D</style></author><author><style face="normal" font="default" size="100%">Catassi, C</style></author><author><style face="normal" font="default" size="100%">Koletzko, S</style></author><author><style face="normal" font="default" size="100%">Mäki, M</style></author><author><style face="normal" font="default" size="100%">Troncone, R</style></author><author><style face="normal" font="default" size="100%">Zimmer, K P</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">ESPGHAN Working Group on Coeliac Disease Diagnosis</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Coeliac disease diagnosis: ESPGHAN 1990 criteria or need for a change? Results of a questionnaire.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Gastroenterol Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Gastroenterol. Nutr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biopsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Glutens</style></keyword><keyword><style  face="normal" font="default" size="100%">Guideline Adherence</style></keyword><keyword><style  face="normal" font="default" size="100%">Guidelines as Topic</style></keyword><keyword><style  face="normal" font="default" size="100%">Health Care Surveys</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoglobulin A</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestine, Small</style></keyword><keyword><style  face="normal" font="default" size="100%">Physician's Practice Patterns</style></keyword><keyword><style  face="normal" font="default" size="100%">Questionnaires</style></keyword><keyword><style  face="normal" font="default" size="100%">Societies, Medical</style></keyword><keyword><style  face="normal" font="default" size="100%">Transglutaminases</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">54</style></volume><pages><style face="normal" font="default" size="100%">15-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND AND OBJECTIVES: &lt;/b&gt;A revision of criteria for diagnosing coeliac disease (CD) is being conducted by The European Society for Pediatric Gastroenterology, Hepatology, and Nutrition (ESPGHAN). In parallel, we have performed a survey aimed to evaluate present practices for CD among paediatric gastroenterologists and to learn their views on the need for modification of present criteria for CD diagnosis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PATIENTS AND METHODS: &lt;/b&gt;Questionnaires were distributed to experienced paediatric gastroenterologists (ESPGHAN members) via the Internet.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Overall, 95 valid questionnaires were available for analysis, pertaining to 28 different countries, with the majority of responders treating patients with CD for &gt;15 years. Only about 12% of the responders comply with present criteria, noncompliance being related mainly to the challenge policy. Approximately 90% request a revision and modification of the present criteria. Forty-four percent want to omit the small bowel biopsy in symptomatic children with positive anti-tissue transglutaminase immunoglobulin (Ig) A or endomysial IgA antibodies, especially if they are DQ2/DQ8 positive. For silent cases detected by screening with convincingly positive anti-tissue transglutaminase IgA or EMA IgA, about 30% consider that no small bowel biopsy should be required in selected cases. Adding human leukocyte antigen typing in the diagnostic workup was asked for by 42% of the responders. As for gluten challenge, a new policy is advocated restricting its obligation to cases whenever the diagnosis is doubtful or unclear.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Based on these opinions, revision of the ESPGHAN criteria for diagnosing CD is urgently needed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21716133?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cuttini, Marina</style></author><author><style face="normal" font="default" size="100%">Ferrante, Pierpaolo</style></author><author><style face="normal" font="default" size="100%">Mirante, Nadia</style></author><author><style face="normal" font="default" size="100%">Chiandotto, Valeria</style></author><author><style face="normal" font="default" size="100%">Fertz, Mariacristina</style></author><author><style face="normal" font="default" size="100%">Dall'Oglio, Anna Maria</style></author><author><style face="normal" font="default" size="100%">Coletti, Maria Franca</style></author><author><style face="normal" font="default" size="100%">Johnson, Samantha</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cognitive assessment of very preterm infants at 2-year corrected age: performance of the Italian version of the PARCA-R parent questionnaire.</style></title><secondary-title><style face="normal" font="default" size="100%">Early Hum Dev</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Early Hum. Dev.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cognition</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Premature</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Parents</style></keyword><keyword><style  face="normal" font="default" size="100%">Questionnaires</style></keyword><keyword><style  face="normal" font="default" size="100%">ROC Curve</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">88</style></volume><pages><style face="normal" font="default" size="100%">159-63</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Serial assessments of cognitive and language development are recommended for very preterm children, but standardized neuropsychological testing is time-consuming and expensive, as well as tiring for the child.&lt;/p&gt;&lt;p&gt;&lt;b&gt;AIMS: &lt;/b&gt;To validate the Italian version of the PARCA-R parent questionnaire and test its clinical effectiveness in assessing cognitive development of very preterm children at 2 years of corrected age.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;120 consecutive Italian very preterm children (mean gestational age 28.8 weeks, standard deviation 2.1) were assessed in four hospitals through the Mental Development Index (MDI) of the Bayley Scales of Infant Development (BSID-II). Parents completed the PARCA-R questionnaire, designed to measure children's non-verbal and verbal (vocabulary and sentence complexity) cognitive level. The correlation between the MDI and the PARCA-R Parent Report Composite (PRC) was tested through the Pearson correlation coefficient, and the receiver operating characteristic (ROC) curve was used to identify optimal PRC cut-offs.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Significant correlation between the PRC score and MDI (r=0.60, p&lt;0.001) indicated good concurrent validity. The area under the ROC curve was 0.83, and the cut-off of 46 lead to 72.7% sensitivity and 77.1% specificity in identifying children with moderate/severe cognitive delay (MDI&lt;70). Negative predictive value was 96.6 (90.3-99.3). Screening through PARCA-R would reduce the number of children with MDI≥70 undergoing BSID-II or equivalent standardized tool from 109 to 25.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The Italian version of PARCA-R retains good discriminative power for identifying cognitive delay in 2-year very preterm children. It is well accepted by parents, and represents a valid and efficient alternative for developmental screening and outcome measurement.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21862246?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Vuch, Josef</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comments to the editor concerning the paper entitled &quot;Preclinical renal cancer chemopreventive efficacy of geraniol by modulation of multiple molecular pathways&quot; Shiekh Tanveer Ahmad et al.</style></title><secondary-title><style face="normal" font="default" size="100%">Toxicology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Toxicology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Antineoplastic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Kidney Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Terpenes</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Mar 11</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">293</style></volume><pages><style face="normal" font="default" size="100%">123-4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1-3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22210290?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bianco, Anna Monica</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Magnolato, Andrea</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Martellossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A common genetic background could explain early-onset Crohn's disease.</style></title><secondary-title><style face="normal" font="default" size="100%">Med Hypotheses</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Med. Hypotheses</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Crohn Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Linkage</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Biological</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">78</style></volume><pages><style face="normal" font="default" size="100%">520-2</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Crohn's disease (CD) is a multifactorial disease, in which environmental, microbial and genetic factors play important roles. CD is characterized by a chronic granulomatous inflammation by necrotic scarring with aspects of full-thickness wall. In spite of affecting mainly young adults, sometimes, CD can be present in the first year of life (early onset Crohn disease, EOCD) showing an unpredictable course and being often more severe than at older ages. In this paper we propose the hypothesis that EOCD patients should be analyzed using a Mendelian approach with family studies aimed to identify new loci directly involved in the early onset Crohn's disease. So we will leave the classic association study approach used until now for the identification of genes responsible for susceptibility to CD and propose linkage family analysis as alternative and powerful tool for the identification of new genetic variants associated with familiar cases of EOCD.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22309886?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Comar, Manola</style></author><author><style face="normal" font="default" size="100%">Iannacone, Michelle R</style></author><author><style face="normal" font="default" size="100%">Casalicchio, Giorgia</style></author><author><style face="normal" font="default" size="100%">McKay-Chopin, Sandrine</style></author><author><style face="normal" font="default" size="100%">Tommasino, Massimo</style></author><author><style face="normal" font="default" size="100%">Gheit, Tarik</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparison of hybrid capture II, linear array, and a bead-based multiplex genotyping assay for detection of human papillomavirus in women with negative pap test results and atypical squamous cells of undetermined significance.</style></title><secondary-title><style face="normal" font="default" size="100%">J Clin Microbiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Clin. Microbiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Diagnostic Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Papillomavirus Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Sensitivity and Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">Uterine Cervical Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Virology</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">50</style></volume><pages><style face="normal" font="default" size="100%">4041-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Many methods with different levels of analytical sensitivity and clinical specificity have been developed to detect the presence of high-risk (HR) types of the human papillomavirus (HPV) in cervical samples. The Hybrid Capture II (HC-II) assay is broadly used for primary screening. In addition, several HPV genotyping assays, based on PCR methods, display higher sensitivity than the HC-II and are also used in screening programs. We evaluated the performance of three HPV DNA tests, namely, the HC-II, the Linear Array (LA) HPV genotyping assay, and an HPV type-specific E7 PCR bead-based multiplex genotyping assay (TS-MPG) that is a laboratory-developed method for the detection of HPV, in 94 women with atypical squamous cells of undetermined significance (ASC-US) and in cytological samples from 86 women with a negative Pap test. The HPV prevalence with the TS-MPG assay was increased compared to the prevalence with the LA and HC-II assays. The HPV DNA prevalence in women with ASC-US was greater with the TS-MPG assay (46.2%) than with the LA (36.3%) and HC-II (29.7%) assays. The HPV DNA prevalence in the control group was greater with the TS-MPG assay (32.1%) than with the LA assay (10.7%). Two women with ASC-US who were HPV DNA negative by the HC-II and positive by the TS-MPG or/and LA assays had lesions that progressed to low-grade squamous intraepithelial and high-grade squamous intraepithelial lesions. This study shows that the TS-MPG assay exhibited higher analytical sensitivity than the LA and HC-II assays for the detection of HPV DNA, which reduces the potential to incorrectly identify a woman's HPV infection status.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23035194?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Travan, Laura</style></author><author><style face="normal" font="default" size="100%">Demarini, Sergio</style></author><author><style face="normal" font="default" size="100%">Del Frate, Giovanni</style></author><author><style face="normal" font="default" size="100%">Zacchi, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Congenital hemangiopericytoma.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Biopsy, Needle</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemangiopericytoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnetic Resonance Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">Soft Tissue Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Ultrasonography, Prenatal</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">160</style></volume><pages><style face="normal" font="default" size="100%">878</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22177995?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Rocca, Maria Santa</style></author><author><style face="normal" font="default" size="100%">Fabretto, Antonella</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Carlet, Ombretta</style></author><author><style face="normal" font="default" size="100%">Skabar, Aldo</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Pecile, Vanna</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Contribution of SNP arrays in diagnosis of deletion 2p11.2-p12.</style></title><secondary-title><style face="normal" font="default" size="100%">Gene</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Gene</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Multiple</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intellectual Disability</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Deletion</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jan 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">492</style></volume><pages><style face="normal" font="default" size="100%">315-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Deletions of the short arm of chromosome 2 are exceedingly rare, having been reported in few patients. Furthermore most cases with deletion in 2p11.2-p12 have been studied using standard karyotype and so it is not possible to delineate the precise size of deletions. Here, we describe a 9-year-old girl with a 9.4 Mb de novo interstitial deletion of region 2p11.2-p12 identified by SNP array analysis. The deleted region encompasses over 40 known genes, including LRRTM1, CTNNA2 and REEP1, haploinsufficiency of which could explain some clinical features of this patient such as mental retardation, speech delay and gait abnormalities. A comparison of our case with previously reported patients who present deletions in 2p11.2-p12 was carried out. Our case adds new information to the deletion of 2p11.2-p12, improving the knowledge on this rearrangement.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22062632?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Norbedo, Stefania</style></author><author><style face="normal" font="default" size="100%">Perini, Roberto</style></author><author><style face="normal" font="default" size="100%">Amaddeo, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A coughing spine.</style></title><secondary-title><style face="normal" font="default" size="100%">Emerg Med J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Emerg Med J</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cervical Vertebrae</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Dyspnea</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mediastinal Emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Subcutaneous Emphysema</style></keyword><keyword><style  face="normal" font="default" size="100%">Tomography, X-Ray Computed</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">14</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21693479?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Parco, Sergio</style></author><author><style face="normal" font="default" size="100%">Città, Angelo</style></author><author><style face="normal" font="default" size="100%">Vascotto, Fulvia</style></author><author><style face="normal" font="default" size="100%">Tamaro, Giorgio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Celiac disease and immigration in Northeastern Italy: the &quot;drawn double nostalgia&quot; of &quot;cozonac&quot; and &quot;panettone&quot; slices.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Exp Gastroenterol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin Exp Gastroenterol</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">4</style></volume><pages><style face="normal" font="default" size="100%">121-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Many investigators consider children's drawings to be an important test in the evaluation of stress and anxiety, but few studies have examined the reliability and validity of indicators of emotional distress in children's projective drawings. In this report, we describe screening tests in children coming to the Friuli Venezia Giulia region in Northeastern Italy from non-European Union regions and suspected to have celiac disease, the problems involved in diagnosis of the disease, and the &quot;drawn double nostalgia&quot; of Romanian children for both Italian food and traditional Romanian foods. Of 3150 Western European cases, we found 712 with positive antibodies for IgA/IgG antitransglutaminase, 174 with a positive antiendomysium antibody confirmation test, and 20 with an IgA deficit. Of the children examined, 93% were children native to Western Europe, 4% were immigrants from Eastern Europe, and 1.6% originated from Africa. Among these, four Romanian children with celiac disease brought in their drawings, as requested in a hospital questionnaire. The prevalence of celiac disease is destined to increase among immigrants. Economic problems are common, and the twin nostalgia of immigrant children for foods and tastes that are &quot;cozonac&quot; (from the native country) and &quot;panettone&quot; (Italian cake flavor) represents a problem that will be difficult to resolve. Only some children's hospitals in Italy, ie, Burlo Garofolo and Gaslini, public and private foundations, or volunteer associations would be able to deal with this problem.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21753894?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author><author><style face="normal" font="default" size="100%">Caputo, Roberto</style></author><author><style face="normal" font="default" size="100%">de Libero, Cinzia</style></author><author><style face="normal" font="default" size="100%">Di Grande, Laura</style></author><author><style face="normal" font="default" size="100%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Mori, Francesca</style></author><author><style face="normal" font="default" size="100%">Novembre, Elio</style></author><author><style face="normal" font="default" size="100%">Pucci, Neri</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Childhood chronic anterior uveitis associated with vernal keratoconjunctivitis (VKC): successful treatment with topical tacrolimus. Case series.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Rheumatol Online J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr Rheumatol Online J</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">34</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Uveitis treatment involves topical corticosteroids along with cycloplegic-mydriatics. Particularly severe cases may require systemic corticosteroids and immunosuppressive drugs. Vernal keratoconjunctivitis (VKC) treatment consists of a brief period of topical corticosteroids and/or cyclosporine. In patients refractory to traditional treatment, the use of 0.1% topical ophtalmic FK- 506 (tacrolimus) ointment has been occasionally reported.This is the first report of the coexistence of uveitis and VKC. The documented response to topical tacrolimus eyedrop of uveitis and VKC is also of interest, in particular since to our knowledge there are no published reports on its clinical use in uveitis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22047067?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Rimondi, Erika</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Montico, Marcella</style></author><author><style face="normal" font="default" size="100%">D'Ottavio, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Alberico, Salvatore</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Circulating TRAIL shows a significant post-partum decline associated to stressful conditions.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS One</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS ONE</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">C-Reactive Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Blood</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Distress</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Labor, Obstetric</style></keyword><keyword><style  face="normal" font="default" size="100%">Logistic Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Multivariate Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Postpartum Period</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Statistics, Nonparametric</style></keyword><keyword><style  face="normal" font="default" size="100%">Stress, Physiological</style></keyword><keyword><style  face="normal" font="default" size="100%">TNF-Related Apoptosis-Inducing Ligand</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">e27011</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Since circulating levels of TNF-related apoptosis inducing ligand (TRAIL) may be important in the physiopathology of pregnancy, we tested the hypothesis that TRAIL levels change at delivery in response to stressful conditions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS/PRINCIPAL FINDINGS: &lt;/b&gt;We conducted a longitudinal study in a cohort of 73 women examined at week 12, week 16, delivery and in the corresponding cord blood (CB). Serum TRAIL was assessed in relationship with maternal characteristics and to biochemical parameters. TRAIL did not vary between 12 (67.6±27.6 pg/ml, means±SD) and 16 (64.0±16.2 pg/ml) weeks' gestation, while displaying a significant decline after partum (49.3±26.4 pg/ml). Using a cut-off decline &gt;20 pg/ml between week 12 and delivery, the subset of women with the higher decline of circulating TRAIL (41.7%) showed the following characteristics: i) nullipara, ii) higher age, iii) operational vaginal delivery or urgent CS, iv) did not receive analgesia during labor, v) induced labor. CB TRAIL was significantly higher (131.6±52 pg/ml) with respect to the corresponding maternal TRAIL, and the variables significantly associated with the first quartile of CB TRAIL (&lt;90 pg/ml) were higher pre-pregnancy BMI, induction of labor and fetal distress. With respect to the biochemical parameters, maternal TRAIL at delivery showed an inverse correlation with C-reactive protein (CRP), total cortisol, glycemia and insulin at bivariate analysis, but only with CRP at multivariate analysis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Stressful partum conditions and elevated CRP levels are associated with a decrease of circulating TRAIL.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">12</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22194780?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author><author><style face="normal" font="default" size="100%">Pastore, Annalisa</style></author><author><style face="normal" font="default" size="100%">De Rocco, Daniela</style></author><author><style face="normal" font="default" size="100%">Civaschi, Elisa</style></author><author><style face="normal" font="default" size="100%">Di Stazio, Mariateresa</style></author><author><style face="normal" font="default" size="100%">Bottega, Roberta</style></author><author><style face="normal" font="default" size="100%">Melazzini, Federica</style></author><author><style face="normal" font="default" size="100%">Bozzi, Valeria</style></author><author><style face="normal" font="default" size="100%">Pecci, Alessandro</style></author><author><style face="normal" font="default" size="100%">Magrin, Silvana</style></author><author><style face="normal" font="default" size="100%">Balduini, Carlo L</style></author><author><style face="normal" font="default" size="100%">Noris, Patrizia</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical and genetic aspects of Bernard-Soulier syndrome: searching for genotype/phenotype correlations.</style></title><secondary-title><style face="normal" font="default" size="100%">Haematologica</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Haematologica</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Amino Acid Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Bernard-Soulier Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Platelets</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Shape</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemorrhage</style></keyword><keyword><style  face="normal" font="default" size="100%">Homozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Membrane Glycoproteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Sequence Data</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Aggregation</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Glycoprotein GPIb-IX Complex</style></keyword><keyword><style  face="normal" font="default" size="100%">Point Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Ristocetin</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombocytopenia</style></keyword><keyword><style  face="normal" font="default" size="100%">von Willebrand Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">417-23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Bernard-Soulier syndrome is a severe bleeding disease due to a defect of GPIb/IX/V, a platelet complex that binds the von Willebrand factor. Due to the rarity of the disease, there are reports only on a few cases compromising any attempt to establish correlations between genotype and phenotype. In order to identify any associations, we describe the largest case series ever reported, which was evaluated systematically at the same center.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN AND METHODS: &lt;/b&gt;Thirteen patients with the disease and seven obligate carriers were enrolled. We collected clinical aspects and determined platelet features, including number and size, expression of membrane glycoproteins, and ristocetin induced platelet aggregation. Mutations were identified by direct sequencing of the GP1BA, GP1BB, and GP9 genes and their effect was shown by molecular modeling analyses.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Patients all had a moderate thrombocytopenia with giant platelets and a bleeding tendency whose severity varied among individuals. Consistent with expression levels of GPIbα always lower than 10% of control values, platelet aggregation was absent or severely reduced. Homozygous mutations were identified in the GP1BA, GP1BB and GP9 genes; six were novel alterations expected to destabilize the conformation of the respective protein. Except for obligate carriers of a GP9 mutation with a reduced GPIb/IX/V expression and defective aggregation, all the other carriers had no obvious anomalies.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Regardless of mutations identified, the patients' bleeding diathesis did not correlate with thrombocytopenia, which was always moderate, and platelet GPIbα expression, which was always severely impaired. Obligate carriers had features similar to controls though their GPIb/IX/V expression showed discrepancies. Aware of the limitations of our cohort, we cannot define any correlations. However, further investigations should be encouraged to better understand the causes of this rare and underestimated disease.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21173099?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Mazza, Cinzia</style></author><author><style face="normal" font="default" size="100%">Buzi, Fabio</style></author><author><style face="normal" font="default" size="100%">Ortolani, Federica</style></author><author><style face="normal" font="default" size="100%">Vitali, Alberto</style></author><author><style face="normal" font="default" size="100%">Notarangelo, Lucia D</style></author><author><style face="normal" font="default" size="100%">Weber, Giovanna</style></author><author><style face="normal" font="default" size="100%">Bacchetta, Rosa</style></author><author><style face="normal" font="default" size="100%">Soresina, Annarosa</style></author><author><style face="normal" font="default" size="100%">Lougaris, Vassilios</style></author><author><style face="normal" font="default" size="100%">Greggio, Nella A</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Pasic, Srdjan</style></author><author><style face="normal" font="default" size="100%">de Vroede, Monique</style></author><author><style face="normal" font="default" size="100%">Pac, Malgorzata</style></author><author><style face="normal" font="default" size="100%">Kilic, Sara Sebnem</style></author><author><style face="normal" font="default" size="100%">Ozden, Sanal</style></author><author><style face="normal" font="default" size="100%">Rusconi, Roberto</style></author><author><style face="normal" font="default" size="100%">Martino, Silvana</style></author><author><style face="normal" font="default" size="100%">Capalbo, Donatella</style></author><author><style face="normal" font="default" size="100%">Salerno, Mariacarolina</style></author><author><style face="normal" font="default" size="100%">Pignata, Claudio</style></author><author><style face="normal" font="default" size="100%">Radetti, Giorgio</style></author><author><style face="normal" font="default" size="100%">Maggiore, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Plebani, Alessandro</style></author><author><style face="normal" font="default" size="100%">Notarangelo, Luigi D</style></author><author><style face="normal" font="default" size="100%">Badolato, Raffaele</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Clinical heterogeneity and diagnostic delay of autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Homozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyendocrinopathies, Autoimmune</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">139</style></volume><pages><style face="normal" font="default" size="100%">6-11</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Autoimmune polyendocrinopathy-candidiasis-ectodermal dystrophy (APECED) is a rare autosomal recessive organ-specific autoimmune disorder that is characterized by a variable combination of (i) chronic mucocutaneous candidiasis, (ii) polyendocrinopathy and/or hepatitis and (iii) dystrophy of the dental enamel and nails. We analyzed the AIRE (autoimmune regulator) gene in subjects who presented any symptom that has been associated with APECED, including candidiasis and autoimmune endocrinopathy. We observed that 83.3% of patients presented at least two of the three typical manifestations of APECED, while the remaining 16.7% of patients showed other signs of the disease. Analysis of the genetic diagnosis of these subjects revealed that a considerable delay occurs in the majority of patients between the appearance of symptoms and the diagnosis. Overall, the mean diagnostic delay in our patients was 10.2 years. These results suggest that molecular analysis of AIRE should be performed in patients with relapsing mucocutaneous candidiasis for early identification of APECED.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21295522?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Pontillo, Alessandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comments on ''Geranylgeraniol--a new potential therapeutic approach to bisphosphonate associated osteonecrosis of the jaw&quot; by Ziebart T et al. (2011).</style></title><secondary-title><style face="normal" font="default" size="100%">Oral Oncol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Oral Oncol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Bone Density Conservation Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Diphosphonates</style></keyword><keyword><style  face="normal" font="default" size="100%">Diterpenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Jaw Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteonecrosis</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">436-7; author reply 438</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21411362?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Chiaretti, Antonio</style></author><author><style face="normal" font="default" size="100%">Ruggiero, Antonio</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author><author><style face="normal" font="default" size="100%">Pierri, Filomena</style></author><author><style face="normal" font="default" size="100%">Maurizi, Palma</style></author><author><style face="normal" font="default" size="100%">Fantacci, Claudia</style></author><author><style face="normal" font="default" size="100%">Bersani, Giulia</style></author><author><style face="normal" font="default" size="100%">Riccardi, Riccardo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparison of propofol versus propofol-ketamine combination in pediatric oncologic procedures performed by non-anesthesiologists.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Blood Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr Blood Cancer</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Biopsy, Needle</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Marrow Examination</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Conscious Sedation</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypnotics and Sedatives</style></keyword><keyword><style  face="normal" font="default" size="100%">Ketamine</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</style></keyword><keyword><style  face="normal" font="default" size="100%">Physicians</style></keyword><keyword><style  face="normal" font="default" size="100%">Propofol</style></keyword><keyword><style  face="normal" font="default" size="100%">Spinal Puncture</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Dec 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">57</style></volume><pages><style face="normal" font="default" size="100%">1163-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Limited data are available on the best option (short acting sedatives, opioids, or ketamine) in oncologic procedural sedation performed by non-anesthesiologists. The aim of the present prospective study is to compare the safety and efficacy of propofol-ketamine versus propofol alone, managed by trained pediatricians, in children with cancer undergoing painful procedures.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PROCEDURES: &lt;/b&gt;Data on 121 children with acute lymphatic leukemia (ALL) undergoing procedural sedations (lumbar punctures and bone marrow aspirations) were prospectively collected and included drug doses, side effects, pain assessment, and sedation degree. Children were randomly assigned to one of the two groups: P (n = 62) receiving propofol alone and K (n = 59) in whom a ketamine-propofol combination was used.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;In group K, the total dose of propofol required was significantly lower than in group P (3.9 ± 3.6 mg/kg vs. 5.1 ± 3.6 mg/kg; P &lt; 0.001). The incidence of hypotension was also significantly lower (11% vs. 39%; P &lt; 0.001). Major O(2) desaturations (defined as SatO(2) &lt; 88%) occurred principally in group P (7 vs. 1; P = 0.05). Both best analgesia and shorter recovery time were obtained with the propofol-ketamine association. No differences were observed in the degree of sedation and in the awakening quality score between the two groups.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The combination of propofol and ketamine produced statistically significant clinical advantages combined with a higher profile of safety in children with cancer undergoing painful procedures.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21584935?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bellini, Anna</style></author><author><style face="normal" font="default" size="100%">Zanchi, Chiara</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Di Leo, Grazia</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Compliance with the gluten-free diet: the role of locus of control in celiac disease.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Age Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Diet, Gluten-Free</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Internal-External Control</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Patient Compliance</style></keyword><keyword><style  face="normal" font="default" size="100%">Quality of Life</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">158</style></volume><pages><style face="normal" font="default" size="100%">463-466.e5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVES: &lt;/b&gt;To verify whether subjects with celiac disease (CD) have a different locus of control (LoC) compared with healthy subjects, and to evaluate the relationship between LoC and compliance with a prescribed gluten-free diet (GFD) and quality of life (QoL).&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;We studied 156 subjects on a GFD (mean age, 10 years) and 353 healthy controls (mean age, 12 years). All subjects completed tests on the Nowicki-Strickland Locus of Control Scale; the subjects with CD also completed a questionnaire to measure compliance with dietary treatment and the disease's impact on QoL.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;There was no difference in LoC values between patients with CD and controls. Subjects with CD with good dietary compliance had a more internal LoC compared with those who were not compliant (P = .01). Patients who reported a satisfactory QoL had a more internal LoC compared with those who reported negative affects on QoL due to CD (P = .01).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our study confirms the usefulness of the LoC concept for identifying those patients who might be at risk for dietary transgression. Given the enhanced, psychological, and social well being that can result from adherence to a GFD, educational and psychological support can help internalize the LoC in those patients at risk for dietary transgression.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20870245?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Calligaris, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Davide, Zanon</style></author><author><style face="normal" font="default" size="100%">Alessandra, Maestro</style></author><author><style face="normal" font="default" size="100%">De Bortoli, Romina</style></author><author><style face="normal" font="default" size="100%">Chiaretti, Antonio</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Concentrated midazolam for intranasal administration: a pilot study.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Emerg Care</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr Emerg Care</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Administration, Intranasal</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Conscious Sedation</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypnotics and Sedatives</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Midazolam</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Pilot Projects</style></keyword><keyword><style  face="normal" font="default" size="100%">Preoperative Care</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">27</style></volume><pages><style face="normal" font="default" size="100%">245-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21378534?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pensiero, Stefano</style></author><author><style face="normal" font="default" size="100%">Cecchini, Paolo</style></author><author><style face="normal" font="default" size="100%">Michieletto, Paola</style></author><author><style face="normal" font="default" size="100%">Pelizzo, Gloria</style></author><author><style face="normal" font="default" size="100%">Madonia, Maurizio</style></author><author><style face="normal" font="default" size="100%">Parentin, Fulvio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Congenital aplasia of the optic chiasm and esophageal atresia: a case report.</style></title><secondary-title><style face="normal" font="default" size="100%">J Med Case Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Med Case Rep</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">335</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;INTRODUCTION: &lt;/b&gt;The complete absence of the chiasm (chiasmal aplasia) is a rare clinical condition. Hypoplasia of the optic nerve and congenital nystagmus are almost invariably associated characteristics. Microphthalmos or anophthalmos are common features in chiasmal aplasia, while central nervous system abnormalities are less frequent. Esophageal atresia can be isolated or syndromic. In syndromic cases, it is frequently associated with cardiac, limb, renal or vertebral malformations and anal atresia. More rarely, esophageal atresia can be part of anophthalmia-esophageal-genital syndrome, which comprises anophthalmia or microphthalmia, genital abnormalities, vertebral defects and cerebral malformations. Here, a previously unreported case of chiasmal aplasia presenting without microphthalmos and associated with esophageal atresia is described.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CASE PRESENTATION: &lt;/b&gt;Aplasia of the optic chiasm was identified in a Caucasian Italian 8-month-old boy with esophageal atresia. An ultrasound examination carried out at 21 weeks' gestation revealed polyhydramnios. Intrauterine growth retardation, esophageal atresia and a small atrial-septal defect were subsequently detected at 28 weeks' gestation. Repair of the esophageal atresia was carried out shortly after birth. A jejunostomy was carried out at four months to facilitate enteral feeding. The child was subsequently noted to be visually inattentive and to be neurodevelopmentally delayed. Magnetic resonance imaging revealed chiasmal aplasia. No other midline brain defects were found. His karyotype was normal.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;If achiasmia is a spectrum, our patient seems to depict the most severe form, since he appears to have an extremely severe visual impairment. This is in contrast to most of the cases described in the literature, where patients maintain good--or at least useful-- visual function. To the best of our knowledge, the association of optic nerve hypoplasia, complete chiasmal aplasia, esophageal atresia and atrial-septal defect, choanal atresia, hypertelorism and psychomotor retardation has never been described before.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21806818?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Giurici, Nagua</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Consensus on diagnosis and empiric antibiotic therapy of febrile neutropenia.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr Rep</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Feb 24</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">3</style></volume><pages><style face="normal" font="default" size="100%">e4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Controversial issues on the management of empiric therapy and diagnosis of febrile neutropenia (FN) were faced by a Consensus Group of the Italian Association of Pediatric Hematology-Oncology (AIEOP). In this paper we report the suggestions of the consensus process regarding the role of aminoglycosides, glycopeptides and oral antibiotics in empiric therapy of FN, the rules for changing or discontinuing the therapy as well as the timing of the blood cultures.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21647277?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Silva, Silvana</style></author><author><style face="normal" font="default" size="100%">Parentin, Fulvio</style></author><author><style face="normal" font="default" size="100%">Michieletto, Paola</style></author><author><style face="normal" font="default" size="100%">Pensiero, Stefano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Corneal curvature and thickness development in premature infants.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Ophthalmol Strabismus</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Pediatr Ophthalmol Strabismus</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child Development</style></keyword><keyword><style  face="normal" font="default" size="100%">Cornea</style></keyword><keyword><style  face="normal" font="default" size="100%">Corneal Pachymetry</style></keyword><keyword><style  face="normal" font="default" size="100%">Eye</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Premature</style></keyword><keyword><style  face="normal" font="default" size="100%">Intraocular Pressure</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Premature Birth</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Jan-Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">48</style></volume><pages><style face="normal" font="default" size="100%">25-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;PURPOSE: &lt;/b&gt;Analysis of postnatal changes in central corneal thickness (CCT) and corneal curvature (CC) in premature infants, their relation, and their possible influence on eye growth and intraocular pressure (IOP) evaluation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;CCT and CC were assessed in both eyes of 56 premature infants, born at 24 to 32 weeks of gestational age (GA), and then two or three times at post-conceptional ages (PCAs) of 28 to 42 weeks.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;CC changed from 65.83 diopters at 28 weeks of PCA to 49.38 diopters at 42 weeks of PCA. CCT decreased from 794 to 559 μm at the same ages. The reductions of these two corneal parameters seem to be related to each other and begin immediately after birth.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;In light of the few data available in the literature, these data provide more certainty about the CCT values of premature infants. The importance of CCT and CC fast variations after premature birth concerns both the knowledge of anterior segment development and the correct evaluation of IOP in immature eyes; the influence of these two parameters on the methods of IOP evaluation could be more remarkable at the lowest PCAs.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">1</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20411870?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Ziberna, Fabiana</style></author><author><style face="normal" font="default" size="100%">Vatta, Serena</style></author><author><style face="normal" font="default" size="100%">Quaglia, Sara</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Villanacci, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Marzari, Roberto</style></author><author><style face="normal" font="default" size="100%">Florian, Fiorella</style></author><author><style face="normal" font="default" size="100%">Vecchiet, Monica</style></author><author><style face="normal" font="default" size="100%">Sulic, Ana-Marija</style></author><author><style face="normal" font="default" size="100%">Ferrara, Fortunato</style></author><author><style face="normal" font="default" size="100%">Bradbury, Andrew</style></author><author><style face="normal" font="default" size="100%">Sblattero, Daniele</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cryptic genetic gluten intolerance revealed by intestinal antitransglutaminase antibodies and response to gluten-free diet.</style></title><secondary-title><style face="normal" font="default" size="100%">Gut</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Gut</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies, Anti-Idiotypic</style></keyword><keyword><style  face="normal" font="default" size="100%">Asymptomatic Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Diet, Gluten-Free</style></keyword><keyword><style  face="normal" font="default" size="100%">Fatty Acid-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">GTP-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Health Status</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Mucosa</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Peptide Library</style></keyword><keyword><style  face="normal" font="default" size="100%">Transglutaminases</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">60</style></volume><pages><style face="normal" font="default" size="100%">1487-93</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND AND OBJECTIVE: &lt;/b&gt;Antitransglutaminase (anti-TG2) antibodies are synthesised in the intestine and their presence seems predictive of future coeliac disease (CD). This study investigates whether mucosal antibodies represent an early stage of gluten intolerance even in the absence of intestinal damage and serum anti-TG2 antibodies.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This study investigated 22 relatives of patients with CD genetically predisposed to gluten intolerance but negative for both serum anti-TG2 antibodies and intestinal abnormalities. Fifteen subjects were symptomatic and seven were asymptomatic. The presence of immunoglobulin A anti-TG2 antibodies in the intestine was studied by creating phage-antibody libraries against TG-2. The presence of intestinal anti-TG2 antibodies was compared with the serum concentration of the intestinal fatty acid-binding protein (I-FABP), a marker for early intestinal mucosal damage. The effects of a 12-month gluten-free diet on anti-TG2 antibody production and the subjects' clinical condition was monitored. Twelve subjects entered the study as controls.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The intestinal mucosa appeared normal in 18/22; 4 had a slight increase in intraepithelial lymphocytes. Mucosal anti-TG2 antibodies were isolated in 15/22 subjects (68%); in particular symptomatic subjects were positive in 13/15 cases and asymptomatic subjects in 2/7 cases (p=0.01). No mucosal antibodies were selected from the controls' biopsies. There was significant correlation between the presence of intestinal anti-TG2 antibodies and positive concentrations of I-FABP (p=0.0008). After a gluten-free diet, 19/22 subjects underwent a second intestinal biopsy, which showed that anti-TG2 antibodies had disappeared in 12/15 (p=0.002), while I-FABP decreased significantly (p&lt;0.0001). The diet resolved both extraintestinal and intestinal symptoms.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;A new form of genetic-dependent gluten intolerance has been described in which none of the usual diagnostic markers is present. Symptoms and intestinal anti-TG2 antibodies respond to a gluten free-diet. The detection of intestinal anti-TG2 antibodies by the phage-antibody libraries has an important diagnostic and therapeutic impact for the subjects with gluten-dependent intestinal or extraintestinal symptoms. Clinical trial number NCT00677495.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">11</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21471568?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fabretto, Antonella</style></author><author><style face="normal" font="default" size="100%">Shardlow, Alison</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author><author><style face="normal" font="default" size="100%">Hladnik, Uros</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A case of lymphedema-distichiasis syndrome carrying a new de novo frameshift FOXC2 mutation.</style></title><secondary-title><style face="normal" font="default" size="100%">Ophthalmic Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ophthalmic Genet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Abnormalities, Multiple</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Eye Abnormalities</style></keyword><keyword><style  face="normal" font="default" size="100%">Eyelashes</style></keyword><keyword><style  face="normal" font="default" size="100%">Face</style></keyword><keyword><style  face="normal" font="default" size="100%">Forkhead Transcription Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Frameshift Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphedema</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Syndrome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">31</style></volume><pages><style face="normal" font="default" size="100%">98-100</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;PURPOSE: &lt;/b&gt;Lymphedema-Distichiasis (LD, OMIM 153400) is an autosomal dominant disorder with variable expression. The mutated gene implicated is FOXC2, which encodes for a forkhead transcription factor involved in the development of the lymphatic and vascular system. LD is characterized by late childhood or pubertal onset lymphedema of the limbs and distichiasis. Other associations have been reported, including congenital heart disease, ptosis, scoliosis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Here we describe a case of LD carrying a de novo frameshift mutation of FOXC2 who presented a prepubertal onset of lower limbs lymphedema and mild distichiasis associated with other anomalies such as webbing neck and ptosis.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">2</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20450314?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Londero, Margherita</style></author><author><style face="normal" font="default" size="100%">Pastore, Serena</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio A</style></author><author><style face="normal" font="default" size="100%">Bruno, Irene</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A child with pain after mild trauma.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antigens, CD</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD31</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, CD34</style></keyword><keyword><style  face="normal" font="default" size="100%">Antigens, Differentiation, Myelomonocytic</style></keyword><keyword><style  face="normal" font="default" size="100%">Biopsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Factor VIII</style></keyword><keyword><style  face="normal" font="default" size="100%">Fingers</style></keyword><keyword><style  face="normal" font="default" size="100%">Hand Injuries</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemangioendothelioma</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunohistochemistry</style></keyword><keyword><style  face="normal" font="default" size="100%">Injury Severity Score</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteolysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain Measurement</style></keyword><keyword><style  face="normal" font="default" size="100%">S100 Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Vascular Neoplasms</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">157</style></volume><pages><style face="normal" font="default" size="100%">693</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20553843?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Corallini, Federica</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Castellino, Gabriella</style></author><author><style face="normal" font="default" size="100%">Montecucco, Maurizio</style></author><author><style face="normal" font="default" size="100%">Trotta, Francesco</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Circulating levels of frizzled-related protein (FRZB) are increased in patients with early rheumatoid arthritis and decrease in response to disease-modifying antirheumatic drugs.</style></title><secondary-title><style face="normal" font="default" size="100%">Ann Rheum Dis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ann. Rheum. Dis.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Rheumatoid</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Glycoproteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">69</style></volume><pages><style face="normal" font="default" size="100%">1733-4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20447952?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Confalonieri, Marco</style></author><author><style face="normal" font="default" size="100%">D'Agaro, Pierlanfranco</style></author><author><style face="normal" font="default" size="100%">Campello, Cesare</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Corticosteroids do not cause harmful increase of viral load in severe H1N1 virus infection.</style></title><secondary-title><style face="normal" font="default" size="100%">Intensive Care Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Intensive Care Med</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Antiviral Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchoalveolar Lavage Fluid</style></keyword><keyword><style  face="normal" font="default" size="100%">Extracorporeal Membrane Oxygenation</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucocorticoids</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza A Virus, H1N1 Subtype</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Methylprednisolone</style></keyword><keyword><style  face="normal" font="default" size="100%">Oseltamivir</style></keyword><keyword><style  face="normal" font="default" size="100%">Respiration, Artificial</style></keyword><keyword><style  face="normal" font="default" size="100%">Severity of Illness Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Viral Load</style></keyword><keyword><style  face="normal" font="default" size="100%">World Health Organization</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">36</style></volume><pages><style face="normal" font="default" size="100%">1780-1</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">10</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/20631982?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Moroi, K</style></author><author><style face="normal" font="default" size="100%">Sato, T</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Comparison between procaine and isocarboxazid metabolism in vitro by a liver microsomal amidase-esterase.</style></title><secondary-title><style face="normal" font="default" size="100%">Biochem Pharmacol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Biochem. Pharmacol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Amidohydrolases</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Esterases</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydrogen-Ion Concentration</style></keyword><keyword><style  face="normal" font="default" size="100%">In Vitro Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Isocarboxazid</style></keyword><keyword><style  face="normal" font="default" size="100%">Kinetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Metals</style></keyword><keyword><style  face="normal" font="default" size="100%">Microsomes, Liver</style></keyword><keyword><style  face="normal" font="default" size="100%">Phospholipids</style></keyword><keyword><style  face="normal" font="default" size="100%">Procaine</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Rats</style></keyword><keyword><style  face="normal" font="default" size="100%">Subcellular Fractions</style></keyword><keyword><style  face="normal" font="default" size="100%">Temperature</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">1975</style></year><pub-dates><date><style  face="normal" font="default" size="100%">1975 Aug 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">24</style></volume><pages><style face="normal" font="default" size="100%">1517-21</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">16</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/8?dopt=Abstract</style></custom1></record></records></xml>