<?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%">Mancini, C</style></author><author><style face="normal" font="default" size="100%">Giorgio, E</style></author><author><style face="normal" font="default" size="100%">Rubegni, A</style></author><author><style face="normal" font="default" size="100%">Pradotto, L</style></author><author><style face="normal" font="default" size="100%">Bagnoli, S</style></author><author><style face="normal" font="default" size="100%">Rubino, E</style></author><author><style face="normal" font="default" size="100%">Prontera, P</style></author><author><style face="normal" font="default" size="100%">Cavalieri, S</style></author><author><style face="normal" font="default" size="100%">Di Gregorio, E</style></author><author><style face="normal" font="default" size="100%">Ferrero, M</style></author><author><style face="normal" font="default" size="100%">Pozzi, E</style></author><author><style face="normal" font="default" size="100%">Riberi, E</style></author><author><style face="normal" font="default" size="100%">Ferrero, P</style></author><author><style face="normal" font="default" size="100%">Nigro, P</style></author><author><style face="normal" font="default" size="100%">Mauro, A</style></author><author><style face="normal" font="default" size="100%">Zibetti, M</style></author><author><style face="normal" font="default" size="100%">Tessa, A</style></author><author><style face="normal" font="default" size="100%">Barghigiani, M</style></author><author><style face="normal" font="default" size="100%">Antenora, A</style></author><author><style face="normal" font="default" size="100%">Sirchia, F</style></author><author><style face="normal" font="default" size="100%">Piacentini, S</style></author><author><style face="normal" font="default" size="100%">Silvestri, G</style></author><author><style face="normal" font="default" size="100%">De Michele, G</style></author><author><style face="normal" font="default" size="100%">Filla, A</style></author><author><style face="normal" font="default" size="100%">Orsi, L</style></author><author><style face="normal" font="default" size="100%">Santorelli, F M</style></author><author><style face="normal" font="default" size="100%">Brusco, A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Prevalence and phenotype of the c.1529C&gt;T SPG7 variant in adult-onset cerebellar ataxia in Italy.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Neurol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Neurol.</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%">26</style></volume><pages><style face="normal" font="default" size="100%">80-86</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 PURPOSE: &lt;/b&gt;Hereditary ataxias are heterogeneous groups of neurodegenerative disorders, characterized by cerebellar syndromes associated with dysarthria, oculomotor and corticospinal signs, neuropathy and cognitive impairment. Recent reports have suggested mutations in the SPG7 gene, causing the most common form of autosomal recessive spastic paraplegia (MIM#607259), as a main cause of ataxias. The majority of described patients were homozygotes or compound heterozygotes for the c.1529C&gt;T (p.Ala510Val) change. We screened a cohort of 895 Italian patients with ataxia for p.Ala510Val in order to define the prevalence and genotype-phenotype correlation of this variant.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We set up a rapid assay for c.1529C&gt;T using restriction enzyme analysis after polymerase chain reaction amplification. We confirmed the diagnosis with Sanger sequencing.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We identified eight homozygotes and 13 compound heterozygotes, including two novel variants affecting splicing. Mutated patients showed a pure cerebellar ataxia at onset, evolving in mild spastic ataxia (alternatively) associated with dysarthria (~80% of patients), urinary urgency (~30%) and pyramidal signs (~70%). Comparing homozygotes and compound heterozygotes, we noted a difference in age at onset and Scale for the Assessment and Rating of Ataxia score between the two groups, supporting an earlier and more severe phenotype in compound heterozygotes versus homozygotes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The SPG7 c.1529C&gt;T (p.Ala510Val) mutants accounted for 2.3% of cerebellar ataxia cases in Italy, suggesting that this variant should be considered as a priority test in the presence of late-onset pure ataxia. Moreover, the heterozygous/homozygous genotype appeared to predict the onset of clinical manifestation and disease progression.&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/30098094?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%">Lezo, Antonella</style></author><author><style face="normal" font="default" size="100%">Capriati, Teresa</style></author><author><style face="normal" font="default" size="100%">Spagnuolo, Maria Immacolata</style></author><author><style face="normal" font="default" size="100%">Lacitignola, Laura</style></author><author><style face="normal" font="default" size="100%">Goreva, Irina</style></author><author><style face="normal" font="default" size="100%">Di Leo, Grazia</style></author><author><style face="normal" font="default" size="100%">Cecchi, Nicola</style></author><author><style face="normal" font="default" size="100%">Gandullia, Paolo</style></author><author><style face="normal" font="default" size="100%">Amarri, Sergio</style></author><author><style face="normal" font="default" size="100%">Forchielli, Maria Luisa</style></author><author><style face="normal" font="default" size="100%">Dipasquale, Valeria</style></author><author><style face="normal" font="default" size="100%">Parma, Barbara</style></author><author><style face="normal" font="default" size="100%">Gatti, Simona</style></author><author><style face="normal" font="default" size="100%">Ravaioli, Elisa</style></author><author><style face="normal" font="default" size="100%">Salvatore, Silvia</style></author><author><style face="normal" font="default" size="100%">Mainetti, Martina</style></author><author><style face="normal" font="default" size="100%">Norsa, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Pellegrino, Maristella</style></author><author><style face="normal" font="default" size="100%">Fornaro, Martina</style></author><author><style face="normal" font="default" size="100%">Fiorito, Valentina</style></author><author><style face="normal" font="default" size="100%">Lanari, Marcello</style></author><author><style face="normal" font="default" size="100%">Giaquinto, Ester</style></author><author><style face="normal" font="default" size="100%">Verduci, Elvira</style></author><author><style face="normal" font="default" size="100%">Baldassarre, Maria Elisabetta</style></author><author><style face="normal" font="default" size="100%">Diamanti, Antonella</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Paediatric Home Artificial Nutrition in Italy: Report from 2016 Survey on Behalf of Artificial Nutrition Network of Italian Society for Gastroenterology, Hepatology and Nutrition (SIGENP).</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%">Adolescent</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 Nutritional Physiological Phenomena</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Enteral Nutrition</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Health Care Surveys</style></keyword><keyword><style  face="normal" font="default" size="100%">Home Care Services</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%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Nutritional Status</style></keyword><keyword><style  face="normal" font="default" size="100%">Parenteral Nutrition, Home</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</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%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Sep 16</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;Home Artificial Nutrition (HAN) is a safe and efficacious technique that insures children's reintegration into the family, society and school. Epidemiological data on paediatric HAN in Italy are not available.&lt;/p&gt;&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;to detect the prevalence and incidence of Home Parenteral Nutrition (HPN) and Home Enteral Nutrition (HEN), either via tube or mouth, in Italy in 2016.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;a specific form was sent to all registered SIGENP members and investigators of local HAN centres, inviting them to provide the requested centre's data and demographics, underlying diseases and HAN characteristics of the patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;we recorded 3403 Italian patients on HAN aged 0 to 19 years from 22 centres: 2277 HEN, 950 Oral Nutritional Supplements (ONS) and 179 HPN programs. The prevalence of HEN (205 pts/million inhabitants) and HPN (16 pts/million inhabitants) has dramatically increased in Italy in the last 9 years. Neurodisabling conditions were the first indication for HEN by tube or mouth while HPN is mainly requested in digestive disorders.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;HAN is a widespread and rapidly growing treatment in Italy, as well as in other European countries. Awareness of its extent and characteristics helps improving HAN service and patients' quality of life.&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/30223620?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%">Zanchi, Chiara</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%">Germani, Claudio</style></author><author><style face="normal" font="default" size="100%">Giorgi, Rita</style></author><author><style face="normal" font="default" size="100%">Calligaris, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Norbedo, Stefania</style></author><author><style face="normal" font="default" size="100%">Liccari, Giulio</style></author><author><style face="normal" font="default" size="100%">Cozzi, Giorgio</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%">Pain Intensity and Risk of Bone Fracture in Children With Minor Extremity Injuries.</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><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Jan 23</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;Injuries are one of the most common causes of pediatric emergency department (ED) visit. The aim of this study was to investigate the relationship between the intensity of pain at the ED visit of children presenting with an extremity injury and the risk of fracture.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We conducted a retrospective study, considering all patients presenting to the ED of a children's hospital in Italy, with an accidental extremity injury, between May and December 2015. We selected all children aged 8 to 17 years who underwent an x-ray. Children with major, multiple, or nonextremity injuries were excluded. Age, sex, spontaneous and palpation pain, local swelling, time between injury, and medical evaluation were recorded. Sensibility and specificity of spontaneous and palpation pain in detecting a fracture were calculated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We reviewed 994 medical records; of these, 344 (34.6%) reported a fracture. Children's median age was 12 years (interquartile range [IQR], 10-14). Median spontaneous pain at the ED visit was not significantly different between children with and without a fracture: 4.0 (1.0-6.0) and 5 (1.0-6.0), respectively (P = 0.129). Children with mild palpation pain and children without an increase of pain of at least 2 points between spontaneous and palpation pain were fractured in 3.2% and 0.97% of cases, respectively.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;In this series, pain intensity in children with a minor extremity injury was not a good marker of fracture. Nevertheless, children with mild palpation pain or with a mild increase of pain between spontaneous and palpation pain had a low risk of fracture.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29369266?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%">Princivalle, Andrea</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Butturini, Giovanni</style></author><author><style face="normal" font="default" size="100%">Bassi, Claudio</style></author><author><style face="normal" font="default" size="100%">Perbellini, Luigi</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pancreatic ductal adenocarcinoma can be detected by analysis of volatile organic compounds (VOCs) in alveolar air.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Cancer</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 May 04</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">529</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;In the last decade many studies showed that the exhaled breath of subjects suffering from several pathological conditions has a peculiar volatile organic compound (VOC) profile. The objective of the present work was to analyse the VOCs in alveolar air to build a diagnostic tool able to identify the presence of pancreatic ductal adenocarcinoma in patients with histologically confirmed disease.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The concentration of 92 compounds was measured in the end-tidal breath of 65 cases and 102 controls. VOCs were measured with an ion-molecule reaction mass spectrometry. To distinguish between subjects with pancreatic adenocarcinomas and controls, an iterated Least Absolute Shrinkage and Selection Operator multivariate Logistic Regression model was elaborated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The final predictive model, based on 10 VOCs, significantly and independently associated with the outcome had a sensitivity and specificity of 100 and 84% respectively, and an area under the ROC curve of 0.99. For further validation, the model was run on 50 other subjects: 24 cases and 26 controls; 23 patients with histological diagnosis of pancreatic adenocarcinomas and 25 controls were correctly identified by the model.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Pancreatic cancer is able to alter the concentration of some molecules in the blood and hence of VOCs in the alveolar air in equilibrium. The detection and statistical rendering of alveolar VOC composition can be useful for the clinical diagnostic approach of pancreatic neoplasms with excellent sensitivity and specificity.&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/29728093?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%">Mangogna, Alessandro</style></author><author><style face="normal" font="default" size="100%">Belmonte, Beatrice</style></author><author><style face="normal" font="default" size="100%">Agostinis, Chiara</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Gulino, Alessandro</style></author><author><style face="normal" font="default" size="100%">Ferrara, Ines</style></author><author><style face="normal" font="default" size="100%">Zanconati, Fabrizio</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Romano, Federico</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%">Pathological Significance and Prognostic Value of Surfactant Protein D in Cancer.</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%">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%">9</style></volume><pages><style face="normal" font="default" size="100%">1748</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Surfactant protein D (SP-D) is a pattern recognition molecule belonging to the Collectin (collagen-containing C-type lectin) family that has pulmonary as well as extra-pulmonary existence. In the lungs, it is a well-established opsonin that can agglutinate a range of microbes, and enhance their clearance  phagocytosis and super-oxidative burst. It can interfere with allergen-IgE interaction and suppress basophil and mast cell activation. However, it is now becoming evident that SP-D is likely to be an innate immune surveillance molecule against tumor development. SP-D has been shown to induce apoptosis in sensitized eosinophils derived from allergic patients and a leukemic cell line  p53 pathway. Recently, SP-D has been shown to suppress lung cancer progression  interference with the epidermal growth factor signaling. In addition, a truncated form of recombinant human SP-D has been reported to induce apoptosis in pancreatic adenocarcinoma  Fas-mediated pathway in a p53-independent manner. To further establish a correlation between SP-D presence/levels and normal and cancer tissues, we performed a bioinformatics analysis, using Oncomine dataset and the survival analysis platforms Kaplan-Meier plotter, to assess if SP-D can serve as a potential prognostic marker for human lung cancer, in addition to human gastric, breast, and ovarian cancers. We also analyzed immunohistochemically the presence of SP-D in normal and tumor human tissues. We conclude that (1) in the lung, gastric, and breast cancers, there is a lower expression of SP-D than normal tissues; (2) in ovarian cancer, there is a higher expression of SP-D than normal tissue; and (3) in lung cancer, the presence of SP-D could be associated with a favorable prognosis. On the contrary, at non-pulmonary sites such as gastric, breast, and ovarian cancers, the presence of SP-D could be associated with unfavorable prognosis. Correlation between the levels of SP-D and overall survival requires further investigation. Our analysis involves a large number of dataset; therefore, any trend observed is reliable. Despite apparent complexity within the results, it is evident that cancer tissues that produce less levels of SP-D compared to their normal tissue counterparts are probably less susceptible to SP-D-mediated immune surveillance mechanisms  infiltrating immune cells.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30127783?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%">Lucafò, Marianna</style></author><author><style face="normal" font="default" size="100%">Franca, Raffaella</style></author><author><style face="normal" font="default" size="100%">Selvestrel, Davide</style></author><author><style face="normal" font="default" size="100%">Curci, Debora</style></author><author><style face="normal" font="default" size="100%">Pugnetti, Letizia</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacogenetics of treatments for inflammatory bowel disease.</style></title><secondary-title><style face="normal" font="default" size="100%">Expert Opin Drug Metab Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Expert Opin Drug Metab Toxicol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">Epigenesis, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastrointestinal Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Markers</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%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharmacogenetics</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">1209-1223</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;Inflammatory bowel disease is a chronic inflammation of the gut whose pathogenesis is still unclear. Although no curative therapy is currently available, a number of drugs are used in induction and maintenance therapy; however, for most of these drugs, a high inter-individual variability in response is observed. Among the factors of this variability, genetics plays an important role. Areas covered: This review summarizes the results of pharmacogenetic studies, considering the most important drugs used and in particular aminosalycilates, glucocorticoids, thiopurines, monoclonal antibodies and thalidomide. Most studies used a candidate gene approach, even if significant breakthroughs have been obtained recently from applying genome-wide studies. When available, also investigations considering epigenetics and pharmacogenetic dosing guidelines have been included. Expert opinion: Only for thiopurines, genetic markers identified as predictors of efficacy or adverse events have allowed the development of dosing guidelines. For the other drugs, encouraging results are available and great expectations rely on the study of epigenetics and integration with pharmacokinetic information, especially useful for biologics. However, to improve therapy of IBD patients with these drugs, for implementation in the clinics of pharmacogenetics, informatic clinical decision support systems and training about pharmacogenetics of health providers are needed.&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/30465611?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%">Rupel, Katia</style></author><author><style face="normal" font="default" size="100%">Zupin, Luisa</style></author><author><style face="normal" font="default" size="100%">Colliva, Andrea</style></author><author><style face="normal" font="default" size="100%">Kamada, Anselmo</style></author><author><style face="normal" font="default" size="100%">Poropat, Augusto</style></author><author><style face="normal" font="default" size="100%">Ottaviani, Giulia</style></author><author><style face="normal" font="default" size="100%">Gobbo, Margherita</style></author><author><style face="normal" font="default" size="100%">Fanfoni, Lidia</style></author><author><style face="normal" font="default" size="100%">Gratton, Rossella</style></author><author><style face="normal" font="default" size="100%">Santoro, Massimo</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%">Photobiomodulation at Multiple Wavelengths Differentially Modulates Oxidative Stress  and .</style></title><secondary-title><style face="normal" font="default" size="100%">Oxid Med Cell Longev</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Oxid Med Cell Longev</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%">Aged, 80 and over</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%">Keratinocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Lasers, Semiconductor</style></keyword><keyword><style  face="normal" font="default" size="100%">Low-Level Light Therapy</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%">Neutrophils</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Stomatitis</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%">2018</style></volume><pages><style face="normal" font="default" size="100%">6510159</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Photobiomodulation (PBM) is emerging as an effective strategy for the management of multiple inflammatory conditions, including oral mucositis (OM) in cancer patients who receive chemotherapy or radiotherapy. Still, the poor understanding of the mechanisms by which the light interacts with biological tissues and the heterogeneity of light sources and protocols employed worldwide significantly limits its applicability. Reactive oxygen species (ROS) are massively generated during the early phases of OM and play a major role in the pathogenesis of inflammation in general. Here, we report the results of a clinical and experimental study, aimed at evaluating the effect of laser light at different wavelengths on oxidative stress  in oncologic patients suffering from OM and  in two cell types abundantly present within the inflamed oral mucosa, neutrophil polymorphonuclear (PMN) granulocytes, and keratinocytes. In addition to standard ROS detection methods, we exploited a roGFP2-Orp1 genetically encoded sensor, allowing specific, quantitative, and dynamic imaging of redox events in living cells in response to oxidative stress and PBM. We found that the various wavelengths differentially modulate ROS production. In particular, the 660 nm laser light increases ROS production when applied either before or after an oxidative stimulus. In contrast, the 970 nm laser light exerted a moderate antioxidant activity both in the saliva of OM patients and in both cell types. The most marked reduction in the levels of ROS was detected in cells exposed either to the 800 nm laser light or to the combination of the three wavelengths. Overall, our study demonstrates that PBM exerts different effects on the redox state of both PMNs and keratinocytes depending on the used wavelength and prompts the validation of a multiwavelength protocol in the clinical settings.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30534349?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><translated-authors><author><style face="normal" font="default" size="100%">GBD 2017 Population and Fertility Collaborators</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Population and fertility by age and sex for 195 countries and territories, 1950-2017: a systematic analysis for the Global Burden of Disease Study 2017.</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%">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%">Birth Rate</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%">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%">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%">Maternal Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Mortality</style></keyword><keyword><style  face="normal" font="default" size="100%">Population Density</style></keyword><keyword><style  face="normal" font="default" size="100%">Population Growth</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 11 10</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">392</style></volume><pages><style face="normal" font="default" size="100%">1995-2051</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;Population estimates underpin demographic and epidemiological research and are used to track progress on numerous international indicators of health and development. To date, internationally available estimates of population and fertility, although useful, have not been produced with transparent and replicable methods and do not use standardised estimates of mortality. We present single-calendar year and single-year of age estimates of fertility and population by sex with standardised and replicable methods.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We estimated population in 195 locations by single year of age and single calendar year from 1950 to 2017 with standardised and replicable methods. We based the estimates on the demographic balancing equation, with inputs of fertility, mortality, population, and migration data. Fertility data came from 7817 location-years of vital registration data, 429 surveys reporting complete birth histories, and 977 surveys and censuses reporting summary birth histories. We estimated age-specific fertility rates (ASFRs; the annual number of livebirths to women of a specified age group per 1000 women in that age group) by use of spatiotemporal Gaussian process regression and used the ASFRs to estimate total fertility rates (TFRs; the average number of children a woman would bear if she survived through the end of the reproductive age span [age 10-54 years] and experienced at each age a particular set of ASFRs observed in the year of interest). Because of sparse data, fertility at ages 10-14 years and 50-54 years was estimated from data on fertility in women aged 15-19 years and 45-49 years, through use of linear regression. Age-specific mortality data came from the Global Burden of Diseases, Injuries, and Risk Factors Study (GBD) 2017 estimates. Data on population came from 1257 censuses and 761 population registry location-years and were adjusted for underenumeration and age misreporting with standard demographic methods. Migration was estimated with the GBD Bayesian demographic balancing model, after incorporating information about refugee migration into the model prior. Final population estimates used the cohort-component method of population projection, with inputs of fertility, mortality, and migration data. Population uncertainty was estimated by use of out-of-sample predictive validity testing. With these data, we estimated the trends in population by age and sex and in fertility by age between 1950 and 2017 in 195 countries and territories.&lt;/p&gt;&lt;p&gt;&lt;b&gt;FINDINGS: &lt;/b&gt;From 1950 to 2017, TFRs decreased by 49·4% (95% uncertainty interval [UI] 46·4-52·0). The TFR decreased from 4·7 livebirths (4·5-4·9) to 2·4 livebirths (2·2-2·5), and the ASFR of mothers aged 10-19 years decreased from 37 livebirths (34-40) to 22 livebirths (19-24) per 1000 women. Despite reductions in the TFR, the global population has been increasing by an average of 83·8 million people per year since 1985. The global population increased by 197·2% (193·3-200·8) since 1950, from 2·6 billion (2·5-2·6) to 7·6 billion (7·4-7·9) people in 2017; much of this increase was in the proportion of the global population in south Asia and sub-Saharan Africa. The global annual rate of population growth increased between 1950 and 1964, when it peaked at 2·0%; this rate then remained nearly constant until 1970 and then decreased to 1·1% in 2017. Population growth rates in the southeast Asia, east Asia, and Oceania GBD super-region decreased from 2·5% in 1963 to 0·7% in 2017, whereas in sub-Saharan Africa, population growth rates were almost at the highest reported levels ever in 2017, when they were at 2·7%. The global average age increased from 26·6 years in 1950 to 32·1 years in 2017, and the proportion of the population that is of working age (age 15-64 years) increased from 59·9% to 65·3%. At the national level, the TFR decreased in all countries and territories between 1950 and 2017; in 2017, TFRs ranged from a low of 1·0 livebirths (95% UI 0·9-1·2) in Cyprus to a high of 7·1 livebirths (6·8-7·4) in Niger. The TFR under age 25 years (TFU25; number of livebirths expected by age 25 years for a hypothetical woman who survived the age group and was exposed to current ASFRs) in 2017 ranged from 0·08 livebirths (0·07-0·09) in South Korea to 2·4 livebirths (2·2-2·6) in Niger, and the TFR over age 30 years (TFO30; number of livebirths expected for a hypothetical woman ageing from 30 to 54 years who survived the age group and was exposed to current ASFRs) ranged from a low of 0·3 livebirths (0·3-0·4) in Puerto Rico to a high of 3·1 livebirths (3·0-3·2) in Niger. TFO30 was higher than TFU25 in 145 countries and territories in 2017. 33 countries had a negative population growth rate from 2010 to 2017, most of which were located in central, eastern, and western Europe, whereas population growth rates of more than 2·0% were seen in 33 of 46 countries in sub-Saharan Africa. In 2017, less than 65% of the national population was of working age in 12 of 34 high-income countries, and less than 50% of the national population was of working age in Mali, Chad, and Niger.&lt;/p&gt;&lt;p&gt;&lt;b&gt;INTERPRETATION: &lt;/b&gt;Population trends create demographic dividends and headwinds (ie, economic benefits and detriments) that affect national economies and determine national planning needs. Although TFRs are decreasing, the global population continues to grow as mortality declines, with diverse patterns at the national level and across age groups. To our knowledge, this is the first study to provide transparent and replicable estimates of population and fertility, which can be used to inform decision making and to monitor progress.&lt;/p&gt;&lt;p&gt;&lt;b&gt;FUNDING: &lt;/b&gt;Bill &amp; Melinda Gates Foundation.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">10159</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30496106?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%">Fornasaro, Stefano</style></author><author><style face="normal" font="default" size="100%">Vicario, Annalisa</style></author><author><style face="normal" font="default" size="100%">De Leo, Luigina</style></author><author><style face="normal" font="default" size="100%">Bonifacio, Alois</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</style></author><author><style face="normal" font="default" size="100%">Sergo, Valter</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Potential use of MCR-ALS for the identification of coeliac-related biochemical changes in hyperspectral Raman maps from pediatric intestinal biopsies.</style></title><secondary-title><style face="normal" font="default" size="100%">Integr Biol (Camb)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Integr Biol (Camb)</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 06 18</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">356-363</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Raman hyperspectral imaging is an emerging practice in biological and biomedical research for label free analysis of tissues and cells. Using this method, both spatial distribution and spectral information of analyzed samples can be obtained. The current study reports the first Raman microspectroscopic characterisation of colon tissues from patients with Coeliac Disease (CD). The aim was to assess if Raman imaging coupled with hyperspectral multivariate image analysis is capable of detecting the alterations in the biochemical composition of intestinal tissues associated with CD. The analytical approach was based on a multi-step methodology: duodenal biopsies from healthy and coeliac patients were measured and processed with Multivariate Curve Resolution Alternating Least Squares (MCR-ALS). Based on the distribution maps and the pure spectra of the image constituents obtained from MCR-ALS, interesting biochemical differences between healthy and coeliac patients has been derived. Noticeably, a reduced distribution of complex lipids in the pericryptic space, and a different distribution and abundance of proteins rich in beta-sheet structures was found in CD patients. The output of the MCR-ALS analysis was then used as a starting point for two clustering algorithms (k-means clustering and hierarchical clustering methods). Both methods converged with similar results providing precise segmentation over multiple Raman images of studied tissues.&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/29756143?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%">van Setten, Jessica</style></author><author><style face="normal" font="default" size="100%">Brody, Jennifer A</style></author><author><style face="normal" font="default" size="100%">Jamshidi, Yalda</style></author><author><style face="normal" font="default" size="100%">Swenson, Brenton R</style></author><author><style face="normal" font="default" size="100%">Butler, Anne M</style></author><author><style face="normal" font="default" size="100%">Campbell, Harry</style></author><author><style face="normal" font="default" size="100%">Del Greco, Fabiola M</style></author><author><style face="normal" font="default" size="100%">Evans, Daniel S</style></author><author><style face="normal" font="default" size="100%">Gibson, Quince</style></author><author><style face="normal" font="default" size="100%">Gudbjartsson, Daniel F</style></author><author><style face="normal" font="default" size="100%">Kerr, Kathleen F</style></author><author><style face="normal" font="default" size="100%">Krijthe, Bouwe P</style></author><author><style face="normal" font="default" size="100%">Lyytikäinen, Leo-Pekka</style></author><author><style face="normal" font="default" size="100%">Müller, Christian</style></author><author><style face="normal" font="default" size="100%">Müller-Nurasyid, Martina</style></author><author><style face="normal" font="default" size="100%">Nolte, Ilja M</style></author><author><style face="normal" font="default" size="100%">Padmanabhan, Sandosh</style></author><author><style face="normal" font="default" size="100%">Ritchie, Marylyn D</style></author><author><style face="normal" font="default" size="100%">Robino, Antonietta</style></author><author><style face="normal" font="default" size="100%">Smith, Albert V</style></author><author><style face="normal" font="default" size="100%">Steri, Maristella</style></author><author><style face="normal" font="default" size="100%">Tanaka, Toshiko</style></author><author><style face="normal" font="default" size="100%">Teumer, Alexander</style></author><author><style face="normal" font="default" size="100%">Trompet, Stella</style></author><author><style face="normal" font="default" size="100%">Ulivi, Sheila</style></author><author><style face="normal" font="default" size="100%">Verweij, Niek</style></author><author><style face="normal" font="default" size="100%">Yin, Xiaoyan</style></author><author><style face="normal" font="default" size="100%">Arnar, David O</style></author><author><style face="normal" font="default" size="100%">Asselbergs, Folkert W</style></author><author><style face="normal" font="default" size="100%">Bader, Joel S</style></author><author><style face="normal" font="default" size="100%">Barnard, John</style></author><author><style face="normal" font="default" size="100%">Bis, Josh</style></author><author><style face="normal" font="default" size="100%">Blankenberg, Stefan</style></author><author><style face="normal" font="default" size="100%">Boerwinkle, Eric</style></author><author><style face="normal" font="default" size="100%">Bradford, Yuki</style></author><author><style face="normal" font="default" size="100%">Buckley, Brendan M</style></author><author><style face="normal" font="default" size="100%">Chung, Mina K</style></author><author><style face="normal" font="default" size="100%">Crawford, Dana</style></author><author><style face="normal" font="default" size="100%">den Hoed, Marcel</style></author><author><style face="normal" font="default" size="100%">Denny, Josh C</style></author><author><style face="normal" font="default" size="100%">Dominiczak, Anna F</style></author><author><style face="normal" font="default" size="100%">Ehret, Georg B</style></author><author><style face="normal" font="default" size="100%">Eijgelsheim, Mark</style></author><author><style face="normal" font="default" size="100%">Ellinor, Patrick T</style></author><author><style face="normal" font="default" size="100%">Felix, Stephan B</style></author><author><style face="normal" font="default" size="100%">Franco, Oscar H</style></author><author><style face="normal" font="default" size="100%">Franke, Lude</style></author><author><style face="normal" font="default" size="100%">Harris, Tamara B</style></author><author><style face="normal" font="default" size="100%">Holm, Hilma</style></author><author><style face="normal" font="default" size="100%">Ilaria, Gandin</style></author><author><style face="normal" font="default" size="100%">Iorio, Annamaria</style></author><author><style face="normal" font="default" size="100%">Kähönen, Mika</style></author><author><style face="normal" font="default" size="100%">Kolcic, Ivana</style></author><author><style face="normal" font="default" size="100%">Kors, Jan A</style></author><author><style face="normal" font="default" size="100%">Lakatta, Edward G</style></author><author><style face="normal" font="default" size="100%">Launer, Lenore J</style></author><author><style face="normal" font="default" size="100%">Lin, Honghuang</style></author><author><style face="normal" font="default" size="100%">Lin, Henry J</style></author><author><style face="normal" font="default" size="100%">Loos, Ruth J F</style></author><author><style face="normal" font="default" size="100%">Lubitz, Steven A</style></author><author><style face="normal" font="default" size="100%">Macfarlane, Peter W</style></author><author><style face="normal" font="default" size="100%">Magnani, Jared W</style></author><author><style face="normal" font="default" size="100%">Leach, Irene Mateo</style></author><author><style face="normal" font="default" size="100%">Meitinger, Thomas</style></author><author><style face="normal" font="default" size="100%">Mitchell, Braxton D</style></author><author><style face="normal" font="default" size="100%">Munzel, Thomas</style></author><author><style face="normal" font="default" size="100%">Papanicolaou, George J</style></author><author><style face="normal" font="default" size="100%">Peters, Annette</style></author><author><style face="normal" font="default" size="100%">Pfeufer, Arne</style></author><author><style face="normal" font="default" size="100%">Pramstaller, Peter P</style></author><author><style face="normal" font="default" size="100%">Raitakari, Olli T</style></author><author><style face="normal" font="default" size="100%">Rotter, Jerome I</style></author><author><style face="normal" font="default" size="100%">Rudan, Igor</style></author><author><style face="normal" font="default" size="100%">Samani, Nilesh J</style></author><author><style face="normal" font="default" size="100%">Schlessinger, David</style></author><author><style face="normal" font="default" size="100%">Silva Aldana, Claudia T</style></author><author><style face="normal" font="default" size="100%">Sinner, Moritz F</style></author><author><style face="normal" font="default" size="100%">Smith, Jonathan D</style></author><author><style face="normal" font="default" size="100%">Snieder, Harold</style></author><author><style face="normal" font="default" size="100%">Soliman, Elsayed Z</style></author><author><style face="normal" font="default" size="100%">Spector, Timothy D</style></author><author><style face="normal" font="default" size="100%">Stott, David J</style></author><author><style face="normal" font="default" size="100%">Strauch, Konstantin</style></author><author><style face="normal" font="default" size="100%">Tarasov, Kirill V</style></author><author><style face="normal" font="default" size="100%">Thorsteinsdottir, Unnur</style></author><author><style face="normal" font="default" size="100%">Uitterlinden, André G</style></author><author><style face="normal" font="default" size="100%">Van Wagoner, David R</style></author><author><style face="normal" font="default" size="100%">Völker, Uwe</style></author><author><style face="normal" font="default" size="100%">Völzke, Henry</style></author><author><style face="normal" font="default" size="100%">Waldenberger, Melanie</style></author><author><style face="normal" font="default" size="100%">Jan Westra, Harm</style></author><author><style face="normal" font="default" size="100%">Wild, Philipp S</style></author><author><style face="normal" font="default" size="100%">Zeller, Tanja</style></author><author><style face="normal" font="default" size="100%">Alonso, Alvaro</style></author><author><style face="normal" font="default" size="100%">Avery, Christy L</style></author><author><style face="normal" font="default" size="100%">Bandinelli, Stefania</style></author><author><style face="normal" font="default" size="100%">Benjamin, Emelia J</style></author><author><style face="normal" font="default" size="100%">Cucca, Francesco</style></author><author><style face="normal" font="default" size="100%">Dörr, Marcus</style></author><author><style face="normal" font="default" size="100%">Ferrucci, Luigi</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Gudnason, Vilmundur</style></author><author><style face="normal" font="default" size="100%">Hayward, Caroline</style></author><author><style face="normal" font="default" size="100%">Heckbert, Susan R</style></author><author><style face="normal" font="default" size="100%">Hicks, Andrew A</style></author><author><style face="normal" font="default" size="100%">Jukema, J Wouter</style></author><author><style face="normal" font="default" size="100%">Kääb, Stefan</style></author><author><style face="normal" font="default" size="100%">Lehtimäki, Terho</style></author><author><style face="normal" font="default" size="100%">Liu, Yongmei</style></author><author><style face="normal" font="default" size="100%">Munroe, Patricia B</style></author><author><style face="normal" font="default" size="100%">Parsa, Afshin</style></author><author><style face="normal" font="default" size="100%">Polasek, Ozren</style></author><author><style face="normal" font="default" size="100%">Psaty, Bruce M</style></author><author><style face="normal" font="default" size="100%">Roden, Dan M</style></author><author><style face="normal" font="default" size="100%">Schnabel, Renate B</style></author><author><style face="normal" font="default" size="100%">Sinagra, Gianfranco</style></author><author><style face="normal" font="default" size="100%">Stefansson, Kari</style></author><author><style face="normal" font="default" size="100%">Stricker, Bruno H</style></author><author><style face="normal" font="default" size="100%">van der Harst, Pim</style></author><author><style face="normal" font="default" size="100%">van Duijn, Cornelia M</style></author><author><style face="normal" font="default" size="100%">Wilson, James F</style></author><author><style face="normal" font="default" size="100%">Gharib, Sina A</style></author><author><style face="normal" font="default" size="100%">de Bakker, Paul I W</style></author><author><style face="normal" font="default" size="100%">Isaacs, Aaron</style></author><author><style face="normal" font="default" size="100%">Arking, Dan E</style></author><author><style face="normal" font="default" size="100%">Sotoodehnia, Nona</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">PR interval genome-wide association meta-analysis identifies 50 loci associated with atrial and atrioventricular electrical activity.</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%">Atrial Function</style></keyword><keyword><style  face="normal" font="default" size="100%">Atrioventricular Node</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrocardiography</style></keyword><keyword><style  face="normal" font="default" size="100%">Electrophysiological Phenomena</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</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%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</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 07 25</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">2904</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Electrocardiographic PR interval measures atrio-ventricular depolarization and conduction, and abnormal PR interval is a risk factor for atrial fibrillation and heart block. Our genome-wide association study of over 92,000 European-descent individuals identifies 44 PR interval loci (34 novel). Examination of these loci reveals known and previously not-yet-reported biological processes involved in cardiac atrial electrical activity. Genes in these loci are over-represented in cardiac disease processes including heart block and atrial fibrillation. Variants in over half of the 44 loci were associated with atrial or blood transcript expression levels, or were in high linkage disequilibrium with missense variants. Six additional loci were identified either by meta-analysis of ~105,000 African and European-descent individuals and/or by pleiotropic analyses combining PR interval with heart rate, QRS interval, and atrial fibrillation. These findings implicate developmental pathways, and identify transcription factors, ion-channel genes, and cell-junction/cell-signaling proteins in atrio-ventricular conduction, identifying potential targets for drug development.&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/30046033?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%">Gurnari, G</style></author><author><style face="normal" font="default" size="100%">Monaco, S</style></author><author><style face="normal" font="default" size="100%">Romano, A</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%">Dello Iacono, I</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%">Calvani, M</style></author><author><style face="normal" font="default" size="100%">Giannone, A</style></author><author><style face="normal" font="default" size="100%">Calabrò, C</style></author><author><style face="normal" font="default" size="100%">Scala, G</style></author><author><style face="normal" font="default" size="100%">Verga, M C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Predictive value of the number of adverse reaction episodes for the IgE-mediated food allergy diagnosis.</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 Dec 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;INTRODUCTION AND OBJECTIVES: &lt;/b&gt;The reproducibility of the adverse reaction increases the suggestiveness of a history of food allergy. However, the positive predictive value (PPV) of multiple adverse reaction episodes for the diagnosis of IgE-mediated food allergy is not known. This evaluation was the objective of our study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PATIENTS AND METHODS: &lt;/b&gt;We retrospectively studied 180 children with a history of non-anaphylactic adverse reactions after the ingestion of a food. All children had the prick test positive for the offending food and performed the oral food challenge (OFC) within 12 months after the last adverse reaction episode (ARE). We have evaluated whether increasing the number of ARE increased the probability that the OFC would be positive (failed).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;93 patients (52%) presented one ARE, 49 (27%) presented two ARE, 24 (13%) presented three ARE, 14 (8%) patients presented≥four ARE. The OFC was positive in 94/180 (52%). The outcome of the OFC was found to be positively correlated with the number of ARE (OR=1.56; 95% CI=1.16-2.09; p=0.003). A PPV=100% was observed with a number of ARE≥five.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The number of ARE is an important predictor of the diagnosis of food allergy, although less than we would have imagined. The number of ARE could be used to increase the predictability of the diagnostic tests currently in use, to define clinical prediction rules alternative to OFC and easy to use in clinical practice.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/30573320?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%">Rami, Damiano</style></author><author><style face="normal" font="default" size="100%">Zacchi, Paola</style></author><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Stampalija, Tamara</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%">Vidergar, Romana</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Celeghini, Claudio</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Sargent, Ian</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%">Pre-eclampsia affects procalcitonin production in placental tissue.</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><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Calcitonin</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%">Macrophages</style></keyword><keyword><style  face="normal" font="default" size="100%">Placenta</style></keyword><keyword><style  face="normal" font="default" size="100%">Pre-Eclampsia</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Trophoblasts</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</style></keyword><keyword><style  face="normal" font="default" size="100%">Up-Regulation</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 04</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">79</style></volume><pages><style face="normal" font="default" size="100%">e12823</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;Procalcitonin (PCT) is the prohormone of calcitonin which is usually released from neuroendocrine cells of the thyroid gland (parafollicular) and the lungs (K cells). PCT is synthesized by almost all cell types and tissues, including monocytes and parenchymal tissue, upon LPS stimulation. To date, there is no evidence for PCT expression in the placenta both in physiological and pathological conditions.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHOD: &lt;/b&gt;Circulating and placental PCT levels were analysed in pre-eclamptic (PE) and control patients. Placental cells and macrophages (PBDM), stimulated with PE sera, were analysed for PCT expression. The effect of anti-TNF-α antibody was analysed.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Higher PCT levels were detected in PE sera and in PE placentae compared to healthy women. PE trophoblasts showed increased PCT expression compared to those isolated from healthy placentae. PE sera induced an upregulation of PCT production in macrophages and placental cells. The treatment of PBDM with PE sera in the presence of anti-TNF-α completely abrogated the effect induced by pathologic sera.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Trophoblast cells are the main producer of PCT in PE placentae. TNF-α, in association with other circulating factors present in PE sera, upregulates PCT production in macrophages and normal placental cells, thus contributing to the observed increased in circulating PCT in PE sera.&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/29427369?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%">Romano, Claudio</style></author><author><style face="normal" font="default" size="100%">Oliva, Salvatore</style></author><author><style face="normal" font="default" size="100%">Martellossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Miele, Erasmo</style></author><author><style face="normal" font="default" size="100%">Arrigo, Serena</style></author><author><style face="normal" font="default" size="100%">Graziani, Maria Giovanna</style></author><author><style face="normal" font="default" size="100%">Cardile, Sabrina</style></author><author><style face="normal" font="default" size="100%">Gaiani, Federica</style></author><author><style face="normal" font="default" size="100%">de'Angelis, Gian Luigi</style></author><author><style face="normal" font="default" size="100%">Torroni, Filippo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pediatric gastrointestinal bleeding: Perspectives from the Italian Society of Pediatric Gastroenterology.</style></title><secondary-title><style face="normal" font="default" size="100%">World J Gastroenterol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">World J. Gastroenterol.</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%">Diagnostic Imaging</style></keyword><keyword><style  face="normal" font="default" size="100%">Endoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastroenterology</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastrointestinal Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastrointestinal Hemorrhage</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemodynamics</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%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Societies, Medical</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 28</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">1328-1337</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;There are many causes of gastrointestinal bleeding (GIB) in children, and this condition is not rare, having a reported incidence of 6.4%. Causes vary with age, but show considerable overlap; moreover, while many of the causes in the pediatric population are similar to those in adults, some lesions are unique to children. The diagnostic approach for pediatric GIB includes definition of the etiology, localization of the bleeding site and determination of the severity of bleeding; timely and accurate diagnosis is necessary to reduce morbidity and mortality. To assist medical care providers in the evaluation and management of children with GIB, the &quot;Gastro-Ped Bleed Team&quot; of the Italian Society of Pediatric Gastroenterology, Hepatology and Nutrition (SIGENP) carried out a systematic search on MEDLINE  PubMed (http://www.ncbi.nlm.nih.gov/pubmed/) to identify all articles published in English from January 1990 to 2016; the following key words were used to conduct the electronic search: &quot;upper GIB&quot; and &quot;pediatric&quot; [all fields]; &quot;lower GIB&quot; and &quot;pediatric&quot; [all fields]; &quot;obscure GIB&quot; and &quot;pediatric&quot; [all fields]; &quot;GIB&quot; and &quot;endoscopy&quot; [all fields]; &quot;GIB&quot; and &quot;therapy&quot; [all fields]. The identified publications included articles describing randomized controlled trials, reviews, case reports, cohort studies, case-control studies and observational studies. References from the pertinent articles were also reviewed. This paper expresses a position statement of SIGENP that can have an immediate impact on clinical practice and for which sufficient evidence is not available in literature. The experts participating in this effort were selected according to their expertise and professional qualifications.&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/28293079?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%">Bertozzi, Mirko</style></author><author><style face="normal" font="default" size="100%">Esposito, Ciro</style></author><author><style face="normal" font="default" size="100%">Vella, Claudio</style></author><author><style face="normal" font="default" size="100%">Briganti, Vito</style></author><author><style face="normal" font="default" size="100%">Zampieri, Nicola</style></author><author><style face="normal" font="default" size="100%">Codrich, Daniela</style></author><author><style face="normal" font="default" size="100%">Ubertazzi, Michele</style></author><author><style face="normal" font="default" size="100%">Trucchi, Alessandro</style></author><author><style face="normal" font="default" size="100%">Magrini, Elisa</style></author><author><style face="normal" font="default" size="100%">Battaglia, Sonia</style></author><author><style face="normal" font="default" size="100%">Bini, Vittorio</style></author><author><style face="normal" font="default" size="100%">Conighi, Maria Luisa</style></author><author><style face="normal" font="default" size="100%">Gulia, Caterina</style></author><author><style face="normal" font="default" size="100%">Farina, Alessandra</style></author><author><style face="normal" font="default" size="100%">Camoglio, Francesco Saverio</style></author><author><style face="normal" font="default" size="100%">Rigamonti, Waifro</style></author><author><style face="normal" font="default" size="100%">Gamba, Piergiorgio</style></author><author><style face="normal" font="default" size="100%">Riccipetitoni, Giovanna</style></author><author><style face="normal" font="default" size="100%">Chiarenza, Salvatore Fabio</style></author><author><style face="normal" font="default" size="100%">Inserra, Alessandro</style></author><author><style face="normal" font="default" size="100%">Appignani, Antonino</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pediatric Ovarian Torsion and its Recurrence: A Multicenter Study.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Adolesc Gynecol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Pediatr Adolesc Gynecol</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%">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%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Laparoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Laparotomy</style></keyword><keyword><style  face="normal" font="default" size="100%">Menarche</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovariectomy</style></keyword><keyword><style  face="normal" font="default" size="100%">Postoperative Complications</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Surveys and Questionnaires</style></keyword><keyword><style  face="normal" font="default" size="100%">Torsion Abnormality</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">30</style></volume><pages><style face="normal" font="default" size="100%">413-417</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;STUDY OBJECTIVE: &lt;/b&gt;To report results of a retrospective multicentric Italian survey concerning the management of pediatric ovarian torsion (OT) and its recurrence.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DESIGN: &lt;/b&gt;Multicenter retrospective cohort study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SETTING: &lt;/b&gt;Italian Units of Pediatric Surgery.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PARTICIPANTS: &lt;/b&gt;Participants were female aged 1-14 years of age with surgically diagnosed OT between 2004 and 2014.&lt;/p&gt;&lt;p&gt;&lt;b&gt;INTERVENTIONS: &lt;/b&gt;Adnexal detorsion, adnexectomy, mass excision using laparoscopy or laparotomy. Different kinds of oophoropexy (OPY) for OT or recurrence, respectively.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MAIN OUTCOME MEASURES: &lt;/b&gt;A total of 124 questionnaires were returned and analyzed to understand the current management of pediatric OT and its recurrence. The questionnaires concerned patient age, presence of menarche, OT site, presence and type of mass, performed procedure, OPY technique adopted, intra- and postoperative complications, recurrence and site, procedure performed for recurrence, OPY technique for recurrence, and 1 year follow-up of detorsed ovaries.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Mean age at surgery was 9.79 ± 3.54 years. Performed procedures were open adnexectomy (52 of 125; 41.6%), laparoscopic adnexectomy (25 of 125; 20%), open detorsion (10 of 125; 8%), and laparoscopic detorsion (38 of 125; 30.4%). Recurrence occurred in 15 of 125 cases (12%) and resulted as significant (P = .012) if associated with a normal ovary at the first episode of torsion. Recurrence occurred only in 1 of 19 cases after OPY (5.2%). Ultrasonographic results of detorsed ovaries were not significant whether an OPY was performed or not (P = 1.00).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Unfortunately, oophorectomy and open technique are still widely adopted even if not advised. Recurrence is not rare and the risk is greater in patients without ovarian masses. OPY does not adversely affect ultrasonographic results at 1 year. When possible OPY should be performed at the first episode of OT.&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/27894860?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%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">De Cunto, Angela</style></author><author><style face="normal" font="default" size="100%">Pellegrin, Andrea</style></author><author><style face="normal" font="default" size="100%">Pecile, Vanna</style></author><author><style face="normal" font="default" size="100%">Spinelli, Alessandro Mauro</style></author><author><style face="normal" font="default" size="100%">Cappellani, Stefania</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phenotypic expression of 19q13.32 microdeletions: Report of a new patient and review of the literature.</style></title><secondary-title><style face="normal" font="default" size="100%">Am J Med Genet A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Am. J. Med. Genet. A</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 Apr 14</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;The phenotypic manifestations of microdeletions in the 19q13.32 region are still poorly known. In this paper we report a patient who presented with hypotonia, developmental delay, facial dysmorphism, micrognathia, kyphoscoliosis, and buried penis. Chromosomal microarray revealed an interstitial 327 kb de novo microdeletion in the 19q13.32 region comprising eight genes (ARGHAP35, NPAS1, TMEM160, ZC3H4, SAE1, BBC3, MIR3190, and MIR3191). Previously reported cases of microdeletions in the 19q13.32 region were reviewed and compared to our patient, highlighting the common features of a possible 19q13.32 microdeletion syndrome.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28411391?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%">Lima, C A D</style></author><author><style face="normal" font="default" size="100%">Javorski, N R</style></author><author><style face="normal" font="default" size="100%">Souza, A P O</style></author><author><style face="normal" font="default" size="100%">Barbosa, A D</style></author><author><style face="normal" font="default" size="100%">Valença, A P M C</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author><author><style face="normal" font="default" size="100%">Souza, P R E</style></author><author><style face="normal" font="default" size="100%">de Azevêdo Silva, J</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%">Polymorphisms in key bone modulator cytokines genes influence bisphosphonates therapy in postmenopausal women.</style></title><secondary-title><style face="normal" font="default" size="100%">Inflammopharmacology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Inflammopharmacology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Density</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Remodeling</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Diphosphonates</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%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoporosis, Postmenopausal</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Postmenopause</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%">25</style></volume><pages><style face="normal" font="default" size="100%">191-201</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Osteoporosis is a multifactorial and debilitating disease resulting from decreased bone mineral density (BMD) and loss of tissue microarchitecture. Ineffective therapies may lead to bone fractures and subsequent death. Single nucleotide polymorphisms (SNPs) in key immune regulator genes have been associated with therapeutic response to bisphosphonates, which are the first therapeutic line of choice for osteoporosis. However, cytokine pathways and their relation with therapeutic adhesion remain to be fully elucidated. Aimed at better understanding these processes, we investigated the response to bisphosphonate therapy in postmenopausal women and four SNPs in key proinflammatory cytokines genes: IL23R +2284 (C&gt;A) (rs10889677), IL17A +672 (G&gt;A) (rs7747909), IL12B +1188 (T&gt;G) (rs3212227) and INF-γ -1616 (G&gt;A) (rs2069705). A total of 69 patients treated with bisphosphonate were followed for a period of 1 up to 4 years, genotyped and compared according to their changes in bone mineral density (BMD) and level of biochemical markers during their treatment. The INF-γ -1616 G/G associated with increased BMD values in femoral neck (GG/AA, p = 0.016) and decreased BMD values in total hip (GG/GA, p = 0.019; GG/AA, p = 0.011). In relation to biochemical markers, INF-γ -1616 SNP associated with increased alkaline phosphatase (GG/AA; p &lt; 0.0001) and parathyroid hormone levels (AA/GA; p = 0.017). Vitamin D values changes were related to IL17A +672 (GG/GA, p = 0.034) and to IL12B +1188 (TT/TG, p = 0.046) SNPs. Besides, significant differences in changes of calcium levels correlated with IL23R +2284 (CC/CA, p = 0.016) genotypes. Altogether, we suggest that these polymorphisms may play an important role for therapeutic decisions in osteoporosis treatment.&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/28220389?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%">Simonini, Gabriele</style></author><author><style face="normal" font="default" size="100%">Bracaglia, Claudia</style></author><author><style face="normal" font="default" size="100%">Cattalini, Marco</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author><author><style face="normal" font="default" size="100%">Brambilla, Alice</style></author><author><style face="normal" font="default" size="100%">de Libero, Cinzia</style></author><author><style face="normal" font="default" size="100%">Pires Marafon, Denise</style></author><author><style face="normal" font="default" size="100%">Caputo, Roberto</style></author><author><style face="normal" font="default" size="100%">Cimaz, Rolando</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Predictors of Relapse after Discontinuing Systemic Treatment in Childhood Autoimmune Chronic Uveitis.</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><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Autoimmune Diseases</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%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Uveitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Withholding Treatment</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">44</style></volume><pages><style face="normal" font="default" size="100%">822-826</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 identify clinical predictors of relapse in childhood autoimmune chronic uveitis after stopping systemic treatment.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A retrospective, multicenter, cohort study.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Ninety-four children in remission, receiving no treatments and with at least a 6-month followup, were enrolled. A higher probability of maintaining remission after discontinuing treatment was shown in idiopathic compared with juvenile idiopathic arthritis uveitis (Mantel-Cox chi-square = 23.21) if inactivity had been obtained within 6 months from starting systemic treatment (Mantel-Cox chi-square = 24.17) and by antitumor necrosis factor-α treatment (Mantel-Cox chi-square = 6.43).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Type of disease, time, and type of systemic therapy to achieve inactivity predict different duration of uveitis remission after treatment withdrawal.&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/28365583?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%">Floridia, M</style></author><author><style face="normal" font="default" size="100%">Masuelli, G</style></author><author><style face="normal" font="default" size="100%">Tamburrini, E</style></author><author><style face="normal" font="default" size="100%">Cetin, I</style></author><author><style face="normal" font="default" size="100%">Liuzzi, G</style></author><author><style face="normal" font="default" size="100%">Martinelli, P</style></author><author><style face="normal" font="default" size="100%">Guaraldi, G</style></author><author><style face="normal" font="default" size="100%">Spinillo, A</style></author><author><style face="normal" font="default" size="100%">Vimercati, A</style></author><author><style face="normal" font="default" size="100%">Maso, G</style></author><author><style face="normal" font="default" size="100%">Pinnetti, C</style></author><author><style face="normal" font="default" size="100%">Frisina, V</style></author><author><style face="normal" font="default" size="100%">Dalzero, S</style></author><author><style face="normal" font="default" size="100%">Ravizza, M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pregnant with HIV before age 25: data from a large national study in Italy, 2001-2016.</style></title><secondary-title><style face="normal" font="default" size="100%">Epidemiol Infect</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Epidemiol. Infect.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</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%">HIV Infections</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%">Odds Ratio</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</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%">145</style></volume><pages><style face="normal" font="default" size="100%">2360-2365</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Young pregnant women with HIV may be at significant risk of unplanned pregnancy, lower treatment coverage, and other adverse pregnancy outcomes. In a large cohort of pregnant women with HIV in Italy, among 2979 pregnancies followed in 2001-2016, 9·0% were in women &lt;25 years, with a significant increase over time (2001-2005: 7·0%; 2006-2010: 9·1%; 2011-2016: 12·2%, P &lt; 0·001). Younger women had a lower rate of planned pregnancy (23·2% vs. 37·7%, odds ratio (OR) 0·50, 95% confidence interval (CI) 0·36-0·69), were more frequently diagnosed with HIV in pregnancy (46·5% vs. 20·9%, OR 3·29, 95% CI 2·54-4·25), and, if already diagnosed with HIV before pregnancy, were less frequently on antiretroviral treatment at conception (&lt;25 years: 56·3%; ⩾25 years: 69·0%, OR 0·58, 95% CI 0·41-0·81). During pregnancy, treatment coverage was almost universal in both age groups (98·5% vs. 99·3%), with no differences in rate of HIV viral suppression at third trimester and adverse pregnancy outcomes. The data show that young women represent a growing proportion of pregnant women with HIV, and are significantly more likely to have unplanned pregnancy, undiagnosed HIV infection, and lower treatment coverage at conception. During pregnancy, antiretroviral treatment, HIV suppression, and pregnancy outcomes are similar compared with older women. Earlier intervention strategies may provide additional benefits in the quality of care for women with HIV.&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/28712385?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%">Lora, Angela</style></author><author><style face="normal" font="default" size="100%">Scrimin, Federica</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%">Barbi, Egidio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A premenarcheal girl with urogenital bleeding.</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%">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%">102</style></volume><pages><style face="normal" font="default" size="100%">472</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/27881375?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%">Fanfani, Francesco</style></author><author><style face="normal" font="default" size="100%">Restaino, Stefano</style></author><author><style face="normal" font="default" size="100%">Cicogna, Stefania</style></author><author><style face="normal" font="default" size="100%">Petrillo, Marco</style></author><author><style face="normal" font="default" size="100%">Montico, Marcella</style></author><author><style face="normal" font="default" size="100%">Perrone, Emanuele</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">De Leo, Rossella</style></author><author><style face="normal" font="default" size="100%">Ceccarello, Matteo</style></author><author><style face="normal" font="default" size="100%">Scambia, Giovanni</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Preoperative Serum Human Epididymis Protein 4 Levels in Early Stage Endometrial Cancer: A Prospective Study.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Gynecol Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int. J. Gynecol. Cancer</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%">Aged, 80 and over</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomarkers, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Endometrial Neoplasms</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%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Staging</style></keyword><keyword><style  face="normal" font="default" size="100%">Preoperative Care</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteins</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 07</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">27</style></volume><pages><style face="normal" font="default" size="100%">1200-1205</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 the study was to evaluate the prognostic value of human epididymis protein 4 (HE4) and cancer antigen 125 markers with pathological prognostic factor to complete the preoperative clinical panel and help the treatment planning.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This prospective multicenter study was conducted in 2 gynecologic oncology centers between 2012 and 2014 (Institute for Maternal and Child Health IRCCS Burlo Garofolo in Trieste and Catholic University of the Sacred Heart in Rome, Italy). We enrolled 153 patients diagnosed with clinical early (International Federation of Gynecology and Obstetrics stages I-II) type I endometrial cancer.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Human epididymis protein 4 levels seemed to be strictly related to age (P &lt; 0.001) and menopausal status (P &lt; 0.002). Compared with myometrial invasion (MI), the HE4 values were significantly higher in case of invasion of greater than 50% of the thickness: MI of greater than 50%, median of 94.85 pmol/L (38.3-820.8 pmol/L), versus MI of less than 50%, median of 65.65 pmol/L (25.1-360.2 pmol/L), (P &lt; 0.001). The HE4 levels increase significantly with increasing tumor size: diameter of larger than 2 cm, median of 86.9 pmol/L (35.8-820.8 pmol/L), versus diameter of smaller than 2 cm, median of 52.2 pmol/L (33.3-146.8 pmol/L), (P &lt; 0.001). In our population, HE4 did not correlate with the histological grade, endometrial cancer type I versus type II (P = 0.86), the lymphovascular infiltration (P = 0.12), and the cervical invasion (P = 0.6). We established a new variable, considering 3 high-risk tumor features: MI of greater than 50% and/or histological G3 and/or type II. Human epididymis protein 4 levels significantly increase in high-risk tumors (high risk HE4, 93.6 pmol/L vs low-medium risk, 65.5 pmol/L; P &lt; 0.001).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;A preoperative HE4 evaluation could help stratify patients with deep invasion and/or metastatic disease and is correlated with other relevant prognostic factors to be considered to tailor an adequate surgical strategy.&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/28557834?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%">Castagnetti, Marco</style></author><author><style face="normal" font="default" size="100%">Bagnara, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Rigamonti, Waifro</style></author><author><style face="normal" font="default" size="100%">Cimador, Marcello</style></author><author><style face="normal" font="default" size="100%">Esposito, Ciro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Preputial reconstruction in hypospadias repair.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Urol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Pediatr Urol</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 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">102-109</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;In principle, the prepuce can be reconstructed during hypospadias repair, but the procedure has not gained wide acceptance and preputial reconstruction (PR) is surrounded by several controversies.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIAL AND METHODS: &lt;/b&gt;A review is provided of the technique for PR, how PR combines with the other steps of hypospadias repair, the risks of complications related to the urethroplasty and specific to PR, and the results of PR with particular regard to the relevance for the patient and his family.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;PR can be important for patients requiring hypospadias repair and their parents. It can be performed in almost all patients with distal hypospadias except perhaps those with the most asymmetrical prepuces or severe ventral skin deficiency. PR does not seem to increase urethroplasty complications, but combination of PR with tubularisation of the urethral plate urethroplasty seems to offer the best chance of success. Specific complications occur in around 8% of patients and include partial or complete dehiscence of the prepuce and secondary phimosis. To prevent the latter, the reconstructed prepuce should be easily retractile at the end of surgery. Technical modifications can help to achieve this goal. Cosmetically, reconstructed prepuces are not fully normal, but the abnormality could be less important for a patient and his parents that the complete absence of the prepuce.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;On the basis of the evidence summarised above, an algorithm for PR in patients with distal hypospadias is proposed. PR can be offered to the vast majority of distal hypospadias patients, although some modification of the technique for hypospadias repair can be required. Retractility of the reconstructed prepuce at the end of surgery seems paramount for final success.&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/27773620?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%">Velkoski, Angelika</style></author><author><style face="normal" font="default" size="100%">Amoroso, Stefano</style></author><author><style face="normal" font="default" size="100%">Brovedani, Pierpaolo</style></author><author><style face="normal" font="default" size="100%">Cont, Gabriele</style></author><author><style face="normal" font="default" size="100%">Trappan, Antonella</style></author><author><style face="normal" font="default" size="100%">Travan, Laura</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Presentation of acute suppurative parotitis in a newborn with incessant crying.</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%">Acute Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Bacterial Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Crying</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, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Parotitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Staphylococcal Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Staphylococcus aureus</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 Mar</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">102</style></volume><pages><style face="normal" font="default" size="100%">F125</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/27986789?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%">Rizzardi, Clara</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Cammisuli, Francesca</style></author><author><style face="normal" font="default" size="100%">Monego, Simeone Dal</style></author><author><style face="normal" font="default" size="100%">DE Spelorzi, Yeraldin Chiquinquira Castillo</style></author><author><style face="normal" font="default" size="100%">Costantinides, Fulvio</style></author><author><style face="normal" font="default" size="100%">Giudici, Fabiola</style></author><author><style face="normal" font="default" size="100%">Pinamonti, Maurizio</style></author><author><style face="normal" font="default" size="100%">Canzonieri, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Melato, Mauro</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%">Puzzling Results from  Germline Mutations Analysis in a Group of Asbestos-Exposed Patients in a High-risk Area of Northeast Italy.</style></title><secondary-title><style face="normal" font="default" size="100%">Anticancer Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Anticancer Res.</style></alt-title></titles><keywords><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%">Asbestos</style></keyword><keyword><style  face="normal" font="default" size="100%">Environmental Exposure</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Germ-Line Mutation</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%">Lung Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesothelioma</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Suppressor Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Ubiquitin Thiolesterase</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">37</style></volume><pages><style face="normal" font="default" size="100%">3073-3083</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;Germline mutations of the oncosuppressor gene breast cancer 1-associated protein 1 (BAP1) were recently related to an autosomal-dominant tumor predisposition syndrome (BAP1-TPDS), characterized by uveal melanoma, malignant mesothelioma (MM), cutaneous melanoma, and other malignancies. The demonstration that BAP1 mutations are strongly associated with MM has provided a real breakthrough in the study of genetic predisposition in MM, that may explain why only a fraction of asbestos-exposed individuals go on to develop MM.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;To evaluate the possible role of BAP1 mutations in the epidemiology of sporadic MM, and their relationship with asbestos exposure, we determined the prevalence of germline BAP1 mutations by the Sanger method in a group of 29 asbestos-exposed patients, 21 of which were diagnosed with MM. They were residents of Trieste, a ship-building town in Northeast Italy with a very high incidence of mesothelioma.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We identified non-obviously pathogenetic germline sequence variants of BAP1 in 3/29 patients and in 2/21 MM cases (10%).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Non obviously pathogenic germline sequence variants of BAP1 were found. Nevertheless, limitations of predictive web tools allowed us to comment on some interesting peculiarities of our 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/28551647?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%">Cocca, Massimiliano</style></author><author><style face="normal" font="default" size="100%">Bedognetti, Davide</style></author><author><style face="normal" font="default" size="100%">La Bianca, Martina</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacogenetics driving personalized medicine: analysis of genetic polymorphisms related to breast cancer medications in Italian isolated populations.</style></title><secondary-title><style face="normal" font="default" size="100%">J Transl Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Transl 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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</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;Breast cancer is the most common cancer in women characterized by a high variable clinical outcome among individuals treated with equivalent regimens and novel targeted therapies. In this study, we performed a population based approach intersecting high-throughput genotype data from Friuli Venezia Giulia (FVG) isolated populations with publically available pharmacogenomics information to estimate the frequency of genotypes correlated with responsiveness to breast cancer treatment thus improving the clinical management of this disease in an efficient and cost effective way.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A list of 80 variants reported to be related to the efficacy or toxicity of breast cancer drugs was obtained from PharmGKB database. Fourty-one were present in FVG, 1000G European (EUR) and ExAC (Non Finnish European) databases. Their frequency was extracted using PLINK software and the differences tested by Fisher's exact test.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Statistical analyses revealed that 13 out of the 41 (32 %) variants were significantly different in frequency in our sample as compared to the EUR/ExAC cohorts. For nine variants the available level of evidence (LOE) included polymorphisms related to cyclophosphamide, tamoxifen, doxorubicin, fluorpyrimidine and paclitaxel. In particular, for trastuzumab two variants were detected: (1) rs1801274-G within FCGR2A and associated with decreased efficacy (LOE 2B); (2) rs1136201-G located within ERBB2 and associated with increased toxicity (LOE 3). Both these two variants were underrepresented in the FVG population compared to EUR/ExAC population thus suggesting a high therapeutic index of this drug in our population. Moreover, as regards fluoropyrimidines, the frequency of two polymorphisms within the DPYD gene associated with drug toxicity (e.g., rs2297595-C allele and rs3918290-T allele, LOE 2A and 1, respectively) was extremely low in FVG population thus suggesting that a larger number of FVG patients could benefit from full dosage of fluoropyrimidine therapy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;All these findings increase the overall knowledge on the prevalence of specific variants related with breast cancer treatment responsiveness in FVG population and highlight the importance of assessing gene polymorphisms related with cancer medications in isolated communities.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26801900?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%">Pascolo, Lorella</style></author><author><style face="normal" font="default" size="100%">Bedolla, Diana E</style></author><author><style face="normal" font="default" size="100%">Vaccari, Lisa</style></author><author><style face="normal" font="default" size="100%">Venturin, Irene</style></author><author><style face="normal" font="default" size="100%">Cammisuli, Francesca</style></author><author><style face="normal" font="default" size="100%">Gianoncelli, Alessandra</style></author><author><style face="normal" font="default" size="100%">Mitri, Elisa</style></author><author><style face="normal" font="default" size="100%">Giolo, Elena</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%">Zweyer, Marina</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pitfalls and promises in FTIR spectromicroscopy analyses to monitor iron-mediated DNA damage in sperm.</style></title><secondary-title><style face="normal" font="default" size="100%">Reprod Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Reprod. Toxicol.</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%">61</style></volume><pages><style face="normal" font="default" size="100%">39-46</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 drugs, chemicals, and environmental factors can impair sperm functionality by inducing DNA damage, one of the important causes of reduced fertility potential. The use of vibrational spectromicroscopy represents a promising approach for monitoring DNA integrity in sperm, although some limitations exist, depending from the experimental conditions. Here, we report that when using FTIR spectromicroscopy to reveal oxidative stress mediated by Fenton's reaction on hydrated sperm samples, DNA damage interpretation is partially compromised by unexpected cell surface precipitates. The precipitates give a broad band in the 1150-1000cm(-1) infrared region, which partially covers one of the signatures of DNA (phosphate stretching bands), and are detected as iron and oxygen containing material when using XRF spectroscopy. On the other hand, the analyses further support the potential of FTIR spectromicroscopy to reveal cellular oxidative damage events such as lipid peroxidation, protein misfolding and aggregations, as well as DNA strain breaks.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26923261?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%">Ciciriello, E</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Planning early childhood audiologic intervention programs on a regional scale: introduction to an Italian study.</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%">3-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Non-uniform, late, or inappropriate care of childhood with permanent hearing impairment (PHI) predisposes many children to develop communicative- behaviour problems and impaired psychosocial adjustment that can persist in adolescence and adulthood.In March 2014, the CCM (Centro Controllo Malattie or Disease Control Centre) of the Italian Ministry of Health funded a project entitled &quot; Preventing Communication Disorders: a Regional Program for Early Identification, Intervention and Care of Hearing Impaired Children&quot;. The project involved 5 tertiary centres with UNHS programs formally approved by the Region. The main purpose of the project is to define and launch an integrated regionally-based public health model for identification, diagnosis and intervention of childhood PHI. The first phase of the project investigated the state of art and produced recommendations for positive changes in identification, diagnosis, therapy and care of childhood PHI in Italy, taking into account diagnostic and treatment innovations, family empowerment, treatment alliance and an interdisciplinary approach. Recommendations drawn from this initial phase will represent the basis for a regional system for early intervention that is validated, integrated and shared between the five regions.&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/27054384?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%">Wanderley-Nogueira, Ana Carolina</style></author><author><style face="normal" font="default" size="100%">Bezerra-Neto, João Pacífico</style></author><author><style face="normal" font="default" size="100%">Kido, Éderson Akio</style></author><author><style face="normal" font="default" size="100%">de Araújo, Flávia Tadeu</style></author><author><style face="normal" font="default" size="100%">Amorim, Lidiane Lindinalva Barbosa</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Benko-Iseppon, Ana Maria</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Plant Elite Squad: First Defense Line and Resistance Genes - Identification, Diversity and Functional Roles.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Protein Pept Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Protein Pept. Sci.</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 24</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;Plants exhibit sensitive mechanisms to respond to environmental stresses, presenting some specific and non-specific reactions when attacked by pathogens, including organisms from different classes and complexity, as viroids, viruses, bacteria, fungi and nematodes. A crucial step to define the fate of the plant facing an invading pathogen is the activation of a compatible Resistance (R) gene, the focus of the present review. Different aspects regarding R-genes and their products are discussed, including pathogen recognition mechanisms, signaling and effects on induced and constitutive defense processes, splicing and post transcriptional mechanisms involved. There are still countless challenges to the complete understanding of the mechanisms involving R-genes in plants, in particular those related to the interactions with other genes of the pathogen and of the host itself, their regulation, acting mechanisms at transcriptional and post-transcriptional levels, as well as the influence of other types of stress over their regulation. A magnification of knowledge is expected when considering the novel information from the omics and systems biology.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27455974?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%">Maria, Ana Carolina Wanderley-Nogueira</style></author><author><style face="normal" font="default" size="100%">Bezerra-Neto, João Pacífico</style></author><author><style face="normal" font="default" size="100%">Kido, Éderson Akio</style></author><author><style face="normal" font="default" size="100%">de Araújo, Flávia Tadeu</style></author><author><style face="normal" font="default" size="100%">Amorim, Lidiane Lindinalva Barbosa</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Benko-Iseppon, Ana Maria</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Plants Defense-related Cyclic Peptides: Diversity, Structure and Applications.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Protein Pept Sci</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Protein Pept. Sci.</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 24</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;Plant growth is prone to several unfavorable factors that may compromise or impair development and survival, including abiotic or biotic stressors. Aiming at defending themselves, plants have developed several strategies to survive and adapt to such adversities. Cyclotides are a family of plant-derived proteins that exhibit a diverse range of biological activities including antimicrobial and insecticidal activities that actively participate in plant defense processes. Three main categories of peptides have been described: (i) Cyclotides (ii) Sunflower Trypsin Inhibitor (SFTI) and (iii) peptides MCoTI-I and II, from Momordica cochinchinensis. They comprise proteins of approximately 30 amino acids, containing a head-to-tail cyclized backbone, with three disulfide bonds configured in a cystine knot topology, therefore bearing greater peptide stability. Given their features and multifunctionality, cyclotides stand out as promising sources for the discovery of new antimicrobial agents. The present review describes cyclotide occurrence, abundance and action in plants, also their diversity and evolution. Considerations regarding their use in the context of biomedical and agronomical sciences uses are also presented.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27455973?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%">Farruggia, Piero</style></author><author><style face="normal" font="default" size="100%">Puccio, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Sala, Alessandra</style></author><author><style face="normal" font="default" size="100%">Todesco, Alessandra</style></author><author><style face="normal" font="default" size="100%">Buffardi, Salvatore</style></author><author><style face="normal" font="default" size="100%">Garaventa, Alberto</style></author><author><style face="normal" font="default" size="100%">Bottigliero, Gaetano</style></author><author><style face="normal" font="default" size="100%">Bianchi, Maurizio</style></author><author><style face="normal" font="default" size="100%">Zecca, Marco</style></author><author><style face="normal" font="default" size="100%">Locatelli, Franco</style></author><author><style face="normal" font="default" size="100%">Pession, Andrea</style></author><author><style face="normal" font="default" size="100%">Pillon, Marta</style></author><author><style face="normal" font="default" size="100%">Favre, Claudio</style></author><author><style face="normal" font="default" size="100%">D'Amico, Salvatore</style></author><author><style face="normal" font="default" size="100%">Provenzi, Massimo</style></author><author><style face="normal" font="default" size="100%">Trizzino, Angela</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Giulio Andrea</style></author><author><style face="normal" font="default" size="100%">Sau, Antonella</style></author><author><style face="normal" font="default" size="100%">Santoro, Nicola</style></author><author><style face="normal" font="default" size="100%">Murgia, Giulio</style></author><author><style face="normal" font="default" size="100%">Casini, Tommaso</style></author><author><style face="normal" font="default" size="100%">Mascarin, Maurizio</style></author><author><style face="normal" font="default" size="100%">Burnelli, Roberta</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">AIEOP Italian Association of Pediatric Hematology and Oncology and Hodgkin Lymphoma Working Group</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">The prognostic value of biological markers in paediatric Hodgkin lymphoma.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Cancer</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Cancer</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%">Antineoplastic Combined Chemotherapy Protocols</style></keyword><keyword><style  face="normal" font="default" size="100%">Biomarkers, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Platelets</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%">Databases, Factual</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Progression</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease-Free Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Eosinophils</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Ferritins</style></keyword><keyword><style  face="normal" font="default" size="100%">Hodgkin Disease</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%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Kaplan-Meier Estimate</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocyte Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Multivariate Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Staging</style></keyword><keyword><style  face="normal" font="default" size="100%">Platelet Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Proportional Hazards Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</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></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%">52</style></volume><pages><style face="normal" font="default" size="100%">33-40</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;Many biological and inflammatory markers have been proposed as having a prognostic value at diagnosis of Hodgkin lymphoma (HL), but very few have been validated in paediatric patients. We explored the significance of these markers in a large population of 769 affected children.&lt;/p&gt;&lt;p&gt;&lt;b&gt;PATIENTS AND METHODS: &lt;/b&gt;By using the database of patients enrolled in A.I.E.O.P. (Associazione Italiana di Emato-Oncologia Pediatrica) trial LH2004 for paediatric HL, we identified 769 consecutive patients treated with curative intent from 1st June 2004 to 1st April 2014 with ABVD (doxorubicin, bleomycin, vinblastine, and dacarbazine), or hybrid COPP/ABV (cyclophosphamide, vincristine, prednisone, procarbazine, doxorubicin, bleomycin and vinblastine) regimens.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;On multivariate analysis with categorical forms, the 5-year freedom from progression survival was significantly lower in patients with stage IV or elevated value of platelets, eosinophils and ferritin at diagnosis. Furthermore, stage IV and eosinophils seem to maintain their predictive value independently of interim (after IV cycles of chemotherapy) positron emission tomography.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Using the combination of four simple markers such as stage IV and elevated levels of platelets, ferritin and eosinophils, it is possible to classify the patients into subgroups with very different outcomes.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26630532?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%">Kamada, Anselmo J</style></author><author><style face="normal" font="default" size="100%">Bianco, Anna M</style></author><author><style face="normal" font="default" size="100%">Zupin, Luisa</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Matte, Maria C C</style></author><author><style face="normal" font="default" size="100%">Medeiros, Rúbia Marília de</style></author><author><style face="normal" font="default" size="100%">Almeida, Sabrina Esteves de Matos</style></author><author><style face="normal" font="default" size="100%">Rocha, Marineide M</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">Chies, José A B</style></author><author><style face="normal" font="default" size="100%">Kuhn, Louise</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%">Protective Role of BST2 Polymorphisms in Mother-to-Child Transmission of HIV-1 and Adult AIDS Progression.</style></title><secondary-title><style face="normal" font="default" size="100%">J Acquir Immune Defic Syndr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Acquir. Immune Defic. Syndr.</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 1</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">72</style></volume><pages><style face="normal" font="default" size="100%">237-41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Bone marrow stromal cell antigen-2 (BST-2)/Tetherin is a restriction factor that prevents Human immunodeficiency virus type 1 (HIV-1) release from infected cells and mediates pro-inflammatory cytokine production. This study investigated the risk conferred by single nucleotide polymorphisms (rs919266, rs9192677, and rs9576) at BST-2 coding gene (BST2) in HIV-1 mother-to-child transmission and in disease progression. Initially, 101 HIV-1+ pregnant women and 331 neonates exposed to HIV-1 from Zambia were enrolled. Additional BST2 single nucleotide polymorphism analyses were performed in 2 cohorts with acquired immunodeficiency syndrome (AIDS) progression: an adult Brazilian cohort (37 rapid, 30 chronic and 21 long-term non-progressors) and an Italian pediatric cohort (21 rapid and 67 slow progressors). The rs9576A allele was nominally associated with protection during breastfeeding (P = 0.019) and individuals carrying rs919266 GA showed slower progression to AIDS (P = 0.033). Despite the influence of rs919266 and rs9576 on BST2 expression being still undetermined, a preventive role by BST2 polymorphisms was found during HIV-1 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/26885809?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%">Ura, Blendi</style></author><author><style face="normal" font="default" size="100%">Scrimin, Federica</style></author><author><style face="normal" font="default" size="100%">Arrigoni, Giorgio</style></author><author><style face="normal" font="default" size="100%">Franchin, Cinzia</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Ricci, Giuseppe</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Proteomic Approach for the Identification of Up-Regulated Proteins Involved in the Metabolic Process of the Leiomyoma.</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><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%">540</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Uterine leiomyoma is the most common benign smooth muscle cell tumor of the uterus. Proteomics is a powerful tool for the analysis of complex mixtures of proteins. In our study, we focused on proteins that were upregulated in the leiomyoma compared to the myometrium. Paired samples of eight leiomyomas and adjacent myometrium were obtained and submitted to two-dimensional gel electrophoresis (2-DE) and mass spectrometry for protein identification and to Western blotting for 2-DE data validation. The comparison between the patterns revealed 24 significantly upregulated (p &lt; 0.05) protein spots, 12 of which were found to be associated with the metabolic processes of the leiomyoma and not with the normal myometrium. The overexpression of seven proteins involved in the metabolic processes of the leiomyoma was further validated by Western blotting and 2D Western blotting. Four of these proteins have never been associated with the leiomyoma before. The 2-DE approach coupled with mass spectrometry, which is among the methods of choice for comparative proteomic studies, identified a number of proteins overexpressed in the leiomyoma and involved in several biological processes, including metabolic processes. A better understanding of the mechanism underlying the overexpression of these proteins may be important for therapeutic purposes.&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/27070597?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%">Vozzi, Diego</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Tricarico, Paola Maura</style></author><author><style face="normal" font="default" size="100%">Knowles, Alessandra</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Vuch, Josef</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</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%">Putative modifier genes in mevalonate kinase deficiency.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Med Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol Med Rep</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%">13</style></volume><pages><style face="normal" font="default" size="100%">3181-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Mevalonate kinase deficiency (MKD) is an autosomal recessive auto‑inflammatory disease, caused by impairment of the mevalonate pathway. Although the molecular mechanism remains to be elucidated, there is clinical evidence suggesting that other regulatory genes may be involved in determining the phenotype. The identification of novel target genes may explain non‑homogeneous genotype‑phenotype correlations, and provide evidence in support of the hypothesis that novel regulatory genes predispose or amplify deregulation of the mevalonate pathway in this orphan disease. In the present study, DNA samples were obtained from five patients with MKD, which were then analyzed using whole exome sequencing. A missense variation in the PEX11γ gene was observed in homozygosis in P2, possibly correlating with visual blurring. The UNG rare gene variant was detected in homozygosis in P5, without correlating with a specific clinical phenotype. A number of other variants were found in the five analyzed DNA samples from the MKD patients, however no correlation with the phenotype was established. The results of the presents study suggested that further analysis, using next generation sequencing approaches, is required on a larger sample size of patients with MKD, who share the same MVK mutations and exhibit 'extreme' clinical phenotypes. As MVK mutations may be associated with MKD, the identification of specific modifier genes may assist in providing an earlier diagnosis.&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/26935981?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%">Brovedani, Pierpaolo</style></author><author><style face="normal" font="default" size="100%">Cont, Gabriele</style></author><author><style face="normal" font="default" size="100%">Travan, Laura</style></author><author><style face="normal" font="default" size="100%">Grassi, Veronica</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%">Pain activates a defined area of the somatosensory and motor cortex in newborn infants.</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%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">104</style></volume><pages><style face="normal" font="default" size="100%">e530-3</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><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/26174848?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%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Lanzi, Gaetana</style></author><author><style face="normal" font="default" size="100%">Yue, Fengming</style></author><author><style face="normal" font="default" size="100%">Giliani, Silvia</style></author><author><style face="normal" font="default" size="100%">Sasaki, Katsunori</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Pelin, Marco</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%">Decorti, Giuliana</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Patients' Induced Pluripotent Stem Cells to Model Drug Induced Adverse Events: A Role in Predicting Thiopurine Induced Pancreatitis?</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Drug Metab</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Drug Metab.</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%">17</style></volume><pages><style face="normal" font="default" size="100%">91-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Induced pluripotent stem cells (iPSC) can be produced from adult cells by transfecting them with a definite set of pluripotency-associated genes. Under adequate growth conditions and stimulation iPSC can differentiate to almost every somatic lineage in the body. Patients' derived iPSC are an innovative model to study mechanisms of adverse drug reactions in individual patients and in cell types that cannot be easily obtained from human subjects. Proof-of concept studies with known toxicants have been performed for liver, cardiovascular and central nervous system cells: neurons obtained from iPSC have been used to elucidate the mechanism of chemotherapy-induced peripheral neuropathy by evaluating the effects of neurotoxic drugs such as vincristine. However, no study has been performed yet on pancreatic tissue and drug induced pancreatitis. Thiopurines (azathioprine and mercaptopurine) are immunosuppressive antimetabolite drugs, commonly used to treat Crohn's disease. About 5% of Crohn's disease patients treated with thiopurines develop pancreatitis, a severe idiosyncratic adverse event; these patients have to stop thiopurine administration and may require medical treatment, with significant personal and social costs. Molecular mechanism of thiopurine induced pancreatitis (TIP) is currently unknown and no fully validated biomarker is available to assist clinicians in preventing this adverse event. Hence, in this review we have reflected upon the probable research applications of exocrine pancreatic cells generated from patient specific iPS cells. Such pancreatic cells can provide excellent insights into the molecular mechanism of TIP. In particular three hypotheses on the mechanism of TIP could be explored: drug biotransformation, innate immunity and adaptative immunity.&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/26526832?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%">Zonta, Francesco</style></author><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author><author><style face="normal" font="default" size="100%">Buratto, Damiano</style></author><author><style face="normal" font="default" size="100%">Crispino, Giulia</style></author><author><style face="normal" font="default" size="100%">Morgan, Anna</style></author><author><style face="normal" font="default" size="100%">Abdulhadi, Khalid</style></author><author><style face="normal" font="default" size="100%">Alkowari, Moza</style></author><author><style face="normal" font="default" size="100%">Badii, Ramin</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</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%">The p.Cys169Tyr variant of connexin 26 is not a polymorphism.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Mol Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum. Mol. Genet.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Amino Acid Substitution</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Connexins</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gap Junctions</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Hearing Loss</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%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Molecular</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Conformation</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Interaction Domains and Motifs</style></keyword><keyword><style  face="normal" font="default" size="100%">Transfection</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 May 1</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">24</style></volume><pages><style face="normal" font="default" size="100%">2641-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Mutations in the GJB2 gene, which encodes the gap junction protein connexin 26 (Cx26), are the primary cause of hereditary prelingual hearing impairment. Here, the p.Cys169Tyr missense mutation of Cx26 (Cx26C169Y), previously classified as a polymorphism, has been identified as causative of severe hearing loss in two Qatari families. We have analyzed the effect of this mutation using a combination of confocal immunofluorescence microscopy and molecular dynamics simulations. At the cellular level, our results show that the mutant protein fails to form junctional channels in HeLa transfectants despite being correctly targeted to the plasma membrane. At the molecular level, this effect can be accounted for by disruption of the disulfide bridge that Cys169 forms with Cys64 in the wild-type structure (Cx26WT). The lack of the disulfide bridge in the Cx26C169Y protein causes a spatial rearrangement of two important residues, Asn176 and Thr177. In the Cx26WT protein, these residues play a crucial role in the intra-molecular interactions that permit the formation of an intercellular channel by the head-to-head docking of two opposing hemichannels resident in the plasma membrane of adjacent cells. Our results elucidate the molecular pathogenesis of hereditary hearing loss due to the connexin mutation and facilitate the understanding of its role in both healthy and affected individuals.&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/25628337?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%">Kleiner, Giulio</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Caruso, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Milani, Daniela</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%">Pediatric patients with inflammatory bowel disease exhibit increased serum levels of proinflammatory cytokines and chemokines, but decreased circulating levels of macrophage inhibitory protein-1β, interleukin-2 and interleukin-17.</style></title><secondary-title><style face="normal" font="default" size="100%">Exp Ther Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Exp Ther Med</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%">9</style></volume><pages><style face="normal" font="default" size="100%">2047-2052</style></pages><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Inflammatory bowel disease (IBD) is a chronic and progressive inflammatory condition of the gastrointestinal tract. Although the causative events that lead to the onset of IBD are yet to be fully elucidated, deregulation of immune and inflammatory mechanisms are hypothesized to significantly contribute to this disorder. Since the onset of IBD is often during infancy, in the present study, the serum values of a large panel of cytokines and chemokines in pediatric patients (&lt;18 years; n=26) were compared with age-matched controls (n=37). While elevations in the serum level of several proinflammatory and immune regulating cytokines were confirmed, such as interleukin (IL)-1β, IL-5, IL-7, interferon (IFN)-γ-inducible protein-10, IL-16, cutaneous T-cell-attracting chemokine, leukemia inhibitory factor, monokine induced by γ-IFN, IFN-α2 and IFN-γ, notably decreased levels of IL-2, IL-17 and macrophage inhibitory protein-1β were also observed. Therefore, while a number of proinflammatory cytokines exhibit increased levels in IBD patients, pediatric IBD patients may also exhibit certain aspects of a reduced immunological response.&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/26136934?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%">Caracciolo, Ilaria</style></author><author><style face="normal" font="default" size="100%">Bassetti, Matteo</style></author><author><style face="normal" font="default" size="100%">Paladini, Giorgio</style></author><author><style face="normal" font="default" size="100%">Luzzati, Roberto</style></author><author><style face="normal" font="default" size="100%">Santon, Daniela</style></author><author><style face="normal" font="default" size="100%">Merelli, Maria</style></author><author><style face="normal" font="default" size="100%">Sabbata, Giovanni De</style></author><author><style face="normal" font="default" size="100%">Carletti, Tea</style></author><author><style face="normal" font="default" size="100%">Marcello, Alessandro</style></author><author><style face="normal" font="default" size="100%">D'Agaro, Pierlanfranco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Persistent viremia and urine shedding of tick-borne encephalitis virus in an infected immunosuppressed patient from a new epidemic cluster in North-Eastern Italy.</style></title><secondary-title><style face="normal" font="default" size="100%">J Clin Virol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Clin. Virol.</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 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">69</style></volume><pages><style face="normal" font="default" size="100%">48-51</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A persistent tick-borne encephalitis virus infection in an immune-suppressed patient is presented. Such an unusual clinical case offers the unique chance of detecting persistent viremia associated to the erythrocyte fraction and shedding of the virus in the urine for more than six weeks. The infection occurred in a new area of the Friuli Venezia-Giulia region (North Eastern Italy) where two additional cases are also being reported.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26209378?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%">Cojutti, Piergiorgio</style></author><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author><author><style face="normal" font="default" size="100%">Crichiutti, Giovanni</style></author><author><style face="normal" font="default" size="100%">Isola, Miriam</style></author><author><style face="normal" font="default" size="100%">Pea, Federico</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacokinetic/pharmacodynamic evaluation of linezolid in hospitalized paediatric patients: a step toward dose optimization by means of therapeutic drug monitoring and Monte Carlo simulation.</style></title><secondary-title><style face="normal" font="default" size="100%">J Antimicrob Chemother</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Antimicrob. Chemother.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acetamides</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Bacterial Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Area Under Curve</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%">Drug Monitoring</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gram-Positive Bacterial Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Hospitalization</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%">Inpatients</style></keyword><keyword><style  face="normal" font="default" size="100%">Linezolid</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Monte Carlo Method</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxazolidinones</style></keyword><keyword><style  face="normal" font="default" size="100%">Plasma</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</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%">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%">70</style></volume><pages><style face="normal" font="default" size="100%">198-206</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 report on linezolid exposure in a paediatric population who routinely underwent therapeutic drug monitoring (TDM) for dosage optimization and to assess the factors affecting interpatient variability.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We performed a retrospective study of patients whose plasma C(min) and Cmax levels were measured during linezolid treatment. Adequate exposure was defined as a C(min) of 2-7 mg/L and/or an estimated AUC24 of 160-300 mg · h/L. Patients were divided into two subgroups (Group 1, 2-11 years; Group 2, 12-18 years). Monte Carlo simulation was performed to investigate whether or not the currently recommended dosages might enable a high probability of target attainment (PTA) of two thresholds for linezolid efficacy (AUC24/MIC ≥ 80 or ≥ 100). Data on demographic characteristics, disease, microbiology and haematochemical parameters and outcomes were collected.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;A total of 23 patients were included. Standard dosages were suboptimal in 50.0% and 44.4% of patients in Group 1 and Group 2, respectively. Among those who underwent multiple instances of TDM, the dosages were increased in 33.3% of cases in both groups, and decreased in 6.6% and 9.5% of cases in Group 1 and Group 2, respectively. Co-treatment with phenobarbital, proton pump inhibitors and amiodarone accounted for most of the variability in C(min) (adjusted R(2) of 0.692). Simulations showed a PTA of ≥ 90% with the current dosing regimens in both groups only for pathogens with an MIC ≤ 1 mg/L.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Higher dosages of linezolid may be needed, especially in Group 1 when in the presence of pathogens with an MIC &gt;1 mg/L. The role of TDM should be encouraged for optimization of linezolid exposure in the paediatric setting in the presence of infections caused by pathogens with borderline susceptibility and/or for patients co-treated with drugs that may alter linezolid exposure.&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/25182066?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%">Cojutti, Piergiorgio</style></author><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author><author><style face="normal" font="default" size="100%">Pea, Federico</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacokinetics and pharmacodynamics of continuous-infusion meropenem in pediatric hematopoietic stem cell transplant patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Antimicrob Agents Chemother</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Antimicrob. Agents Chemother.</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%">59</style></volume><pages><style face="normal" font="default" size="100%">5535-41</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 explored the pharmacokinetics and the pharmacodynamics of continuous-infusion meropenem in a population of pediatric hematopoietic stem cell transplant (HSCT) patients who underwent therapeutic drug monitoring. The relationship between meropenem clearance (CLM) and estimated creatinine clearance (CLCR) was assessed by nonlinear regression. A Monte Carlo simulation was performed to investigate the predictive performance of five dosing regimens (15 to 90 mg/kg of body weight/day) for the empirical treatment of severe Gram-negative-related infections in relation to four different categories of renal function. The optimal target was defined as a probability of target attainment (PTA) of ≥90% at steady-state concentration-to-MIC ratios (C SS/MIC) of ≥1 and ≥4 for MICs of up to 8 mg/liter. A total of 21 patients with 44 meropenem C SS were included. A good relationship between CLM and estimated CLCR was observed (r (2) = 0.733). Simulations showed that at an MIC of 2 mg/liter, the administration of continuous-infusion meropenem at doses of 15, 30, 45, and 60 mg/kg/day may achieve a PTA of ≥90% at a C SS/MIC ratio of ≥4 in the CLCR categories of 40 to &lt;80, 80 to &lt;120, 120 to &lt;200, and 200 to &lt;300 ml/min/1.73 m(2), respectively. At an MIC of 8 mg/liter, doses of up to 90 mg/kg/day by continuous infusion may achieve optimal PTA only in the CLCR categories of 40 to &lt;80 and 80 to &lt;120 ml/min/1.73 m(2). Continuous-infusion meropenem at dosages up to 90 mg/kg/day might be effective for optimal treatment of severe Gram-negative-related infections in pediatric HSCT patients, even when caused by carbapenem-resistant pathogens with an MIC of up to 8 mg/liter.&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/26124157?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%">Iossa, Sandra</style></author><author><style face="normal" font="default" size="100%">Costa, Valerio</style></author><author><style face="normal" font="default" size="100%">Corvino, Virginia</style></author><author><style face="normal" font="default" size="100%">Auletta, Gennaro</style></author><author><style face="normal" font="default" size="100%">Barruffo, Luigi</style></author><author><style face="normal" font="default" size="100%">Cappellani, Stefania</style></author><author><style face="normal" font="default" size="100%">Ceglia, Carlo</style></author><author><style face="normal" font="default" size="100%">Cennamo, Giovanni</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Adamo Pio</style></author><author><style face="normal" font="default" size="100%">D'Amico, Alessandra</style></author><author><style face="normal" font="default" size="100%">Di Paolo, Nilde</style></author><author><style face="normal" font="default" size="100%">Forte, Raimondo</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Laria, Carla</style></author><author><style face="normal" font="default" size="100%">Lombardo, Barbara</style></author><author><style face="normal" font="default" size="100%">Malesci, Rita</style></author><author><style face="normal" font="default" size="100%">Vitale, Andrea</style></author><author><style face="normal" font="default" size="100%">Marciano, Elio</style></author><author><style face="normal" font="default" size="100%">Franzè, Annamaria</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phenotypic and genetic characterization of a family carrying two Xq21.1-21.3 interstitial deletions associated with syndromic hearing loss.</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%">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%">8</style></volume><pages><style face="normal" font="default" size="100%">18</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;Sensorineural hearing impairment is a common pathological manifestation in patients affected by X-linked intellectual disability. A few cases of interstitial deletions at Xq21 with several different phenotypic characteristics have been described, but to date, a complete molecular characterization of the deletions harboring disease-causing genes is still missing. Thus, the aim of this study is to realize a detailed clinical and molecular analysis of a family affected by syndromic X-linked hearing loss with intellectual disability.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Clinical analyses revealed a very complex phenotype that included inner ear malformations, vestibular problems, choroideremia and hypotonia with a peculiar pattern of phenotypic variability. Genomic analysis revealed, for the first time, the presence of two close interstitial deletions in the Xq21.1-21.3, harboring 11 protein coding, 9 non-coding genes and 19 pseudogenes. Among these, 3 protein coding genes have already been associated with X-linked hearing loss, intellectual disability and choroideremia.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;In this study we highlighted the presence of peculiar genotypic and phenotypic details in a family affected by syndromic X-linked hearing loss with intellectual disability. We identified two, previously unreported, Xq21.1-21.3 interstitial deletions. The two rearrangements, containing several genes, segregate with the clinical features, suggesting their role in the pathogenicity. However, not all the observed phenotypic features can be clearly associated with the known genes thus, further study is necessary to determine regions involved.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25821518?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%">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%">Phleboliths as a marker of slow-flow venous malformation.</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">100</style></volume><pages><style face="normal" font="default" size="100%">1012</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><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/26242634?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%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">Chinello, Matteo</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 pneumonia that does not improve.</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%">Airway Obstruction</style></keyword><keyword><style  face="normal" font="default" size="100%">Bronchoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Foreign Bodies</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Pneumonia</style></keyword><keyword><style  face="normal" font="default" size="100%">Radiography, Thoracic</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 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">100</style></volume><pages><style face="normal" font="default" size="100%">18, 55</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/24821991?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%">Pizzol, Antonio</style></author><author><style face="normal" font="default" size="100%">Sonzogni, Aurelio</style></author><author><style face="normal" font="default" size="100%">Gregori, Massimo</style></author><author><style face="normal" font="default" size="100%">Granzotto, Marilena</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%">Polyclonal gammopathy after BKV infection in HSCT recipient: a novel trigger for plasma cells replication?</style></title><secondary-title><style face="normal" font="default" size="100%">Virol J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Virol. J.</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%">12</style></volume><pages><style face="normal" font="default" size="100%">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;BK polyomavirus infects most of the general population. However, its clinical manifestations are almost exclusively seen in immunocompromised patients, particularly in kidney and hematopoietic stem cell transplantation recipients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CASE PRESENTATION: &lt;/b&gt;A 15-y-old female suffering from common B-cell acute lymphoblastic leukaemia underwent hematopoietic stem cell transplantation. The patient had reactivation of BKPyV infection and developed an haemorrhagic cystitis. Three months after transplant, BKPyV viremia and viruria increased and she developed a severe nephropathy associated to a polyclonal gammopathy with high levels of isolated IgM.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;This case report describes a rare and unexpected polyclonal gammopathy developed during a polyomavirus-associated nephropathy confirmed by immunohistochemical and laboratory analyses.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25886491?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%">Robino, Antonietta</style></author><author><style face="normal" font="default" size="100%">Bevilacqua, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Pirastu, Nicola</style></author><author><style face="normal" font="default" size="100%">Situlin, Roberta</style></author><author><style face="normal" font="default" size="100%">Di Lenarda, Roberto</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Navarra, Chiara Ottavia</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Polymorphisms in sweet taste genes (TAS1R2 and GLUT2), sweet liking, and dental caries prevalence in an adult Italian population.</style></title><secondary-title><style face="normal" font="default" size="100%">Genes Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genes 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 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">10</style></volume><pages><style face="normal" font="default" size="100%">485</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 assess the relationship between sweet taste genes and dental caries prevalence in a large sample of adults. In addition, the association between sweet liking and sugar intake with dental caries was investigated. Caries was measured by the decayed, missing, filled teeth (DMFT) index in 647 Caucasian subjects (285 males and 362 females, aged 18-65 years), coming from six villages in northeastern Italy. Sweet liking was assessed using a 9-point scale, and the mean of the liking given by each individual to specific sweet food and beverages was used to create a sweet liking score. Simple sugar consumption was estimated by a dietary history interview, considering both added sugars and sugar present naturally in foods. Our study confirmed that polymorphisms in TAS1R2 and GLUT2 genes are related to DMFT index. In particular, GG homozygous individuals for rs3935570 in TAS1R2 gene (p value = 0.0117) and GG homozygous individuals for rs1499821 in GLUT2 gene (p value = 0.0273) showed higher DMFT levels compared to both heterozygous and homozygous for the alternative allele. Furthermore, while the relationship sugar intake-DMFT did not achieve statistical significance (p value = 0.075), a significant association was identified between sweet liking and DMFT (p value = 0.004), independent of other variables. Our study showed that sweet taste genetic factors contribute to caries prevalence and highlighted the role of sweet liking as a predictor of caries risk. Therefore, these results may open new perspectives for individual risk identification and implementation of target preventive strategies, such as identifying high-risk patients before caries development.&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/26268603?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%">Robinson, Matthew R</style></author><author><style face="normal" font="default" size="100%">Hemani, Gibran</style></author><author><style face="normal" font="default" size="100%">Medina-Gomez, Carolina</style></author><author><style face="normal" font="default" size="100%">Mezzavilla, Massimo</style></author><author><style face="normal" font="default" size="100%">Esko, Tõnu</style></author><author><style face="normal" font="default" size="100%">Shakhbazov, Konstantin</style></author><author><style face="normal" font="default" size="100%">Powell, Joseph E</style></author><author><style face="normal" font="default" size="100%">Vinkhuyzen, Anna</style></author><author><style face="normal" font="default" size="100%">Berndt, Sonja I</style></author><author><style face="normal" font="default" size="100%">Gustafsson, Stefan</style></author><author><style face="normal" font="default" size="100%">Justice, Anne E</style></author><author><style face="normal" font="default" size="100%">Kahali, Bratati</style></author><author><style face="normal" font="default" size="100%">Locke, Adam E</style></author><author><style face="normal" font="default" size="100%">Pers, Tune H</style></author><author><style face="normal" font="default" size="100%">Vedantam, Sailaja</style></author><author><style face="normal" font="default" size="100%">Wood, Andrew R</style></author><author><style face="normal" font="default" size="100%">van Rheenen, Wouter</style></author><author><style face="normal" font="default" size="100%">Andreassen, Ole A</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Metspalu, Andres</style></author><author><style face="normal" font="default" size="100%">Berg, Leonard H van den</style></author><author><style face="normal" font="default" size="100%">Veldink, Jan H</style></author><author><style face="normal" font="default" size="100%">Rivadeneira, Fernando</style></author><author><style face="normal" font="default" size="100%">Werge, Thomas M</style></author><author><style face="normal" font="default" size="100%">Abecasis, Goncalo R</style></author><author><style face="normal" font="default" size="100%">Boomsma, Dorret I</style></author><author><style face="normal" font="default" size="100%">Chasman, Daniel I</style></author><author><style face="normal" font="default" size="100%">de Geus, Eco J C</style></author><author><style face="normal" font="default" size="100%">Frayling, Timothy M</style></author><author><style face="normal" font="default" size="100%">Hirschhorn, Joel N</style></author><author><style face="normal" font="default" size="100%">Hottenga, Jouke Jan</style></author><author><style face="normal" font="default" size="100%">Ingelsson, Erik</style></author><author><style face="normal" font="default" size="100%">Loos, Ruth J F</style></author><author><style face="normal" font="default" size="100%">Magnusson, Patrik K E</style></author><author><style face="normal" font="default" size="100%">Martin, Nicholas G</style></author><author><style face="normal" font="default" size="100%">Montgomery, Grant W</style></author><author><style face="normal" font="default" size="100%">North, Kari E</style></author><author><style face="normal" font="default" size="100%">Pedersen, Nancy L</style></author><author><style face="normal" font="default" size="100%">Spector, Timothy D</style></author><author><style face="normal" font="default" size="100%">Speliotes, Elizabeth K</style></author><author><style face="normal" font="default" size="100%">Goddard, Michael E</style></author><author><style face="normal" font="default" size="100%">Yang, Jian</style></author><author><style face="normal" font="default" size="100%">Visscher, Peter M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Population genetic differentiation of height and body mass index across Europe.</style></title><secondary-title><style face="normal" font="default" size="100%">Nat Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nat. 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 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">47</style></volume><pages><style face="normal" font="default" size="100%">1357-62</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Across-nation differences in the mean values for complex traits are common, but the reasons for these differences are unknown. Here we find that many independent loci contribute to population genetic differences in height and body mass index (BMI) in 9,416 individuals across 14 European countries. Using discovery data on over 250,000 individuals and unbiased effect size estimates from 17,500 sibling pairs, we estimate that 24% (95% credible interval (CI) = 9%, 41%) and 8% (95% CI = 4%, 16%) of the captured additive genetic variance for height and BMI, respectively, reflect population genetic differences. Population genetic divergence differed significantly from that in a null model (height, P &lt; 3.94 × 10(-8); BMI, P &lt; 5.95 × 10(-4)), and we find an among-population genetic correlation for tall and slender individuals (r = -0.80, 95% CI = -0.95, -0.60), consistent with correlated selection for both phenotypes. Observed differences in height among populations reflected the predicted genetic means (r = 0.51; P &lt; 0.001), but environmental differences across Europe masked genetic differentiation for BMI (P &lt; 0.58).&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/26366552?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%">Davanzo, Riccardo</style></author><author><style face="normal" font="default" size="100%">Romagnoli, Costantino</style></author><author><style face="normal" font="default" size="100%">Corsello, Giovanni</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Position Statement on Breastfeeding from the Italian Pediatric Societies.</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%">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%">41</style></volume><pages><style face="normal" font="default" size="100%">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;The 2015 Position Statement on Breastfeeding of The Italian Pediatric Societies (SIP, SIN, SICupp, SIGENP) recognizes breastfeeding as an healthy behaviour with many short and long term benefits for both mother and infant.While protecting, promoting and supporting breastfeeding, neonatologists and pediatricians need specific knowledge, skills and a positive attitude toward breastfeeding. In Maternity Hospitals and in Neonatal Units, appropriate organizative interventions should be applied in order to facilitate the beginning of breastfeeding and the use of mother's/human milk.The Italian Pediatric Societies indicate the desiderable goal of around 6 months exclusive breastfeeding if the infant grows properly according to WHO Growth Charts. In principle, complementary feeding should not be anticipated before 6 months as a nutritional strategy pretending to prevent allergy and/or celiac disease. Eventually, long term breastfeeding should be supported meeting mother's desire.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26498033?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%">Fanfani, Francesco</style></author><author><style face="normal" font="default" size="100%">Monterossi, Giorgia</style></author><author><style face="normal" font="default" size="100%">Fagotti, Anna</style></author><author><style face="normal" font="default" size="100%">Gallotta, Valerio</style></author><author><style face="normal" font="default" size="100%">Costantini, Barbara</style></author><author><style face="normal" font="default" size="100%">Vizzielli, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Petrillo, Marco</style></author><author><style face="normal" font="default" size="100%">Carbone, Maria Vittoria</style></author><author><style face="normal" font="default" size="100%">Scambia, Giovanni</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Positron emission tomography-laparoscopy based method in the prediction of complete cytoreduction in platinum-sensitive recurrent ovarian cancer.</style></title><secondary-title><style face="normal" font="default" size="100%">Ann Surg Oncol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ann. Surg. Oncol.</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%">Algorithms</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytoreduction Surgical Procedures</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%">Laparoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Recurrence, Local</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasm Staging</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms, Glandular and Epithelial</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Positron-Emission Tomography</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%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">22</style></volume><pages><style face="normal" font="default" size="100%">649-54</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;This study was designed to evaluate the positron emission tomography-laparoscopy-based method in the prediction of complete/optimal cytoreduction in platinum sensitive recurrent epithelial ovarian cancer patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We analysed 223 consecutive recurrent epithelial ovarian cancer patients. Inclusion criteria were absence of extra-abdominal disease and Eastern Cooperative Oncology Group Performance Status ≤2. Complete and optimal secondary cytoreduction are defined as macroscopic absence or less than 1 cm of residual tumor at the end of surgery.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Laparoscopy was feasible in 210 of 223 patients (94.2 %). Laparoscopy stated 127 (60.5 %) possible cytoreductions and 83 (39.5 %) systemic chemotherapies. In the same population, AGO score evaluation avowed 150 possible cytoreduction (71.5 %) and 60 unresectable women (28.5 %). Overall, 115 of 210 patients (54.7 %) underwent successful secondary cytoreduction: complete and optimal cytoreduction was obtained in 103 (89.5 %) and 12 (10.5 %) patients, respectively. Laparoscopy obtained a positive predictive value of 91.3 %. Laparoscopy recovered to secondary cytoreduction 13 of 60 patients (21.7 %) deemed as not resectable according to AGO score. Forty-eight of 150 AGO score positive patients (32 %) were judged nonresectable by laparoscopy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;This study confirmed that laparoscopy could be effective for the selection of platinum-sensitive recurrent epithelial ovarian cancer patients suitable for complete cytoreduction.&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/25155399?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%">Tripani, Antonella</style></author><author><style face="normal" font="default" size="100%">Pellizzoni, Sandra</style></author><author><style face="normal" font="default" size="100%">Giuliani, Rosella</style></author><author><style face="normal" font="default" size="100%">Bembich, Stefano</style></author><author><style face="normal" font="default" size="100%">Clarici, Andrea</style></author><author><style face="normal" font="default" size="100%">Lonciari, Isabella</style></author><author><style face="normal" font="default" size="100%">Ammaniti, Massimo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">PRE- AND POSTNATAL MODIFICATIONS IN PARENTAL MENTAL REPRESENTATIONS IN THREE CASES OF FETAL GASTROSCHISIS DIAGNOSED DURING PREGNANCY.</style></title><secondary-title><style face="normal" font="default" size="100%">Infant Ment Health J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Infant Ment Health J</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 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;The aim of this study was to identify possible effects of gastroschisis on parents' intrapsychic dynamics by applying an observational clinical approach. More specifically, we intend to (a) evaluate the representational style of parents informed about the diagnosis of fetal gastroschisis during pregnancy using the Interview of Maternal Representations During Pregnancy and the Interview of Paternal Representations During Pregnancy (M. Ammaniti, C. Candelori, M. Pola, &amp; R. Tambelli, ) and (b) observe whether the baby's birth influences the parents' representational styles through the application of the same tools (the Interview of Maternal Representations After the Birth, M. Ammaniti &amp; R. Tambelli, , and the Interview of Paternal Representations After the Birth, M. Ammaniti &amp; R. Tambelli, ), adapted to the postnatal period. During the prenatal period, all parents showed a restricted/disinvested style. Three parents-one mother and two fathers-changed their styles from restricted/disinvested to integrated between pregnancy and Month 6 after the birth of their child. Clinical data from the interviews and observations are discussed in an attempt at better defining intrapsychic dynamics of parents after a diagnosis of gastroschisis.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26554534?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%">Pillon, R</style></author><author><style face="normal" font="default" size="100%">Ziberna, F</style></author><author><style face="normal" font="default" size="100%">Badina, L</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author><author><style face="normal" font="default" size="100%">Longo, G</style></author><author><style face="normal" font="default" size="100%">Quaglia, S</style></author><author><style face="normal" font="default" size="100%">De Leo, L</style></author><author><style face="normal" font="default" size="100%">Vatta, S</style></author><author><style face="normal" font="default" size="100%">Martelossi, S</style></author><author><style face="normal" font="default" size="100%">Patano, G</style></author><author><style face="normal" font="default" size="100%">Not, T</style></author><author><style face="normal" font="default" size="100%">Berti, I</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Prevalence of celiac disease in patients with severe food allergy.</style></title><secondary-title><style face="normal" font="default" size="100%">Allergy</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Allergy</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">70</style></volume><pages><style face="normal" font="default" size="100%">1346-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The association between food allergy and celiac disease (CD) is still to be clarified. We screened for CD 319 patients with severe food allergy (IgE &gt; 85 kU/l against food proteins and a history of severe allergic reactions) who underwent specific food oral immunotherapy (OIT), together with 128 children with mild allergy who recovered without OIT, and compared the prevalence data with our historical data regarding healthy schoolchildren. Sixteen patients (5%) with severe allergy and one (0.8%) with mild allergy tested positive for both genetic and serological CD markers, while the prevalence among the schoolchildren was 1%. Intestinal biopsies were obtained in 13/16 patients with severe allergy and in the one with mild allergy, confirming the diagnosis of CD. Sufferers from severe food allergy seem to be at a fivefold increased risk of CD. Our findings suggest that routine screening for CD should be recommended in patients with severe food allergy.&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/26179550?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%">Scheffer, Deborah I</style></author><author><style face="normal" font="default" size="100%">Morgan, Anna</style></author><author><style face="normal" font="default" size="100%">Vozzi, Diego</style></author><author><style face="normal" font="default" size="100%">Rubinato, Elisa</style></author><author><style face="normal" font="default" size="100%">Di Stazio, Mariateresa</style></author><author><style face="normal" font="default" size="100%">Muzzi, Enrico</style></author><author><style face="normal" font="default" size="100%">Pensiero, Stefano</style></author><author><style face="normal" font="default" size="100%">Giersch, Anne B</style></author><author><style face="normal" font="default" size="100%">Corey, David P</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%">PSIP1/LEDGF: a new gene likely involved in sensorineural progressive hearing loss.</style></title><secondary-title><style face="normal" font="default" size="100%">Sci Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Sci Rep</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%">5</style></volume><pages><style face="normal" font="default" size="100%">18568</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hereditary Hearing Loss (HHL) is an extremely heterogeneous disorder. Approximately 30 out of 80 known HHL genes are associated with autosomal dominant forms. Here, we identified PSIP1/LEDGF (isoform p75) as a novel strong candidate gene involved in dominant HHL. Using exome sequencing we found a frameshift deletion (c.1554_1555del leading to p.E518Dfs*2) in an Italian pedigree affected by sensorineural mild-to-moderate HHL but also showing a variable eye phenotype (i.e. uveitis, optic neuropathy). This deletion led to a premature stop codon (p.T519X) with truncation of the last 12 amino acids. PSIP1 was recently described as a transcriptional co-activator regulated by miR-135b in vestibular hair cells of the mouse inner ear as well as a possible protector against photoreceptor degeneration. Here, we demonstrate that it is ubiquitously expressed in the mouse inner ear. The PSIP1 mutation is associated with a peculiar audiometric slope toward the high frequencies. These findings indicate that PSIP1 likely plays an important role in HHL.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26689366?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%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Melloni, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Rigolin, Gian Matteo</style></author><author><style face="normal" font="default" size="100%">Agnoletto, Chiara</style></author><author><style face="normal" font="default" size="100%">Voltan, Rebecca</style></author><author><style face="normal" font="default" size="100%">Vozzi, Diego</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">dal Monego, Simeone</style></author><author><style face="normal" font="default" size="100%">Cuneo, Antonio</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</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%">The p53 transcriptional pathway is preserved in ATMmutated and NOTCH1mutated chronic lymphocytic leukemias.</style></title><secondary-title><style face="normal" font="default" size="100%">Oncotarget</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Oncotarget</style></alt-title></titles><keywords><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%">Ataxia Telangiectasia Mutated Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Base Sequence</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, p53</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukemia, Lymphocytic, Chronic, B-Cell</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Molecular</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%">Receptor, Notch1</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Suppressor Protein p53</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 30</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">5</style></volume><pages><style face="normal" font="default" size="100%">12635-45</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;By using next generation sequencing, we have analyzed 108 B chronic lymphocytic leukemia (B-CLL) patients. Among genes involved in the TP53 pathway, we found frequent mutations in ATM (n=18), TP53 (n=10) and NOTCH1 (n=10) genes, rare mutations of NOTCH2 (n=2) and CDKN1A/p21 (n=1) and no mutations in BAX, MDM2, TNFRSF10A and TNFRSF10B genes. The in vitro treatment of primary B-CLL cells with the activator of p53 Nutlin-3 induced the transcription of p53 target genes, without significant differences between the B-CLL without mutations and those harboring either ATM or NOTCH1mutations. On the other hand, the subgroup of TP53mutated B-CLL exhibited a significantly lower induction of the p53 target genes in response to Nutlin-3 as compared to the other B-CLL samples. However, among the TP53mutated B-CLL, those showing mutations in the high hot spot region of the DNA binding domain [273-280 aa] maintained a significantly higher p53-dependent transcriptional activity as compared to the other TP53mutated B-CLL samples. Since the ability to elicit a p53-dependent transcriptional activity in vitro has a positive prognostic significance, our data suggest that ATMmutated, NOTCH1mutated and surprisingly, also a subset of TP53mutated B-CLL patients might benefit from therapeutic combinations including small molecule activator of the p53 pathway.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">24</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25587027?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%">Marzuillo, Pierluigi</style></author><author><style face="normal" font="default" size="100%">Guarino, Stefano</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%">Paracetamol: a focus for the general pediatrician.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Acetaminophen</style></keyword><keyword><style  face="normal" font="default" size="100%">Analgesics, Non-Narcotic</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug Overdose</style></keyword><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%">Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk 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 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">173</style></volume><pages><style face="normal" font="default" size="100%">415-25</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;UNLABELLED: &lt;/b&gt;Paracetamol (acetaminophen) is one of the most popular and widely used drugs for the treatment of pain and fever in children. This drug has multiple mechanisms of action, but its pharmacodynamic is still not well known. The central nervous system is the main site of action and it mirrors the paracetamol effect compartment. The recommended dosages and routes of administration should be different whether paracetamol is used for the treatment of pain or fever. For example, the rectal route, while being efficacious for the treatment of fever, should be avoided in pain management. Paracetamol is a safe drug, but some clinical conditions and concomitant drugs, which are frequent in clinical practice, may increase the risk of paracetamol toxicity. Therefore, it is important to optimize its administration to avoid overdoses and maximize its effect. The principal mediator of the paracetamol toxicity is the N-acetyl-p-benzo-quinone imine (NAPQI), a toxic product of the paracetamol metabolism, which could bind cysteine groups on proteins forming paracetamol-protein adduct in the liver.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Although frequently prescribed, the concept of &quot;effect compartment concentration&quot; and the possible co-factors that could cause toxicity at recommended doses are not familiar to all pediatricians and general practitioners. We reviewed the literature concerning paracetamol mechanisms of action, we highlighted some relevant pharmacodynamic concepts for clinical practice, and we summarized the possible risk factors for toxicity at therapeutic dosages.&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/24374658?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%">Perry, John R B</style></author><author><style face="normal" font="default" size="100%">Day, Felix</style></author><author><style face="normal" font="default" size="100%">Elks, Cathy E</style></author><author><style face="normal" font="default" size="100%">Sulem, Patrick</style></author><author><style face="normal" font="default" size="100%">Thompson, Deborah J</style></author><author><style face="normal" font="default" size="100%">Ferreira, Teresa</style></author><author><style face="normal" font="default" size="100%">He, Chunyan</style></author><author><style face="normal" font="default" size="100%">Chasman, Daniel I</style></author><author><style face="normal" font="default" size="100%">Esko, Tõnu</style></author><author><style face="normal" font="default" size="100%">Thorleifsson, Gudmar</style></author><author><style face="normal" font="default" size="100%">Albrecht, Eva</style></author><author><style face="normal" font="default" size="100%">Ang, Wei Q</style></author><author><style face="normal" font="default" size="100%">Corre, Tanguy</style></author><author><style face="normal" font="default" size="100%">Cousminer, Diana L</style></author><author><style face="normal" font="default" size="100%">Feenstra, Bjarke</style></author><author><style face="normal" font="default" size="100%">Franceschini, Nora</style></author><author><style face="normal" font="default" size="100%">Ganna, Andrea</style></author><author><style face="normal" font="default" size="100%">Johnson, Andrew D</style></author><author><style face="normal" font="default" size="100%">Kjellqvist, Sanela</style></author><author><style face="normal" font="default" size="100%">Lunetta, Kathryn L</style></author><author><style face="normal" font="default" size="100%">McMahon, George</style></author><author><style face="normal" font="default" size="100%">Nolte, Ilja M</style></author><author><style face="normal" font="default" size="100%">Paternoster, Lavinia</style></author><author><style face="normal" font="default" size="100%">Porcu, Eleonora</style></author><author><style face="normal" font="default" size="100%">Smith, Albert V</style></author><author><style face="normal" font="default" size="100%">Stolk, Lisette</style></author><author><style face="normal" font="default" size="100%">Teumer, Alexander</style></author><author><style face="normal" font="default" size="100%">Tšernikova, Natalia</style></author><author><style face="normal" font="default" size="100%">Tikkanen, Emmi</style></author><author><style face="normal" font="default" size="100%">Ulivi, Sheila</style></author><author><style face="normal" font="default" size="100%">Wagner, Erin K</style></author><author><style face="normal" font="default" size="100%">Amin, Najaf</style></author><author><style face="normal" font="default" size="100%">Bierut, Laura J</style></author><author><style face="normal" font="default" size="100%">Byrne, Enda M</style></author><author><style face="normal" font="default" size="100%">Hottenga, Jouke-Jan</style></author><author><style face="normal" font="default" size="100%">Koller, Daniel L</style></author><author><style face="normal" font="default" size="100%">Mangino, Massimo</style></author><author><style face="normal" font="default" size="100%">Pers, Tune H</style></author><author><style face="normal" font="default" size="100%">Yerges-Armstrong, Laura M</style></author><author><style face="normal" font="default" size="100%">Hua Zhao, Jing</style></author><author><style face="normal" font="default" size="100%">Andrulis, Irene L</style></author><author><style face="normal" font="default" size="100%">Anton-Culver, Hoda</style></author><author><style face="normal" font="default" size="100%">Atsma, Femke</style></author><author><style face="normal" font="default" size="100%">Bandinelli, Stefania</style></author><author><style face="normal" font="default" size="100%">Beckmann, Matthias W</style></author><author><style face="normal" font="default" size="100%">Benitez, Javier</style></author><author><style face="normal" font="default" size="100%">Blomqvist, Carl</style></author><author><style face="normal" font="default" size="100%">Bojesen, Stig E</style></author><author><style face="normal" font="default" size="100%">Bolla, Manjeet K</style></author><author><style face="normal" font="default" size="100%">Bonanni, Bernardo</style></author><author><style face="normal" font="default" size="100%">Brauch, Hiltrud</style></author><author><style face="normal" font="default" size="100%">Brenner, Hermann</style></author><author><style face="normal" font="default" size="100%">Buring, Julie E</style></author><author><style face="normal" font="default" size="100%">Chang-Claude, Jenny</style></author><author><style face="normal" font="default" size="100%">Chanock, Stephen</style></author><author><style face="normal" font="default" size="100%">Chen, Jinhui</style></author><author><style face="normal" font="default" size="100%">Chenevix-Trench, Georgia</style></author><author><style face="normal" font="default" size="100%">Collée, J Margriet</style></author><author><style face="normal" font="default" size="100%">Couch, Fergus J</style></author><author><style face="normal" font="default" size="100%">Couper, David</style></author><author><style face="normal" font="default" size="100%">Coviello, Andrea D</style></author><author><style face="normal" font="default" size="100%">Cox, Angela</style></author><author><style face="normal" font="default" size="100%">Czene, Kamila</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Adamo Pio</style></author><author><style face="normal" font="default" size="100%">Davey Smith, George</style></author><author><style face="normal" font="default" size="100%">De Vivo, Immaculata</style></author><author><style face="normal" font="default" size="100%">Demerath, Ellen W</style></author><author><style face="normal" font="default" size="100%">Dennis, Joe</style></author><author><style face="normal" font="default" size="100%">Devilee, Peter</style></author><author><style face="normal" font="default" size="100%">Dieffenbach, Aida K</style></author><author><style face="normal" font="default" size="100%">Dunning, Alison M</style></author><author><style face="normal" font="default" size="100%">Eiriksdottir, Gudny</style></author><author><style face="normal" font="default" size="100%">Eriksson, Johan G</style></author><author><style face="normal" font="default" size="100%">Fasching, Peter A</style></author><author><style face="normal" font="default" size="100%">Ferrucci, Luigi</style></author><author><style face="normal" font="default" size="100%">Flesch-Janys, Dieter</style></author><author><style face="normal" font="default" size="100%">Flyger, Henrik</style></author><author><style face="normal" font="default" size="100%">Foroud, Tatiana</style></author><author><style face="normal" font="default" size="100%">Franke, Lude</style></author><author><style face="normal" font="default" size="100%">Garcia, Melissa E</style></author><author><style face="normal" font="default" size="100%">García-Closas, Montserrat</style></author><author><style face="normal" font="default" size="100%">Geller, Frank</style></author><author><style face="normal" font="default" size="100%">de Geus, Eco E J</style></author><author><style face="normal" font="default" size="100%">Giles, Graham G</style></author><author><style face="normal" font="default" size="100%">Gudbjartsson, Daniel F</style></author><author><style face="normal" font="default" size="100%">Gudnason, Vilmundur</style></author><author><style face="normal" font="default" size="100%">Guenel, Pascal</style></author><author><style face="normal" font="default" size="100%">Guo, Suiqun</style></author><author><style face="normal" font="default" size="100%">Hall, Per</style></author><author><style face="normal" font="default" size="100%">Hamann, Ute</style></author><author><style face="normal" font="default" size="100%">Haring, Robin</style></author><author><style face="normal" font="default" size="100%">Hartman, Catharina A</style></author><author><style face="normal" font="default" size="100%">Heath, Andrew C</style></author><author><style face="normal" font="default" size="100%">Hofman, Albert</style></author><author><style face="normal" font="default" size="100%">Hooning, Maartje J</style></author><author><style face="normal" font="default" size="100%">Hopper, John L</style></author><author><style face="normal" font="default" size="100%">Hu, Frank B</style></author><author><style face="normal" font="default" size="100%">Hunter, David J</style></author><author><style face="normal" font="default" size="100%">Karasik, David</style></author><author><style face="normal" font="default" size="100%">Kiel, Douglas P</style></author><author><style face="normal" font="default" size="100%">Knight, Julia A</style></author><author><style face="normal" font="default" size="100%">Kosma, Veli-Matti</style></author><author><style face="normal" font="default" size="100%">Kutalik, Zoltán</style></author><author><style face="normal" font="default" size="100%">Lai, Sandra</style></author><author><style face="normal" font="default" size="100%">Lambrechts, Diether</style></author><author><style face="normal" font="default" size="100%">Lindblom, Annika</style></author><author><style face="normal" font="default" size="100%">Mägi, Reedik</style></author><author><style face="normal" font="default" size="100%">Magnusson, Patrik K</style></author><author><style face="normal" font="default" size="100%">Mannermaa, Arto</style></author><author><style face="normal" font="default" size="100%">Martin, Nicholas G</style></author><author><style face="normal" font="default" size="100%">Masson, Gisli</style></author><author><style face="normal" font="default" size="100%">McArdle, Patrick F</style></author><author><style face="normal" font="default" size="100%">McArdle, Wendy L</style></author><author><style face="normal" font="default" size="100%">Melbye, Mads</style></author><author><style face="normal" font="default" size="100%">Michailidou, Kyriaki</style></author><author><style face="normal" font="default" size="100%">Mihailov, Evelin</style></author><author><style face="normal" font="default" size="100%">Milani, Lili</style></author><author><style face="normal" font="default" size="100%">Milne, Roger L</style></author><author><style face="normal" font="default" size="100%">Nevanlinna, Heli</style></author><author><style face="normal" font="default" size="100%">Neven, Patrick</style></author><author><style face="normal" font="default" size="100%">Nohr, Ellen A</style></author><author><style face="normal" font="default" size="100%">Oldehinkel, Albertine J</style></author><author><style face="normal" font="default" size="100%">Oostra, Ben A</style></author><author><style face="normal" font="default" size="100%">Palotie, Aarno</style></author><author><style face="normal" font="default" size="100%">Peacock, Munro</style></author><author><style face="normal" font="default" size="100%">Pedersen, Nancy L</style></author><author><style face="normal" font="default" size="100%">Peterlongo, Paolo</style></author><author><style face="normal" font="default" size="100%">Peto, Julian</style></author><author><style face="normal" font="default" size="100%">Pharoah, Paul D P</style></author><author><style face="normal" font="default" size="100%">Postma, Dirkje S</style></author><author><style face="normal" font="default" size="100%">Pouta, Anneli</style></author><author><style face="normal" font="default" size="100%">Pylkäs, Katri</style></author><author><style face="normal" font="default" size="100%">Radice, Paolo</style></author><author><style face="normal" font="default" size="100%">Ring, Susan</style></author><author><style face="normal" font="default" size="100%">Rivadeneira, Fernando</style></author><author><style face="normal" font="default" size="100%">Robino, Antonietta</style></author><author><style face="normal" font="default" size="100%">Rose, Lynda M</style></author><author><style face="normal" font="default" size="100%">Rudolph, Anja</style></author><author><style face="normal" font="default" size="100%">Salomaa, Veikko</style></author><author><style face="normal" font="default" size="100%">Sanna, Serena</style></author><author><style face="normal" font="default" size="100%">Schlessinger, David</style></author><author><style face="normal" font="default" size="100%">Schmidt, Marjanka K</style></author><author><style face="normal" font="default" size="100%">Southey, Mellissa C</style></author><author><style face="normal" font="default" size="100%">Sovio, Ulla</style></author><author><style face="normal" font="default" size="100%">Stampfer, Meir J</style></author><author><style face="normal" font="default" size="100%">Stöckl, Doris</style></author><author><style face="normal" font="default" size="100%">Storniolo, Anna M</style></author><author><style face="normal" font="default" size="100%">Timpson, Nicholas J</style></author><author><style face="normal" font="default" size="100%">Tyrer, Jonathan</style></author><author><style face="normal" font="default" size="100%">Visser, Jenny A</style></author><author><style face="normal" font="default" size="100%">Vollenweider, Peter</style></author><author><style face="normal" font="default" size="100%">Völzke, Henry</style></author><author><style face="normal" font="default" size="100%">Waeber, Gerard</style></author><author><style face="normal" font="default" size="100%">Waldenberger, Melanie</style></author><author><style face="normal" font="default" size="100%">Wallaschofski, Henri</style></author><author><style face="normal" font="default" size="100%">Wang, Qin</style></author><author><style face="normal" font="default" size="100%">Willemsen, Gonneke</style></author><author><style face="normal" font="default" size="100%">Winqvist, Robert</style></author><author><style face="normal" font="default" size="100%">Wolffenbuttel, Bruce H R</style></author><author><style face="normal" font="default" size="100%">Wright, Margaret J</style></author><author><style face="normal" font="default" size="100%">Boomsma, Dorret I</style></author><author><style face="normal" font="default" size="100%">Econs, Michael J</style></author><author><style face="normal" font="default" size="100%">Khaw, Kay-Tee</style></author><author><style face="normal" font="default" size="100%">Loos, Ruth J F</style></author><author><style face="normal" font="default" size="100%">McCarthy, Mark I</style></author><author><style face="normal" font="default" size="100%">Montgomery, Grant W</style></author><author><style face="normal" font="default" size="100%">Rice, John P</style></author><author><style face="normal" font="default" size="100%">Streeten, Elizabeth A</style></author><author><style face="normal" font="default" size="100%">Thorsteinsdottir, Unnur</style></author><author><style face="normal" font="default" size="100%">van Duijn, Cornelia M</style></author><author><style face="normal" font="default" size="100%">Alizadeh, Behrooz Z</style></author><author><style face="normal" font="default" size="100%">Bergmann, Sven</style></author><author><style face="normal" font="default" size="100%">Boerwinkle, Eric</style></author><author><style face="normal" font="default" size="100%">Boyd, Heather A</style></author><author><style face="normal" font="default" size="100%">Crisponi, Laura</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Gieger, Christian</style></author><author><style face="normal" font="default" size="100%">Harris, Tamara B</style></author><author><style face="normal" font="default" size="100%">Ingelsson, Erik</style></author><author><style face="normal" font="default" size="100%">Järvelin, Marjo-Riitta</style></author><author><style face="normal" font="default" size="100%">Kraft, Peter</style></author><author><style face="normal" font="default" size="100%">Lawlor, Debbie</style></author><author><style face="normal" font="default" size="100%">Metspalu, Andres</style></author><author><style face="normal" font="default" size="100%">Pennell, Craig E</style></author><author><style face="normal" font="default" size="100%">Ridker, Paul M</style></author><author><style face="normal" font="default" size="100%">Snieder, Harold</style></author><author><style face="normal" font="default" size="100%">Sørensen, Thorkild I A</style></author><author><style face="normal" font="default" size="100%">Spector, Tim D</style></author><author><style face="normal" font="default" size="100%">Strachan, David P</style></author><author><style face="normal" font="default" size="100%">Uitterlinden, André G</style></author><author><style face="normal" font="default" size="100%">Wareham, Nicholas J</style></author><author><style face="normal" font="default" size="100%">Widen, Elisabeth</style></author><author><style face="normal" font="default" size="100%">Zygmunt, Marek</style></author><author><style face="normal" font="default" size="100%">Murray, Anna</style></author><author><style face="normal" font="default" size="100%">Easton, Douglas F</style></author><author><style face="normal" font="default" size="100%">Stefansson, Kari</style></author><author><style face="normal" font="default" size="100%">Murabito, Joanne M</style></author><author><style face="normal" font="default" size="100%">Ong, Ken K</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Australian Ovarian Cancer Study</style></author><author><style face="normal" font="default" size="100%">GENICA Network</style></author><author><style face="normal" font="default" size="100%">kConFab</style></author><author><style face="normal" font="default" size="100%">LifeLines Cohort Study</style></author><author><style face="normal" font="default" size="100%">InterAct Consortium</style></author><author><style face="normal" font="default" size="100%">Early Growth Genetics (EGG) Consortium</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Parent-of-origin-specific allelic associations among 106 genomic loci for age at menarche.</style></title><secondary-title><style face="normal" font="default" size="100%">Nature</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Nature</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%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Mass Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiovascular Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Type 2</style></keyword><keyword><style  face="normal" font="default" size="100%">Europe</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Loci</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</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%">Hypothalamo-Hypophyseal System</style></keyword><keyword><style  face="normal" font="default" size="100%">Intercellular Signaling Peptides and Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Membrane Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Menarche</style></keyword><keyword><style  face="normal" font="default" size="100%">Obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovary</style></keyword><keyword><style  face="normal" font="default" size="100%">Parents</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Potassium Channels, Tandem Pore Domain</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Quantitative Trait Loci</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, GABA-B</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Retinoic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Ribonucleoproteins</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 Oct 2</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">514</style></volume><pages><style face="normal" font="default" size="100%">92-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Age at menarche is a marker of timing of puberty in females. It varies widely between individuals, is a heritable trait and is associated with risks for obesity, type 2 diabetes, cardiovascular disease, breast cancer and all-cause mortality. Studies of rare human disorders of puberty and animal models point to a complex hypothalamic-pituitary-hormonal regulation, but the mechanisms that determine pubertal timing and underlie its links to disease risk remain unclear. Here, using genome-wide and custom-genotyping arrays in up to 182,416 women of European descent from 57 studies, we found robust evidence (P &lt; 5 × 10(-8)) for 123 signals at 106 genomic loci associated with age at menarche. Many loci were associated with other pubertal traits in both sexes, and there was substantial overlap with genes implicated in body mass index and various diseases, including rare disorders of puberty. Menarche signals were enriched in imprinted regions, with three loci (DLK1-WDR25, MKRN3-MAGEL2 and KCNK9) demonstrating parent-of-origin-specific associations concordant with known parental expression patterns. Pathway analyses implicated nuclear hormone receptors, particularly retinoic acid and γ-aminobutyric acid-B2 receptor signalling, among novel mechanisms that regulate pubertal timing in humans. Our findings suggest a genetic architecture involving at least hundreds of common variants in the coordinated timing of the pubertal transition.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">7520</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25231870?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%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Pelin, Marco</style></author><author><style face="normal" font="default" size="100%">Franca, Raffaella</style></author><author><style face="normal" font="default" size="100%">De Iudicibus, Sara</style></author><author><style face="normal" font="default" size="100%">Cuzzoni, Eva</style></author><author><style face="normal" font="default" size="100%">Favretto, Diego</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%">Decorti, Giuliana</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacogenetics of azathioprine in inflammatory bowel disease: a role for glutathione-S-transferase?</style></title><secondary-title><style face="normal" font="default" size="100%">World J Gastroenterol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">World J. Gastroenterol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">6-Mercaptopurine</style></keyword><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%">Azathioprine</style></keyword><keyword><style  face="normal" font="default" size="100%">Glutathione</style></keyword><keyword><style  face="normal" font="default" size="100%">Glutathione Transferase</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunosuppressive Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidative Stress</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharmacogenetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</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 Apr 7</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">20</style></volume><pages><style face="normal" font="default" size="100%">3534-41</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Azathioprine is a purine antimetabolite drug commonly used to treat inflammatory bowel disease (IBD). In vivo it is active after reaction with reduced glutathione (GSH) and conversion to mercaptopurine. Although this reaction may occur spontaneously, the presence of isoforms M and A of the enzyme glutathione-S-transferase (GST) may increase its speed. Indeed, in pediatric patients with IBD, deletion of GST-M1, which determines reduced enzymatic activity, was recently associated with reduced sensitivity to azathioprine and reduced production of azathioprine active metabolites. In addition to increase the activation of azathioprine to mercaptopurine, GSTs may contribute to azathioprine effects even by modulating GSH consumption, oxidative stress and apoptosis. Therefore, genetic polymorphisms in genes for GSTs may be useful to predict response to azathioprine even if more in vitro and clinical validation studies are needed.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">13</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24707136?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%">Farchi, Sara</style></author><author><style face="normal" font="default" size="100%">Forastiere, Francesco</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Alviti, Sabrina</style></author><author><style face="normal" font="default" size="100%">Arnofi, Antonio</style></author><author><style face="normal" font="default" size="100%">Bernardini, Tommaso</style></author><author><style face="normal" font="default" size="100%">Bin, Maura</style></author><author><style face="normal" font="default" size="100%">Brescianini, Sonia</style></author><author><style face="normal" font="default" size="100%">Colelli, Valentina</style></author><author><style face="normal" font="default" size="100%">Cotichini, Rodolfo</style></author><author><style face="normal" font="default" size="100%">Culasso, Martina</style></author><author><style face="normal" font="default" size="100%">De Bartolo, Paolo</style></author><author><style face="normal" font="default" size="100%">Felice, Laura</style></author><author><style face="normal" font="default" size="100%">Fiano, Valentina</style></author><author><style face="normal" font="default" size="100%">Fioritto, Alessandra</style></author><author><style face="normal" font="default" size="100%">Frizzi, Alfio</style></author><author><style face="normal" font="default" size="100%">Gagliardi, Luigi</style></author><author><style face="normal" font="default" size="100%">Giorgi, Giulia</style></author><author><style face="normal" font="default" size="100%">Grasso, Chiara</style></author><author><style face="normal" font="default" size="100%">La Rosa, Francesca</style></author><author><style face="normal" font="default" size="100%">Loganes, Claudia</style></author><author><style face="normal" font="default" size="100%">Lorusso, Paola</style></author><author><style face="normal" font="default" size="100%">Martini, Valentina</style></author><author><style face="normal" font="default" size="100%">Merletti, Franco</style></author><author><style face="normal" font="default" size="100%">Medda, Emanuela</style></author><author><style face="normal" font="default" size="100%">Montelatici, Veronica</style></author><author><style face="normal" font="default" size="100%">Mugelli, Isabella</style></author><author><style face="normal" font="default" size="100%">Narduzzi, Silvia</style></author><author><style face="normal" font="default" size="100%">Nisticò, Lorenza</style></author><author><style face="normal" font="default" size="100%">Penna, Luana</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Piscicelli, Carlo</style></author><author><style face="normal" font="default" size="100%">Poggesi, Giulia</style></author><author><style face="normal" font="default" size="100%">Porta, Daniela</style></author><author><style face="normal" font="default" size="100%">Ranieli, Antonella</style></author><author><style face="normal" font="default" size="100%">Rapisardi, Gherardo</style></author><author><style face="normal" font="default" size="100%">Rasulo, Assunta</style></author><author><style face="normal" font="default" size="100%">Richiardi, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Rusconi, Franca</style></author><author><style face="normal" font="default" size="100%">Serino, Laura</style></author><author><style face="normal" font="default" size="100%">Stazi, Maria Antonietta</style></author><author><style face="normal" font="default" size="100%">Toccaceli, Virgilia</style></author><author><style face="normal" font="default" size="100%">Todros, Tullia</style></author><author><style face="normal" font="default" size="100%">Tognin, Veronica</style></author><author><style face="normal" font="default" size="100%">Trevisan, Morena</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Volpi, Patrizia</style></author><author><style face="normal" font="default" size="100%">Ziroli, Valentina</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Di Lallo, Domenico</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Piccolipiù, a multicenter birth cohort in Italy: protocol of the study.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC 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%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child Development</style></keyword><keyword><style  face="normal" font="default" size="100%">Child Welfare</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%">Environmental Exposure</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%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Socioeconomic 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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">36</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 fetal and infant life are periods of rapid development, characterized by high susceptibility to exposures. Birth cohorts provide unique opportunities to study early-life exposures in association with child development and health, as well as, with longer follow-up, the early life origin of adult diseases. Piccolipiù is an Italian birth cohort recently set up to investigate the effects of environmental exposures, parental conditions and social factors acting during pre-natal and early post-natal life on infant and child health and development. We describe here its main characteristics.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS/DESIGN: &lt;/b&gt;Piccolipiù is a prospective cohort of expected 3000 newborns, who will be recruiting in six maternity units of five Italian cities (Florence, Rome, Trieste, Turin and Viareggio) since October 2011. Mothers are contacted during pregnancy or at delivery and are offered to participate in the study. Upon acceptance, their newborns are recruited at birth and followed up until at least 18 years of age. At recruitment, the mothers donate a blood sample and complete a baseline questionnaire. Umbilical cord blood, pieces of umbilical cord and heel blood spots are also collected. Postnatal follow-up currently occurs at 6, 12, and 24 months of age using on-line or postal self administered questionnaire; further questionnaires and medical examinations are envisaged. Questionnaires collect information on several factors, including mother's and/or child's environmental exposures, anthropometric measures, reproductive factors, diet, supplements, medical history, cognitive development, mental health and socioeconomic factors. Health promotion materials are also offered to parents.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DISCUSSION: &lt;/b&gt;Piccolipiù will broaden our understanding of the contribution of early-life factors to infant and child health and development. Several hypotheses on the developmental origins of health can be tested or piloted using the data collected from the Piccolipiù cohort. By pooling these data with those collected by other existing birth cohorts it will be possible to validate previous findings and to study rare exposures and outcomes.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/24506846?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%">Biino, Ginevra</style></author><author><style face="normal" font="default" size="100%">Pecci, Alessandro</style></author><author><style face="normal" font="default" size="100%">Civaschi, Elisa</style></author><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author><author><style face="normal" font="default" size="100%">Seri, Marco</style></author><author><style face="normal" font="default" size="100%">Melazzini, Federica</style></author><author><style face="normal" font="default" size="100%">Loffredo, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Russo, Giovanna</style></author><author><style face="normal" font="default" size="100%">Bozzi, Valeria</style></author><author><style face="normal" font="default" size="100%">Notarangelo, Lucia Dora</style></author><author><style face="normal" font="default" size="100%">Gresele, Paolo</style></author><author><style face="normal" font="default" size="100%">Heller, Paula G</style></author><author><style face="normal" font="default" size="100%">Pujol-Moix, Núria</style></author><author><style face="normal" font="default" size="100%">Kunishima, Shinji</style></author><author><style face="normal" font="default" size="100%">Cattaneo, Marco</style></author><author><style face="normal" font="default" size="100%">Bussel, James</style></author><author><style face="normal" font="default" size="100%">De Candia, Erica</style></author><author><style face="normal" font="default" size="100%">Cagioni, Claudia</style></author><author><style face="normal" font="default" size="100%">Ramenghi, Ugo</style></author><author><style face="normal" font="default" size="100%">Barozzi, Serena</style></author><author><style face="normal" font="default" size="100%">Fabris, Fabrizio</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%">Platelet diameters in inherited thrombocytopenias: analysis of 376 patients with all known disorders.</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%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Platelets</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Size</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%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hearing Loss, Sensorineural</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%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Motor Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Myosin Heavy Chains</style></keyword><keyword><style  face="normal" font="default" size="100%">Purpura, Thrombocytopenic, Idiopathic</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombocytopenia</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 Aug 7</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">124</style></volume><pages><style face="normal" font="default" size="100%">e4-e10</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Abnormalities of platelet size are one of the distinguishing features of inherited thrombocytopenias (ITs), and evaluation of blood films is recommended as an essential step for differential diagnosis of these disorders. Nevertheless, what we presently know about this subject is derived mainly from anecdotal evidence. To improve knowledge in this field, we evaluated platelet size on blood films obtained from 376 patients with all 19 forms of IT identified so far and found that these conditions differ not only in mean platelet diameter, but also in platelet diameter distribution width and the percentage of platelets with increased or reduced diameters. On the basis of these findings, we propose a new classification of ITs according to platelet size. It distinguishes forms with giant platelets, with large platelets, with normal or slightly increased platelet size, and with normal or slightly decreased platelet size. We also measured platelet diameters in 87 patients with immune thrombocytopenia and identified cutoff values for mean platelet diameter and the percentage of platelets with increased or reduced size that have good diagnostic accuracy in differentiating ITs with giant platelets and with normal or slightly decreased platelet size from immune thrombocytopenia and all other forms of IT.&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/24990887?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%">Necchi, Vittorio</style></author><author><style face="normal" font="default" size="100%">Sommi, Patrizia</style></author><author><style face="normal" font="default" size="100%">Vitali, Agostina</style></author><author><style face="normal" font="default" size="100%">Vanoli, Alessandro</style></author><author><style face="normal" font="default" size="100%">Savoia, Anna</style></author><author><style face="normal" font="default" size="100%">Ricci, Vittorio</style></author><author><style face="normal" font="default" size="100%">Solcia, Enrico</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Polyubiquitinated proteins, proteasome, and glycogen characterize the particle-rich cytoplasmic structure (PaCS) of neoplastic and fetal cells.</style></title><secondary-title><style face="normal" font="default" size="100%">Histochem Cell Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Histochem. Cell Biol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cytoplasm</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetus</style></keyword><keyword><style  face="normal" font="default" size="100%">Glycogen</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%">Microscopy, Confocal</style></keyword><keyword><style  face="normal" font="default" size="100%">Microscopy, Electron, Transmission</style></keyword><keyword><style  face="normal" font="default" size="100%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Proteasome Endopeptidase Complex</style></keyword><keyword><style  face="normal" font="default" size="100%">Ubiquitinated Proteins</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%">141</style></volume><pages><style face="normal" font="default" size="100%">483-97</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A particle-rich cytoplasmic structure (PaCS) concentrating ubiquitin-proteasome system (UPS) components and barrel-like particles in clear, cytoskeleton- and organelle-free areas has recently been described in some neoplasms and in genetic or infectious diseases at risk of neoplasia. Ultrastructurally similar particulate cytoplasmic structures, interpreted as glycogen deposits, have previously been reported in clear-cell neoplasms and some fetal tissues. It remains to be investigated whether the two structures are the same, colocalize UPS components and polysaccharides, and have a role in highly proliferative cells such as fetal and neoplastic cells. We used immunogold electron microscopy and confocal immunofluorescence microscopy to examine human and mouse fetal tissues and human neoplasms. Fetal and neoplastic cells both showed colocalization of polyubiquitinated proteins, 19S and 20S proteasomes, and polysaccharides, both glycogen and chondroitin sulfate, inside cytoplasmic structures showing all distinctive features of PaCSs. Poorly demarcated and/or hybrid (ribosomes admixed) UPS- and glycogen-enriched areas, likely stages in PaCS development, were also seen in some fetal cells, with special reference to those, like primary alveolar pulmonary cells or pancreatic centroacinar cells, having a crucial role in organogenesis. UPS- and glycogen-rich PaCSs developed extensively in clear-cell neoplasms of the kidney, ovary, pancreas, and other organs, as well as, in infantile, development-related tumors replicating fetal patterns, such as choroid plexus papilloma. UPS-mediated, ATP-dependent proteolysis and its potential energy source, glycogen metabolism, may have a crucial, synergic role in embryo-/organogenesis and carcinogenesis.&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/24577783?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%">Robino, Antonietta</style></author><author><style face="normal" font="default" size="100%">Mezzavilla, Massimo</style></author><author><style face="normal" font="default" size="100%">Pirastu, Nicola</style></author><author><style face="normal" font="default" size="100%">Dognini, Maddalena</style></author><author><style face="normal" font="default" size="100%">Tepper, Beverly J</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 population-based approach to study the impact of PROP perception on food liking in populations along the Silk Road.</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%">Armenia</style></keyword><keyword><style  face="normal" font="default" size="100%">Azerbaijan</style></keyword><keyword><style  face="normal" font="default" size="100%">Food</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Association Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</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%">Propylthiouracil</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, G-Protein-Coupled</style></keyword><keyword><style  face="normal" font="default" size="100%">Tajikistan</style></keyword><keyword><style  face="normal" font="default" size="100%">Taste</style></keyword><keyword><style  face="normal" font="default" size="100%">Taste Perception</style></keyword><keyword><style  face="normal" font="default" size="100%">Uzbekistan</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%">9</style></volume><pages><style face="normal" font="default" size="100%">e91716</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Taste is one of the main factors determining food choices. Differences in PROP bitter taste perception have been implicated in individual differences in food preferences and selection. The present study examined associations between, PROP phenotypes, self-reported food liking and TAS2R38 polymorphisms, the major gene implicated in PROP bitterness, in six different populations of the Caucasus and Central Asia, located along the ancient Silk Road. Differences in the distribution of PROP phenotypes across populations were detected, with a higher frequency of super tasters in Tajikistan (31.3%) and Armenia (39.0%) and a higher frequency of non tasters in Georgia (50.9%). While no relationships were observed between PROP phenotypes and food liking using standard statistical tests, we used an approach based on comparison of distance matrices derived from these data. The first matrix compared the food liking ratings of each population to all others pairwise using the Kruskal-Wallis test (at p&lt;0.00063), and the second one compared the distribution of PROP phenotypes across all populations in a similar manner calculating the chi-square statistic as a distance measure. A strong correlation between the two matrices was found (Mantel test: r = 0.67, p-value = 0.03), suggesting that the pattern of food liking across populations was closely related to the distribution of PROP phenotypes. This same relationship was not observed when TAS2R38 genotypes were substituted for PROP phenotypes in this analysis. Our data suggest that a population-based approach utilizing distance matrices is a useful technique for detecting PROP-related differences in food liking and can be applied to other taste phenotypes.&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/24626196?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%">Ura, Blendi</style></author><author><style face="normal" font="default" size="100%">Feriotto, Giordana</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Bilel, Sabrine</style></author><author><style face="normal" font="default" size="100%">Zweyer, Marina</style></author><author><style face="normal" font="default" size="100%">Celeghini, Claudio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Potential role of circulating microRNAs as early markers of preeclampsia.</style></title><secondary-title><style face="normal" font="default" size="100%">Taiwan J Obstet Gynecol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Taiwan J 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%">Biomarkers</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%">MicroRNAs</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Pilot Projects</style></keyword><keyword><style  face="normal" font="default" size="100%">Pre-Eclampsia</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</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 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">53</style></volume><pages><style face="normal" font="default" size="100%">232-4</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 identify microRNAs (miRNAs) differentially expressed at early stages of gestation (12-14 weeks) in the serum of pregnant women, who later developed severe preeclampsia (sPE) in the third trimester of pregnancy (n = 24) compared to women with normal pregnancy (n = 24).&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS AND METHODS: &lt;/b&gt;Sera from 12-14-week-gestation whole blood were subjected to microarray analysis with TaqMan Low Density Array chips (human microRNA panel V3.0), and to quantitative real-time polymerase chain reaction.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;By using the TaqMan Low Density Array chip technology, 19 mature miRNAs appeared differentially expressed in the group of women who later developed sPE as compared to normal women. The expression of four miRNAs (miR-1233, miR-520, miR-210, miR-144) was validated by quantitative real-time polymerase chain reaction analysis. MiR-1233 was the most overexpressed in the serum of women who later developed sPE.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Circulating miRNAs deserve further investigation in order to explore their potential role in the pathogenesis of preeclampsia. In particular, miR-1233 might represent a potential marker of early sPE.&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/25017274?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%">Badina, Laura</style></author><author><style face="normal" font="default" size="100%">Ferrara, Giovanna</style></author><author><style face="normal" font="default" size="100%">Guastalla, Pierpaolo</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 precordial rub in a boy with a severe attack of ulcerative colitis.</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%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Colitis, Ulcerative</style></keyword><keyword><style  face="normal" font="default" size="100%">Diagnosis, Differential</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Intestinal Perforation</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%">Pericarditis</style></keyword><keyword><style  face="normal" font="default" size="100%">Radiography, Thoracic</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 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">30</style></volume><pages><style face="normal" font="default" size="100%">268</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A case of a pneumomediastinum mimicking a pericarditis in a boy with an occult perforation due to ulcerative colitis is reported. Pneumomediastinum is a rare complication of severe attacks of ulcerative colitis, with or without the previous development of a toxic megacolon, that should be considered in the differential diagnosis.&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/24694884?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%">Giuliani, Rosella</style></author><author><style face="normal" font="default" size="100%">Tripani, Antonella</style></author><author><style face="normal" font="default" size="100%">Pellizzoni, Sandra</style></author><author><style face="normal" font="default" size="100%">Clarici, Andrea</style></author><author><style face="normal" font="default" size="100%">Lonciari, Isabella</style></author><author><style face="normal" font="default" size="100%">D'Ottavio, Giuseppina</style></author><author><style face="normal" font="default" size="100%">Schleef, Jurgen</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pregnancy and postpartum following a prenatal diagnosis of fetal thoracoabdominal malformation: the parental perspective.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Surg</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Surg.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Counseling</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystic Adenomatoid Malformation of Lung, Congenital</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hernia, Diaphragmatic</style></keyword><keyword><style  face="normal" font="default" size="100%">Hernias, Diaphragmatic, Congenital</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydronephrosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Kidney Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Longitudinal Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Musculoskeletal Abnormalities</style></keyword><keyword><style  face="normal" font="default" size="100%">Parents</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Psychological Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Stress, Psychological</style></keyword><keyword><style  face="normal" font="default" size="100%">Ultrasonography, Prenatal</style></keyword><keyword><style  face="normal" font="default" size="100%">Urogenital Abnormalities</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 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">49</style></volume><pages><style face="normal" font="default" size="100%">353-8</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;PURPOSE: &lt;/b&gt;The study's aim was to evaluate how information related to a prenatal diagnosis of fetal malformation could modify parenthood experience descriptions during pregnancy and after the child's birth.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A longitudinal case-control clinical study was conducted. Data on parenthood experience descriptions collected using a validated semantic differential technique during pregnancy and after the child's birth were compared between seven couples of parents receiving a prenatal diagnosis of fetal malformation and seven couples without any fetal diagnosis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Our results show that during pregnancy parents in the clinical group describe themselves as more fragile, passive, and timid [p=0.007] than those in the control group. On the other hand, after the child's birth, there are no significant differences between groups.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Data are discussed with reference to better knowledge of the psychological dynamics involved in becoming a parent and to rational planning of support for parents receiving a diagnosis of fetal malformation.&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/24528985?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%">Gortani, Giulia</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%">Procedural sedation for intra-articular corticosteroid injections in juvenile idiopathic arthritis (JIA) should be a standard of care.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Arthritis, Juvenile</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%">Glucocorticoids</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%">Pain</style></keyword><keyword><style  face="normal" font="default" size="100%">Patient Preference</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%">173</style></volume><pages><style face="normal" font="default" size="100%">831</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/24384792?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%">Roia, Anna</style></author><author><style face="normal" font="default" size="100%">Paviotti, Elena</style></author><author><style face="normal" font="default" size="100%">Ferluga, Valentina</style></author><author><style face="normal" font="default" size="100%">Montico, Marcella</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Ronfani, Luca</style></author><author><style face="normal" font="default" size="100%">Tamburlini, Giorgio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Promoting effective child development practices in the first year of life: does timing make a difference?</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Pediatr</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">14</style></volume><pages><style face="normal" font="default" size="100%">222</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;There is an increasing need for parenting programs aimed at promoting parent-child interaction. A variety of interventions have been proposed. The use of audiovisual materials for parents has been shown to be effective but limited information is available on the optimal timing for its use, particularly for new parents during the first year of life of their children. The aim of this study is to compare the effectiveness of a video administered at two different times to first-time parents in modifying parental knowledge, attitudes and intentions with regards to effective care practices.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Open randomized controlled trial carried out in a referral mother and child hospital. Eligible parents were randomly assigned to receive a video at one month (early intervention) or at seven months (late intervention) of age of their child. The video addressed four specific activities related to early child development: reading aloud to the baby, early exposure to music, promotion of early socialization for parents and for children. The primary outcome was the proportion of parents who declared that their knowledge, attitudes and intentions changed after having seen the video at one or seven months of age of the child.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;One hundred and five families were randomly allocated either to the early (53) or to the late (52) intervention group. For 99 families (52 in the early and 47 in the late group) a complete outcome evaluation was available. Parents included in the early administration group more frequently reported modifications in their knowledge of the suggested practices while parents in the late group more frequently reported a change in their attitudes. This finding was consistent across all four practices. The video was found to influence parental intentions in the great majority of interviewed parents with no significant difference between groups (82.7% and 87.2% in the early and late intervention group, respectively).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Audiovisual materials can be an effective complementary tool in programs aimed at supporting parents, particularly those dealing with their first baby. The results provide some useful insights into the differential benefits of using audiovisual aids at different times during the first year of life of the baby.&lt;/p&gt;&lt;p&gt;&lt;b&gt;TRIAL REGISTRATION: &lt;/b&gt;ClinicalTrials.gov NCT02120430.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25193490?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, M</style></author><author><style face="normal" font="default" size="100%">Pastore, S</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author><author><style face="normal" font="default" size="100%">Barbi, E</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pain in cognitively impaired children: a focus for general pediatricians.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Analgesics</style></keyword><keyword><style  face="normal" font="default" size="100%">Cerebral Palsy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Cognition Disorders</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</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%">Quality of Life</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 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">172</style></volume><pages><style face="normal" font="default" size="100%">9-14</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;UNLABELLED: &lt;/b&gt;Pain in children with cognitive impairment and cerebral palsy is a particularly relevant issue due to its high prevalence and impact on quality of life. We review available evidence about prevalence of pain, causes and specific treatment, recognition and use of specific pain scales, physiology, and consequences of pain in this subset of patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Pain is very common and is a critical determinant of quality of life in children with cognitive impairment and cerebral palsy. The diseases and associated complications that frequently expose these patients to pain can be treated and pain prevented. For patients with communication difficulties, appropriate, effective, validated tools are available and should be used to diagnose pain in itself, to &gt;choose analgesic treatment and to determine effectiveness of these therapies. The level of awareness of pediatricians towards this issue seems to be quite low.&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/22426858?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%">Tisato, Veronica</style></author><author><style face="normal" font="default" size="100%">Toffoli, Barbara</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Bernardi, Stella</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</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%">Patients affected by metabolic syndrome show decreased levels of circulating platelet derived growth factor (PDGF)-BB.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin 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%">Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CXCL10</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%">Interleukin-6</style></keyword><keyword><style  face="normal" font="default" size="100%">Linear Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Metabolic Syndrome X</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Obesity</style></keyword><keyword><style  face="normal" font="default" size="100%">Pilot Projects</style></keyword><keyword><style  face="normal" font="default" size="100%">Proto-Oncogene Proteins c-sis</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Messenger</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</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 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">32</style></volume><pages><style face="normal" font="default" size="100%">259-64</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 &amp; AIMS: &lt;/b&gt;The development and/or progression of metabolic syndrome (MetS) in overweight and obese individuals have been associated to low-grade inflammation, but few studies have simultaneously analyzed the circulating levels of several cytokines.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;In this pilot study, a group of 27 cytokines and growth factors was analyzed in the serum of obese patients (n=40) diagnosed for MetS in comparison with sex- and age-matched control subjects without MetS (n=53) by using a multiplex immunoassay. Release of cytokines was measured in culture supernatants of human primary endothelial cells, THP-1 macrophagic cells and HuH-7 hepatoma cells upon exposure to a high fat mixture.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;While the majority of cytokines did not show significant differences between the investigated groups, the circulating levels of CXCL10/IP-10 and IL-6 were higher in the MetS group versus overweight control group. In contrast, PDGF-BB serum levels were significantly decreased in MetS patients. The in vitro addition of a high fat mixture increased the release of IL-6 and/or CXCL10/IP-10 in the culture supernatant of human primary endothelial cells and THP-1 macrophagic cells, while the same mixture significantly decreased the release of PDGF-BB by human THP-1 macrophagic and HuH-7 hepatoma cells.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;The current demonstration that MetS is associated with decrease of the pro-fibrotic PDGF cytokine is a completely novel finding, which adds complexity to the interplay between inflammation and fibrosis in patients affected by MetS.&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/22840561?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%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Norcio, Alessia</style></author><author><style face="normal" font="default" size="100%">Addobbati, Riccardo</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%">Presence of CTAK/CCL27, MCP-3/CCL7 and LIF in human colostrum and breast milk.</style></title><secondary-title><style face="normal" font="default" size="100%">Cytokine</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cytokine</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CCL27</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CCL7</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Colostrum</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%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukemia Inhibitory Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Milk, Human</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 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">61</style></volume><pages><style face="normal" font="default" size="100%">26-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Human colostrum and breast milk are known to contain high levels of cytokines and chemokines, which are thought to contribute to the development of the newborn. The aim of this study was to investigate the difference in the presence and levels of 21 soluble cytokines and chemokines in paired samples of human colostrum (day 2 after delivery) and breast milk (day 4-5 after delivery) by using the multiplex technology. Of the 21 cytokine investigated in 10 pairs of samples, only β-NGF was absent in both colostrum and milk, while INF-α2, SCF and TNF-β were present in colostrum but not in human milk. As a general rule, colostrum contained higher concentrations of cytokines and chemokines with respect to breast milk. The majority of cytokines, detected in colostrum alone or in colostrum and human milk (IL-1α, IL-2Rα, IL-3, IL-16, IL-18, GRO-α, HGF, IFN-α2, M-CSF, MIF, MIG, TNF-β, SDF-1α, TRAIL) have been described in previous studies, while for the first time we describe the presence of additional cytokines either in colostrum alone (SCF) or in both colostrum and breast milk (CTAK/CCL27, MCP-3/CCL7, LIF). Our data confirm and expand previous studies showing that some cytokines/chemokines, which might contribute to the development of the gastro-intestinal and nervous systems, are overexpressed in human colostrum and breast milk, and might contribute to the development of these systems.&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/23040056?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%">Naviglio, Samuele</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%">Pathergy as a cause of false-positive tuberculin skin test.</style></title><secondary-title><style face="normal" font="default" size="100%">Pediatr Infect Dis J</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pediatr. Infect. Dis. J.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Behcet Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">False Positive Reactions</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%">Hypersensitivity</style></keyword><keyword><style  face="normal" font="default" size="100%">Needles</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin</style></keyword><keyword><style  face="normal" font="default" size="100%">Skin Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Tuberculin Test</style></keyword><keyword><style  face="normal" font="default" size="100%">Tuberculosis, Gastrointestinal</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%">31</style></volume><pages><style face="normal" font="default" size="100%">104</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/22217973?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 Vries, E</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">European Society for Immunodeficiencies (ESID) members</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Patient-centred screening for primary immunodeficiency, a multi-stage diagnostic protocol designed for non-immunologists: 2011 update.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Exp Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Exp. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Age of Onset</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Clinical Protocols</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytotoxicity Tests, Immunologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Early Diagnosis</style></keyword><keyword><style  face="normal" font="default" size="100%">General Practice</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunologic Deficiency Syndromes</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunophenotyping</style></keyword><keyword><style  face="normal" font="default" size="100%">Incidence</style></keyword><keyword><style  face="normal" font="default" size="100%">Infection</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphocyte Subsets</style></keyword><keyword><style  face="normal" font="default" size="100%">Mass Screening</style></keyword><keyword><style  face="normal" font="default" size="100%">Medical History Taking</style></keyword><keyword><style  face="normal" font="default" size="100%">Patient-Centered Care</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Physical Examination</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 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">167</style></volume><pages><style face="normal" font="default" size="100%">108-19</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Members of the European Society for Immunodeficiencies (ESID) and other colleagues have updated the multi-stage expert-opinion-based diagnostic protocol for non-immunologists incorporating newly defined primary immunodeficiency diseases (PIDs). The protocol presented here aims to increase the awareness of PIDs among doctors working in different fields. Prompt identification of PID is important for prognosis, but this may not be an easy task. The protocol therefore starts from the clinical presentation of the patient. Because PIDs may present at all ages, this protocol is aimed at both adult and paediatric physicians. The multi-stage design allows cost-effective screening for PID of the large number of potential cases in the early phases, with more expensive tests reserved for definitive classification in collaboration with a specialist in the field of immunodeficiency at a later stage.&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/22132890?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%">Gonelli, Arianna</style></author><author><style face="normal" font="default" size="100%">Radillo, Oriano</style></author><author><style face="normal" font="default" size="100%">Drioli, Sara</style></author><author><style face="normal" font="default" size="100%">Rimondi, Erika</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Maria Bonora, Gian</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pegylated TRAIL retains anti-leukemic cytotoxicity and exhibits improved signal transduction activity with respect to TRAIL.</style></title><secondary-title><style face="normal" font="default" size="100%">Invest New Drugs</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Invest New Drugs</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antineoplastic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase 3</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Movement</style></keyword><keyword><style  face="normal" font="default" size="100%">Dose-Response Relationship, Drug</style></keyword><keyword><style  face="normal" font="default" size="100%">HL-60 Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal Stromal Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitogen-Activated Protein Kinase 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Mitogen-Activated Protein Kinase 3</style></keyword><keyword><style  face="normal" font="default" size="100%">Phosphorylation</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyethylene Glycols</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Fusion Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</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%">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%">30</style></volume><pages><style face="normal" font="default" size="100%">828-32</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 improve the pharmacokinetic profile of tumor necrosis factor-related apoptosis inducing ligand (TRAIL) an N-terminal specific pegylation was performed to generate pegylated TRAIL (PEG-TRAIL). In in vitro experiments, we found that although PEG-TRAIL was slightly less efficient than recombinant TRAIL in promoting leukemic cell apoptosis, it showed an improved ability to promote migration of bone-marrow mesenchymal stem cells and to elicit the ERK1/2 intracellular signal transduction pathway. Overall, these data suggest that TRAIL pegylation retains, or even enhances, the biological activities of TRAIL relevant for its therapeutic applications.&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/21125311?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 Seta, F</style></author><author><style face="normal" font="default" size="100%">Banco, R</style></author><author><style face="normal" font="default" size="100%">Turrisi, A</style></author><author><style face="normal" font="default" size="100%">Airoud, M</style></author><author><style face="normal" font="default" size="100%">De Leo, R</style></author><author><style face="normal" font="default" size="100%">Stabile, G</style></author><author><style face="normal" font="default" size="100%">Ceccarello, M</style></author><author><style face="normal" font="default" size="100%">Restaino, S</style></author><author><style face="normal" font="default" size="100%">De Santo, D</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pelvic inflammatory disease (PID) from Chlamydia trachomatis versus PID from Neisseria gonorrhea: from clinical suspicion to therapy.</style></title><secondary-title><style face="normal" font="default" size="100%">G Ital Dermatol Venereol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">G Ital Dermatol Venereol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chlamydia Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">Chlamydia trachomatis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gonorrhea</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Neisseria gonorrhoeae</style></keyword><keyword><style  face="normal" font="default" size="100%">Pelvic Inflammatory Disease</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%">147</style></volume><pages><style face="normal" font="default" size="100%">423-30</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Pelvic inflammatory disease (PID) is the most significant complication of sexually transmitted infections in childbearing-age women and it represents an important public health problem because of its long-term sequelae (chronic pelvic pain, tubal infertility, ectopic pregnancy). Prior to the mid 1970s PID was considered a monoetiologic infection, due primarily to Neisseria gonorrhea. Now it is well documented as a polymicrobial process, with a great number of microrganisms involved. In addition to Neisseria gonorrhea and Chlamydia trachomatis, other vaginal microrganisms (anaerobes, Gardnerella vaginalis, Haemophilus influenzae, enteric Gram negative rods, Streptococco agalactie, Mycoplasma genitalium) also have been associated with PID. There is a wide variation in PID clinical features; the type and severity of symptoms vary by microbiologic etiology. Women who have chlamydial PID seem more likely than women who have gonococcal PID to be asymptomatic. Since clinical diagnosis is imprecise, the suspicion of PID should be confirmed by genital assessment for signs of inflammation or infection, blood test and imaging evaluation. Laparoscopic approach is considered the gold standard. According to the polymicrobial etiology of PID, antibiotic treatment must provide broad spectrum coverage of likely pathogens. Early administration of antibiotics is necessary to reduce the risk of long-term sequelae.&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/23007248?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%">Borelli, Violetta</style></author><author><style face="normal" font="default" size="100%">Trevisan, Elisa</style></author><author><style face="normal" font="default" size="100%">Vita, Francesca</style></author><author><style face="normal" font="default" size="100%">Bottin, Cristina</style></author><author><style face="normal" font="default" size="100%">Melato, Mauro</style></author><author><style face="normal" font="default" size="100%">Rizzardi, Clara</style></author><author><style face="normal" font="default" size="100%">Zabucchi, Giuliano</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Peroxidase-like activity of ferruginous bodies isolated by exploiting their magnetic property.</style></title><secondary-title><style face="normal" font="default" size="100%">J Toxicol Environ Health A</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Toxicol. Environ. Health Part A</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Air Pollutants, Occupational</style></keyword><keyword><style  face="normal" font="default" size="100%">Asbestos</style></keyword><keyword><style  face="normal" font="default" size="100%">Asbestosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Benzidines</style></keyword><keyword><style  face="normal" font="default" size="100%">Catalysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line</style></keyword><keyword><style  face="normal" font="default" size="100%">Chromogenic Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytotoxins</style></keyword><keyword><style  face="normal" font="default" size="100%">Ferric Compounds</style></keyword><keyword><style  face="normal" font="default" size="100%">Ferritins</style></keyword><keyword><style  face="normal" font="default" size="100%">Ferrosoferric Oxide</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%">Lung</style></keyword><keyword><style  face="normal" font="default" size="100%">Magnetic Phenomena</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesothelioma</style></keyword><keyword><style  face="normal" font="default" size="100%">Mineral Fibers</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Peroxidases</style></keyword><keyword><style  face="normal" font="default" size="100%">Respiratory Mucosa</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">75</style></volume><pages><style face="normal" font="default" size="100%">603-23</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Ferruginous bodies (FB) are polymorphic structures whose formation is macrophage dependent, and are composed of a core, which may consist of an asbestos fiber coated with proteins, among which ferritin is the main component. Within ferritin, the ferric and ferrous ions are coordinated as ferrihydrite, which is the main iron (Fe) storage compound. However, when ferritin accumulates in some tissues following Fe overload it also contains magnetite along with ferrihydrite, which endows it with magnetic properties. Recently studies showed that magnetite exerts peroxidase-like activity, and since ferruginous bodies display magnetic properties, it was postulated that these particular structures may also contain magnetite within the ferritin coating, and thus may also exert peroxidase-like activity. Histochemical analysis for peroxidase of isolated FB smears demonstrated positive staining. Samples isolated from 4 different autopsy lung fragments were also able to oxidize 3,3',5,5'-tetramethyl-benzidine to a blue colored compound that absorbs at 655 nm. This activity was (1) azide and heat insensitive with optimal pH from 5 to 6, and (2) highly variable, changing more than 25-fold from one sample to another. These findings, together with evidence that the peroxidase-like activity of ferruginous bodies has a hydrogen peroxide and substrate requirement different from that of human myeloperoxidase, can exclude that this enzyme gives a significant contribution to the formation of FB. Standard Fe-rich asbestos fibers also express a peroxidase-like activity, but this appears negligible compared to that of ferruginous bodies. Strong acidification of standard Fe-containing asbestos fibers or magnetically isolated ferruginous bodies liberates a high amount of peroxidase-like activity, which is probably accounted for by the release of Fe ions. Further, FB also damage mesothelial cells in vitro. Data suggest that FB exert peroxidase-like activity and cytotoxic activity against mesothelial cells, and hence may be an important factor in pathogenesis of asbestos-related diseases.&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/22712847?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%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">De Iudicibus, Sara</style></author><author><style face="normal" font="default" size="100%">Franca, Raffaella</style></author><author><style face="normal" font="default" size="100%">Addobbati, Riccardo</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Personalized therapies in pediatric inflammatory and autoimmune diseases.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Pharm Des</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Pharm. Des.</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%">Autoimmune Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</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%">Immunogenetic Phenomena</style></keyword><keyword><style  face="normal" font="default" size="100%">Individualized Medicine</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharmacogenetics</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">5766-75</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Pediatric inflammatory and autoimmune diseases are a wide array of systemic or organ-specific conditions, characterized by an exaggerated immune reactivity, which generally occurs in immunogenetically predisposed children. Among the most important ones, in terms of their diffusion and morbidity in the population worldwide, pediatric inflammatory bowel disease (IBD) and juvenile rheumatoid arthritis (JRA) have to be considered. The aim of personalized therapy is to give to each patient the most appropriate drug and dose regimen, in order to maximize treatment response and reduce the risk of adverse events. In general, several therapeutic options exist for pediatric inflammatory and autoimmune conditions, therefore the perspective of pharmacological tools that allow identification of patients with increased risk of treatment issues related to a particular medication, in terms of lack of efficacy or increased probability of adverse events, is particularly desirable and promising. The present review will be focused on the personalized therapy approaches already available or in development for pediatric patients with IBD or JRA, comprising pharmacokinetic, pharmacodynamic and pharmacogenetic assays.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">35</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22726111?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%">Faletra, F</style></author><author><style face="normal" font="default" size="100%">Berti, I</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Pecile, V</style></author><author><style face="normal" font="default" size="100%">Cleva, L</style></author><author><style face="normal" font="default" size="100%">Alberini, E</style></author><author><style face="normal" font="default" size="100%">Bruno, I</style></author><author><style face="normal" font="default" size="100%">Gasparini, P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phylloid pattern of hypomelanosis closely related to chromosomal abnormalities in the 13q detected by SNP array analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">Dermatology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Dermatology (Basel)</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 13</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypopigmentation</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mosaicism</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></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">225</style></volume><pages><style face="normal" font="default" size="100%">294-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Phylloid hypomelanosis is a distinct type of pigmentary mosaicism characterized by congenital hypochromic macules resembling a floral ornament with various elements such as round or oval patches, asymmetrical macules similar to begonia leaves, or oblong lesions. It has been found to be predominantly associated with abnormalities in chromosome 13 and sometimes as-sociated with different extracutaneous abnormalities. Here, we report 2 new cases of phylloid hypomelanosis due to mosaicism involving chromosome 13. The first one is a mosaicism for a supernumerary marker belonging to chromosome 13 and the second one is the first report of phylloid hypomelanosis associated with a mosaic deletion of 13q. Because of the extremely low level of mosaicism in these 2 cases, SNP array analysis on skin fibroblasts was carried out, showing a 13q21.33-q34 duplication (71,024,411-115,103,529) and a 13q13.3-q34 (38,368,012-115,103,529) deletion. Both cases underline on the one hand the strict connection between phylloid hypomelanosis and anomalies of chromosome 13, and on the other hand the relevance of the SNP array analysis on skin fibroblasts in the detection of low-level mosaicism.&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/23095783?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%">Pontillo, Alessandra</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Kamada, Anselmo J</style></author><author><style face="normal" font="default" size="100%">Pancotto, Joao A T</style></author><author><style face="normal" font="default" size="100%">Donadi, Eduardo A</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Sandrin-Garcia, Paula</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Polimorphisms in inflammasome genes are involved in the predisposition to systemic lupus erythematosus.</style></title><secondary-title><style face="normal" font="default" size="100%">Autoimmunity</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Autoimmunity</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%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis Regulatory Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</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%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Haplotypes</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammasomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Lupus Erythematosus, Systemic</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></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">45</style></volume><pages><style face="normal" font="default" size="100%">271-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Recent findings provide evidence of inflammasome critical role in the predisposition to autoimmune disorders. The involvement of inflammasome in the pathogenesis of systemic lupus erythematosus (SLE) has been hypothesized even if no significant association within inflammasome genes mutations or polymorphisms and lupus has been reported yet. We analyzed 14 single nucleotide polymorphisms (SNPs) within 7 inflammasome genes (NLRP1, NLRP3, NLRC4, AIM2, CARD8, CASP1, IL1B) in 144 patients affected by systemic lupus erythematosus and in 158 healthy controls from Southern Brazilian (state of São Paulo) with the aim of disclosing the possible role of inflammasome genes in the susceptibility of SLE. Our results demonstrated that NLRP1 rs2670660 SNP and the NLRP1 rs12150220-rs2670660 A-G haplotype were associated with SLE in our study population, and in particular with the development of nephritis, rash and arthritis. These findings are concordant with previously reported association of NLRP1 with vitiligo and type-1 diabetes underlining once more the involvement of NALP1 inflammasome in the pathogenesis of autoimmune disorders.&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/22235789?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%">da Silva, Ronaldo Celerino</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">Zanin, Valentina</style></author><author><style face="normal" font="default" size="100%">Arraes, Luiz Claudio</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%">Polymorphisms in DC-SIGN and L-SIGN genes are associated with HIV-1 vertical transmission in a Northeastern Brazilian population.</style></title><secondary-title><style face="normal" font="default" size="100%">Hum Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Hum. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Adhesion Molecules</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%">Exons</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%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infectious Disease Transmission, Vertical</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%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Promoter Regions, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Cell Surface</style></keyword><keyword><style  face="normal" font="default" size="100%">Tandem Repeat Sequences</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%">73</style></volume><pages><style face="normal" font="default" size="100%">1159-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;DC-SIGN and L-SIGN are receptors expressed on specialized macrophages in decidua, (Hofbauer and placental capillary endothelial cells), known to interact with several pathogens, including HIV-1. To disclose the possible involvement of these molecules in the susceptibility to HIV vertical transmission, we analyzed DC-SIGN and L-SIGN gene single nucleotide polymorphisms (SNPs) in 192 HIV-1 positive children and 58 HIV-1 negative children all born to HIV-1 positive mothers, as well as 96 healthy uninfected children not exposed to HIV-1, all from Northeast Brazil. The frequency of three SNPs in the DC-SIGN promoter (-139G&gt;A, -201G&gt;T and -336A&gt;G) were significantly different when comparing HIV positive children with HIV-1 exposed uninfected children, indicating an association with susceptibility to HIV-1 vertical transmission. This genetic association suggests that DC-SIGN molecule may play a role in susceptibility to HIV-1 infection through vertical transmission.&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/22902397?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%">Pontillo, Alessandra</style></author><author><style face="normal" font="default" size="100%">Oshiro, Telma M</style></author><author><style face="normal" font="default" size="100%">Girardelli, Martina</style></author><author><style face="normal" font="default" size="100%">Kamada, Anselmo J</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Duarte, Alberto J S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Polymorphisms in inflammasome' genes and susceptibility to HIV-1 infection.</style></title><secondary-title><style face="normal" font="default" size="100%">J Acquir Immune Defic Syndr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Acquir. Immune Defic. Syndr.</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%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis Regulatory Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Calcium-Binding Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">CARD Signaling Adaptor Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Carrier Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Caspase 1</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%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammasomes</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-1beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Intracellular Signaling Peptides and Proteins</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%">Neoplasm Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</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 Feb 1</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">59</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;The involvement of inflammasome genes in the susceptibility to HIV-1 infection was investigated. Twelve single nucleotide polymorphisms within NLRP1, NLRP3, NLRC4, CARD8, CASP1, and IL1B genes were analyzed in 150 HIV-1-infected Brazilian subjects and 158 healthy controls. The 2 polymorphisms rs10754558 in NLRP3 and rs1143634 in IL1B were significantly associated to the HIV-1 infection. These findings supported the previously hypothesized involvement of NALP3-inflammasome in HIV-1 pathogenesis, underlining once more the key role of inflammation and innate immunity in the susceptibility to HIV-1 infection.&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/22227487?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%">Norcio, Alessia</style></author><author><style face="normal" font="default" size="100%">Toffoli, Barbara</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</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%">Potential role of TRAIL in the management of autoimmune diabetes mellitus.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Pharm Des</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Pharm. Des.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Autoimmunity</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Type 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypoglycemic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin</style></keyword><keyword><style  face="normal" font="default" size="100%">Insulin-Secreting Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Islets of Langerhans</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%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">18</style></volume><pages><style face="normal" font="default" size="100%">5759-65</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Type 1 diabetes mellitus (T1DM) is an autoimmune disease, due to the immune-mediated destruction of pancreatic β-cells, whose incidence has been steadily increasing during the last decades. Insulin replacement therapy can treat T1DM, which, however, is still associated with substantial morbidity and mortality. For this reason, great effort is being put into developing strategies that could eventually prevent and/or cure this disease. These strategies are mainly focused on blocking the immune system from attacking β-cells together with functional islet restoration either by regeneration or transplantation. Recent experimental evidences suggest that TNFrelated apoptosis-inducing ligand (TRAIL), which is an immune system modulator protein, could represent an interesting candidate for the cure for T1DM and/or its complications. Here we review the evidences on the potential role of TRAIL in the management of T1DM.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">35</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/22726118?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%">Parentin, Fulvio</style></author><author><style face="normal" font="default" size="100%">Lepore, Loredana</style></author><author><style face="normal" font="default" size="100%">Rabach, Ingrid</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%">Paediatric Behçet's disease presenting with recurrent papillitis and episcleritis: 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%">81</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;Behçet's disease is a chronic multisystem vasculitis characterized by mucocutaneous, articular, neurological, gastrointestinal and ophthalmological lesions. Ocular involvement is mainly represented by recurrent uveitis, especially posterior uveitis; however, iridocyclitis, retinal and choroidal vasculitis, optic neuritis and retinal vascular occlusion can also occur.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CASE PRESENTATION: &lt;/b&gt;A 12-year-old Caucasian boy with a history of recurrent buccal aphthosis and nonspecific gastrointestinal symptoms was admitted to our hospital with blurred vision associated with acute episcleritis and papillitis. The patient's pathergy test was positive, suggesting a diagnosis of Behçet's disease. Corticosteroid and cyclosporine therapy was started, but further episodes were noted in both eyes. The patient was then switched to intravenous infliximab, with complete resolution of the inflammation after the second infusion.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Episcleritis and papillitis should be added to the list of uncommon manifestations of pediatric Behçet's disease. Infliximab is an effective, new therapeutic approach for Behçet's disease that is refractory to the conventional corticosteroid and immunosuppressive therapy.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21352523?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%">Di Mario, S</style></author><author><style face="normal" font="default" size="100%">Spettoli, D</style></author><author><style face="normal" font="default" size="100%">Alessandrini, C</style></author><author><style face="normal" font="default" size="100%">Erenbourg, A</style></author><author><style face="normal" font="default" size="100%">Ronfani, L</style></author><author><style face="normal" font="default" size="100%">Basevi, V</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Periodontal infection and preterm birth: successful periodontal therapy reduces the risk of preterm birth.</style></title><secondary-title><style face="normal" font="default" size="100%">BJOG</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BJOG</style></alt-title></titles><keywords><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%">Periodontal Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Complications, Infectious</style></keyword><keyword><style  face="normal" font="default" size="100%">Premature Birth</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%">Risk Factors</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%">118</style></volume><pages><style face="normal" font="default" size="100%">635; author reply 635-6</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/21392234?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%">Cesaro, Simone</style></author><author><style face="normal" font="default" size="100%">Zanazzo, Andrea Giulio</style></author><author><style face="normal" font="default" size="100%">Frenos, Stefano</style></author><author><style face="normal" font="default" size="100%">Luksch, Roberto</style></author><author><style face="normal" font="default" size="100%">Pegoraro, Anna</style></author><author><style face="normal" font="default" size="100%">Tridello, Gloria</style></author><author><style face="normal" font="default" size="100%">Dallorso, Sandro</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A Phase II study on the safety and efficacy of a single dose of pegfilgrastim for mobilization and transplantation of autologous hematopoietic stem cells in pediatric oncohematology patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Transfusion</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Transfusion</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%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulocyte Colony-Stimulating Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematopoietic Stem Cell Mobilization</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%">Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Peripheral Blood Stem Cell Transplantation</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Transplantation, Autologous</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%">51</style></volume><pages><style face="normal" font="default" size="100%">2480-7</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 use of pegfilgrastim in pediatric patients as a mobilizing agent in association with chemotherapy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN AND METHODS: &lt;/b&gt;This was a prospective, multicenter, Phase II study to evaluate the safety and efficacy of a single dose of 100 µg/kg pegfilgrastim in mobilizing peripheral blood stem cells (PBSCs) in pediatric patients. The primary endpoint of the study was the percentage of good mobilizers with pegfilgrastim (blood peak of CD34+ cells ≥ 20 × 10(6) /L). The results were compared with a historical control group.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Thirty of 36 recruited patients were classified as good mobilizers (83%). The median value of circulating CD34+ at leukapheresis was 143 × 10(6) /L (range, 20 × 10(6) -1988 × 10(6) /L). No significant adverse effects were associated with the use of pegfilgrastim and no patient was withdrawn from using the drug. A blood peak of 20 × 10(6) /L or more CD34+ was observed in 33 of 36 control patients (92%) and the median CD34+ count at leukapheresis was 158 × 10(6) /kg (range, 28 × 10(6) -4529 × 10(6) /kg; p = 0.7). No significant differences were found between the two groups in terms of toxicity or other variables of mobilization. As at October 2008, 23 patients of the pegfilgrastim group and 32 patients of the filgrastim group underwent autologous transplant. No significant differences were found in terms of early toxicity, myeloid recovery, and Day 100 survival.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;A single dose of 100 µg/kg pegfilgrastim was safe and effective for PBSC collection in pediatric patients. We suggest that these results support the use of pegfilgrastim for pediatric patients.&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/21542852?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%">Bezzerri, Valentino</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Pio</style></author><author><style face="normal" font="default" size="100%">Rimessi, Alessandro</style></author><author><style face="normal" font="default" size="100%">Lanzara, Carmen</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Nicolis, Elena</style></author><author><style face="normal" font="default" size="100%">Tamanini, Anna</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Tebon, Maela</style></author><author><style face="normal" font="default" size="100%">Bisoffi, Giulia</style></author><author><style face="normal" font="default" size="100%">Drumm, Mitchell L</style></author><author><style face="normal" font="default" size="100%">Knowles, Michael R</style></author><author><style face="normal" font="default" size="100%">Pinton, Paolo</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Berton, Giorgio</style></author><author><style face="normal" font="default" size="100%">Cabrini, Giulio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phospholipase C-β3 is a key modulator of IL-8 expression in cystic fibrosis bronchial epithelial cells.</style></title><secondary-title><style face="normal" font="default" size="100%">J Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adenosine Triphosphate</style></keyword><keyword><style  face="normal" font="default" size="100%">Calcium</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Transformed</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystic Fibrosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Epithelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Frequency</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Green Fluorescent Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Host-Pathogen Interactions</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-8</style></keyword><keyword><style  face="normal" font="default" size="100%">Isoenzymes</style></keyword><keyword><style  face="normal" font="default" size="100%">Lung Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Microscopy, Fluorescence</style></keyword><keyword><style  face="normal" font="default" size="100%">Phospholipase C beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Kinase C</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Kinase C beta</style></keyword><keyword><style  face="normal" font="default" size="100%">Pseudomonas aeruginosa</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA Interference</style></keyword><keyword><style  face="normal" font="default" size="100%">Toll-Like Receptors</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription Factor RelA</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 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">186</style></volume><pages><style face="normal" font="default" size="100%">4946-58</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Respiratory insufficiency is the major cause of morbidity and mortality in patients affected by cystic fibrosis (CF). An excessive neutrophilic inflammation, mainly orchestrated by the release of IL-8 from bronchial epithelial cells and amplified by chronic bacterial infection with Pseudomonas aeruginosa, leads to progressive tissue destruction. The anti-inflammatory drugs presently used in CF patients have several limitations, indicating the need for identifying novel molecular targets. To address this issue, we preliminarily studied the association of 721 single nucleotide polymorphisms from 135 genes potentially involved in signal transduction implicated in neutrophil recruitment in a cohort of F508del homozygous CF patients with either severe or mild progression of lung disease. The top ranking association was found for a nonsynonymous polymorphism of the phospholipase C-β3 (PLCB3) gene. Studies in bronchial epithelial cells exposed to P. aeruginosa revealed that PLCB3 is implicated in extracellular nucleotide-dependent intracellular calcium signaling, leading to activation of the protein kinase Cα and Cβ and of the nuclear transcription factor NF-κB p65. The proinflammatory pathway regulated by PLCB3 acts by potentiating the Toll-like Receptors' signaling cascade and represents an interesting molecular target to attenuate the excessive recruitment of neutrophils without completely abolishing the inflammatory response.&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/21411730?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%">Padovan, Lara</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</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 polymorphism in PRF1 gene is associated with HIV-1 vertical transmission in Brazilian children.</style></title><secondary-title><style face="normal" font="default" size="100%">AIDS</style></secondary-title><alt-title><style face="normal" font="default" size="100%">AIDS</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Brazil</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV Infections</style></keyword><keyword><style  face="normal" font="default" size="100%">HIV-1</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%">Infectious Disease Transmission, Vertical</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pore Forming Cytotoxic Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</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 Feb 20</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">535-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We investigated the possible association between PRF1 gene polymorphisms and HIV-1 vertical transmission in Brazilian children by analyzing PRF1 gene coding and untranslated regions in 173 perinatally infected children (HIV+), 51 exposed uninfected (HIV-), and 171 HIV-unexposed uninfected children. Seven single nucleotide polymorphisms were identified in our samples. The rs885822 C allele and CC genotype were significantly more frequent in HIV-negative than in HIV-positive patients and associated with a protective effect toward HIV vertical transmission.&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/21157294?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%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">Amato, Annalisa</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Bezzerri, Valentino</style></author><author><style face="normal" font="default" size="100%">Braggion, Cesare</style></author><author><style face="normal" font="default" size="100%">Casciaro, Rosaria</style></author><author><style face="normal" font="default" size="100%">Castaldo, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Colombo, Carla</style></author><author><style face="normal" font="default" size="100%">Covone, Angela Elvira</style></author><author><style face="normal" font="default" size="100%">De Rose, Virginia</style></author><author><style face="normal" font="default" size="100%">Gagliardini, Rolando</style></author><author><style face="normal" font="default" size="100%">Lanzara, Carmen</style></author><author><style face="normal" font="default" size="100%">Minicucci, Laura</style></author><author><style face="normal" font="default" size="100%">Morgutti, Marcello</style></author><author><style face="normal" font="default" size="100%">Nicolis, Elena</style></author><author><style face="normal" font="default" size="100%">Pardo, Francesca</style></author><author><style face="normal" font="default" size="100%">Quattrucci, Serena</style></author><author><style face="normal" font="default" size="100%">Raia, Valeria</style></author><author><style face="normal" font="default" size="100%">Ravazzolo, Roberto</style></author><author><style face="normal" font="default" size="100%">Seia, Manuela</style></author><author><style face="normal" font="default" size="100%">Stanzial, Valentino</style></author><author><style face="normal" font="default" size="100%">Termini, Lisa</style></author><author><style face="normal" font="default" size="100%">Zazzeron, Laura</style></author><author><style face="normal" font="default" size="100%">Cabrini, Giulio</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 polymorphism in the 5' UTR of the DEFB1 gene is associated with the lung phenotype in F508del homozygous Italian cystic fibrosis patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Chem Lab Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Chem. Lab. Med.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">5' Untranslated Regions</style></keyword><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">beta-Defensins</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystic Fibrosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cystic Fibrosis Transmembrane Conductance Regulator</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</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%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Genetic</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 Jan</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">49</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;&lt;b&gt;BACKGROUND: &lt;/b&gt;The identification of cystic fibrosis (CF) patients who are at greater risk of lung damage could be clinically valuable. Thus, we attempted to replicate previous findings and verify the possible association between three single nucleotide polymorphisms (SNPs c.-52G&gt;A, c.-44C&gt;G and c.-20G&gt;A) in the 5' untranslated region (5' UTR) of the β defensin 1 (DEFB1) gene and the CF pulmonary phenotype.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Genomic DNA from 92 Italian CF patients enrolled in different regional CF centres was extracted from peripheral blood and genotyped for DEFB1 SNPs using TaqMan(®) allele specific probes. In order to avoid genetic confounding causes that can account for CF phenotype variability, all patients were homozygous for the F508del CFTR mutation, and were then classified on the basis of clinical and functional data as mild lung phenotype (Mp, n=50) or severe lung phenotype patients (Sp, n=42).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;For the c.-20G&gt;A SNP, the frequency of the A allele, as well as the AA genotype, were significantly more frequent in Mp than in Sp patients, and thus this was associated with a protective effect against severe pulmonary disease (OR=0.48 and 0.28, respectively). The effect of the c.-20G&gt;A A allele is consistent with a recessive model, and the protective effect against Sp is exerted only when it is present in homozygosis. For the other two SNPs, no differences were observed as allelic and genotypic frequency in the two subgroups of CF patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our results, although necessary to be confirmed in larger and multiethnic populations, reinforce DEFB1 as a candidate modifier gene of the CF pulmonary phenotype.&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/21077791?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%">Bramuzzo, Matteo</style></author><author><style face="normal" font="default" size="100%">Lazzerini, Marzia</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Prevalence of anaemia in children with thromboembolism in IBD.</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%">Anemia, Iron-Deficiency</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%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Stroke</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 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">96</style></volume><pages><style face="normal" font="default" size="100%">783</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><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/21377991?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%">Auriti, Cinzia</style></author><author><style face="normal" font="default" size="100%">Fiscarelli, Ersilia</style></author><author><style face="normal" font="default" size="100%">Ronchetti, Maria Paola</style></author><author><style face="normal" font="default" size="100%">Argentieri, Marta</style></author><author><style face="normal" font="default" size="100%">Marrocco, Gabriella</style></author><author><style face="normal" font="default" size="100%">Quondamcarlo, Anna</style></author><author><style face="normal" font="default" size="100%">Seganti, Giulio</style></author><author><style face="normal" font="default" size="100%">Bagnoli, Francesco</style></author><author><style face="normal" font="default" size="100%">Buonocore, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Serra, Giovanni</style></author><author><style face="normal" font="default" size="100%">Bacolla, Gianfranco</style></author><author><style face="normal" font="default" size="100%">Mastropasqua, Savino</style></author><author><style face="normal" font="default" size="100%">Mari, Annibale</style></author><author><style face="normal" font="default" size="100%">Corchia, Carlo</style></author><author><style face="normal" font="default" size="100%">Prencipe, Giusi</style></author><author><style face="normal" font="default" size="100%">Piersigilli, Fiammetta</style></author><author><style face="normal" font="default" size="100%">Ravà, Lucilla</style></author><author><style face="normal" font="default" size="100%">Di Ciommo, Vincenzo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Procalcitonin in detecting neonatal nosocomial sepsis.</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><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Mar 15</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;OBJECTIVE: To investigate the accuracy of procalcitonin (PCT) as a diagnostic marker of nosocomial sepsis (NS) and define the most accurate cut-off to distinguish infected from uninfected neonates. SETTING: Six neonatal intensive care units (NICUs). PATIENTS: 762 neonates admitted to six NICUs during a 28-month observational study for whom at least one serum sample was taken on admission. MAIN OUTCOME MEASURES: Positive and negative predictive values at different PCT cut-off levels. RESULTS: The overall probability of an NS was doubled or more if PCT was &gt;0.5 ng/ml. In very-low-birth-weight (VLBW) infants, a cut-off of &gt;2.4 ng/ml gave a positive predictive value of NS near to 50% with a probability of a false-positive diagnosis of NS in about 10% of the patients. CONCLUSIONS: In VLBW neonates, a serum PCT value &gt;2.4 ng/ml prompts early empirical antibiotic therapy, while in normal-birth-weight infants, a PCT value ≤2.4 ng/ml carries a low risk of missing an NS.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21406453?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%">Davanzo, Riccardo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Promoting mother’s milk use in very low birth weight infants: when nutritional hierarchy deals with the professional value system.</style></title><secondary-title><style face="normal" font="default" size="100%">J Hum Lact</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Hum Lact</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Attitude of Health Personnel</style></keyword><keyword><style  face="normal" font="default" size="100%">Breast Feeding</style></keyword><keyword><style  face="normal" font="default" size="100%">Health Promotion</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, Very Low Birth Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Intensive Care Units, Neonatal</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%">27</style></volume><pages><style face="normal" font="default" size="100%">329-30</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/22048755?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 Seta, F</style></author><author><style face="normal" font="default" size="100%">Banco, R</style></author><author><style face="normal" font="default" size="100%">Guaschino, S</style></author><author><style face="normal" font="default" size="100%">De Santo, D</style></author><author><style face="normal" font="default" size="100%">Turrisi, A</style></author><author><style face="normal" font="default" size="100%">Piva, C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">[Proteomic applications in gynecology-obstetrics].</style></title><secondary-title><style face="normal" font="default" size="100%">Minerva Ginecol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Minerva Ginecol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Endometriosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genital Diseases, Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Genital Neoplasms, Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Polycystic Ovary Syndrome</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%">Proteomics</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 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">63</style></volume><pages><style face="normal" font="default" size="100%">39-46</style></pages><language><style face="normal" font="default" size="100%">ita</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Proteomics has recently emerged as a powerful approach both for discovering biomarkers as well as for understanding the physiopathology of unclear gynecological-obstetrical disorders. Currently, several biological fluids and fetal tissues were successfully tested, including maternal plasma, amniotic fluid, cervical-vaginal fluid, urine, saliva, placental trophoblast, amnio-chorionic membranes and cord blood. The potential of proteomics on the polycystic ovary syndrome (PCOS) involves biomarkers discovery for a more accurate diagnosis of the syndrome and identification, within the patients with PCOS, those who respond more easily to treatment and those who will be at increased risk for future metabolic complications. The proteomic approach applied to patients with endometriosis would allow not only a non-invasive early diagnosis, but also a staging of the disease and a prediction of infertility risk. Proteomics also involves oncological field, in order to discover biomarkers that allow early diagnosis and prognosis of female genital malignancies. In addition to this, proteomics could be used to understand and predict obstetrical complications such as recurrent spontaneous abortion, preterm birth and preeclampsia. However, further studies are needed on a larger cohort of patients to introduce these biomarkers in clinical practice.&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/21311419?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%">Paugh, Steven W</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author><author><style face="normal" font="default" size="100%">Evans, William E</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Pharmacogenomics in pediatric leukemia.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Opin Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Opin. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Antineoplastic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Predisposition to Disease</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%">Individualized Medicine</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharmacogenetics</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Precursor Cell Lymphoblastic Leukemia-Lymphoma</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 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">22</style></volume><pages><style face="normal" font="default" size="100%">703-10</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 OF REVIEW: &lt;/b&gt;The therapeutic index of many medications, especially in children, is very narrow with substantial risk for toxicity at doses required for therapeutic effects. This is particularly relevant to cancer chemotherapy, when the risk of toxicity must be balanced against potential suboptimal (low) systemic exposure that can be less effective in patients with higher rates of drug clearance. The purpose of this review is to discuss genetic factors that lead to interpatient differences in the pharmacokinetics and pharmacodynamics of these medications.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RECENT FINDINGS: &lt;/b&gt;Genome-wide agonistic studies of pediatric patient populations are revealing genome variations that may affect susceptibility to specific diseases and that influence the pharmacokinetic and pharmacodynamic characteristics of medications. Several genetic factors with relatively small effect may be combined in the determination of a pharmacogenomic phenotype and considering these polygenic models may be mandatory in order to predict the related drug response phenotypes. These findings have potential to yield new insights into disease pathogenesis, and lead to molecular diagnostics that can be used to optimize the treatment of childhood cancers.&lt;/p&gt;&lt;p&gt;&lt;b&gt;SUMMARY: &lt;/b&gt;Advances in genome technology, and their comprehensive and systematic deployment to elucidate the genomic basis of interpatient differences in drug response and disease risk, hold great promise to ultimately enhance the efficacy and reduce the toxicity of drug therapy in children.&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/20861736?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%">Vilca, Iris</style></author><author><style face="normal" font="default" size="100%">Munitis, Pablo Garcia</style></author><author><style face="normal" font="default" size="100%">Pistorio, Angela</style></author><author><style face="normal" font="default" size="100%">Ravelli, Angelo</style></author><author><style face="normal" font="default" size="100%">Buoncompagni, Antonella</style></author><author><style face="normal" font="default" size="100%">Bica, Blanca</style></author><author><style face="normal" font="default" size="100%">Campos, Lucia</style></author><author><style face="normal" font="default" size="100%">Häfner, Renate</style></author><author><style face="normal" font="default" size="100%">Hofer, Michael</style></author><author><style face="normal" font="default" size="100%">Ozen, Seza</style></author><author><style face="normal" font="default" size="100%">Huemer, Christian</style></author><author><style face="normal" font="default" size="100%">Bae, Sang Cheol</style></author><author><style face="normal" font="default" size="100%">Sztajnbok, Flavio</style></author><author><style face="normal" font="default" size="100%">Arguedas, Olga</style></author><author><style face="normal" font="default" size="100%">Foeldvari, Ivan</style></author><author><style face="normal" font="default" size="100%">Huppertz, Hans Iko</style></author><author><style face="normal" font="default" size="100%">Gamir, María Luz</style></author><author><style face="normal" font="default" size="100%">Magnusson, Bo</style></author><author><style face="normal" font="default" size="100%">Dressler, Frank</style></author><author><style face="normal" font="default" size="100%">Uziel, Yosef</style></author><author><style face="normal" font="default" size="100%">van Rossum, Marion A J</style></author><author><style face="normal" font="default" size="100%">Hollingworth, Peter</style></author><author><style face="normal" font="default" size="100%">Cawkwell, Gail</style></author><author><style face="normal" font="default" size="100%">Martini, Alberto</style></author><author><style face="normal" font="default" size="100%">Ruperto, Nicolino</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Pediatric Rheumatology International Trials Organisation (PRINTO)</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Predictors of poor response to methotrexate in polyarticular-course juvenile idiopathic arthritis: analysis of the PRINTO methotrexate trial.</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%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies, Antinuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Arthritis, Juvenile</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%">Disability Evaluation</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%">Immunosuppressive Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Methotrexate</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</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 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">69</style></volume><pages><style face="normal" font="default" size="100%">1479-83</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 determine whether baseline demographic, clinical, articular and laboratory variables predict methotrexate (MTX) poor response in polyarticular-course juvenile idiopathic arthritis.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Patients newly treated for 6 months with MTX enrolled in the Paediatric Rheumatology International Trials Organization (PRINTO) MTX trial. Bivariate and logistic regression analyses were used to identify baseline predictors of poor response according to the American College of Rheumatology pediatric (ACR-ped) 30 and 70 criteria.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;In all, 405/563 (71.9%) of patients were women; median age at onset and disease duration were 4.3 and 1.4 years, respectively, with anti-nuclear antibody (ANA) detected in 259/537 (48.2%) patients. With multivariate logistic regression analysis, the most important determinants of ACR-ped 70 non-responders were: disease duration &gt; 1.3 years (OR 1.93), ANA negativity (OR 1.77), Childhood Health Assessment Questionnaire (CHAQ) disability index &gt; 1.125 (OR 1.65) and the presence of right and left wrist activity (OR 1.55). Predictors of ACR-ped 30 non-responders were: ANA negativity (OR 1.92), CHAQ disability index &gt; 1.14 (OR 2.18) and a parent's evaluation of child's overall well-being &lt; or = 4.69 (OR 2.2).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The subgroup of patients with longer disease duration, ANA negativity, higher disability and presence of wrist activity were significantly associated with a poorer response to a 6-month MTX course.&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/20525842?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%">Lapolla, A</style></author><author><style face="normal" font="default" size="100%">Bonomo, M</style></author><author><style face="normal" font="default" size="100%">Dalfrà, M G</style></author><author><style face="normal" font="default" size="100%">Parretti, E</style></author><author><style face="normal" font="default" size="100%">Mannino, D</style></author><author><style face="normal" font="default" size="100%">Mello, G</style></author><author><style face="normal" font="default" size="100%">Di Cianni, G</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">GISOGD</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Prepregnancy BMI influences maternal and fetal outcomes in women with isolated gestational hyperglycaemia: a multicentre study.</style></title><secondary-title><style face="normal" font="default" size="100%">Diabetes Metab</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Diabetes Metab.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Blood Glucose</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Mass Index</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Macrosomia</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucose Tolerance Test</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperglycemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Statistical</style></keyword><keyword><style  face="normal" font="default" size="100%">Obesity</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%">Pregnancy Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Time Factors</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%">36</style></volume><pages><style face="normal" font="default" size="100%">265-70</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;AIM: &lt;/b&gt;This multicentre study analyzed the maternal and fetal outcomes of women who had one elevated 3-h oral glucose tolerance test (isolated gestational hyperglycaemia [IGH]).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;From 1999 to 2003, data were collected for 606 IGH women from 31 Italian obstetric or diabetic centres, including time and mode of delivery, gestational hypertension, preeclampsia, eclampsia, congenital malformations, and neonatal mortality and morbidity, to compare them with the general pregnant Italian population. A prognostic model for the outcome of pregnancy was constructed, and the concurrence of certain specified conditions was considered a positive outcome, whereas pregnancies that failed to meet one or more of the stated conditions were classified as &quot;complicated&quot;.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Macrosomia was significantly more frequent in women with IGH than in the normal pregnant population (10.7 vs 7.4%, respectively; P=0.003). Stillbirth and neonatal mortality rates did not differ from those in normal pregnancies, while a slight rise in the frequency of major malformations was not statistically significant (1.48 vs 0.89%, respectively; P&lt;0.11). Multivariate logistic analyses confirmed that the prepregnancy body mass index (BMI) was an independent predictor of a complicated pregnancy. As for fetal growth, multivariate logistic analyses according to BMI showed that being overweight or obese were strong predictors of macrosomia.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;These findings in a large cohort of Italian women with IGH confirm the detrimental effect of even minimally altered glucose tolerance on fetal outcome. Also, prepregnancy obesity plays an important role in raising the risk of adverse perinatal outcomes in such patients.&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/20598607?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%">Cattaneo, Adriano</style></author><author><style face="normal" font="default" size="100%">Gafurov, Ilkhom</style></author><author><style face="normal" font="default" size="100%">Bomestar, Tamara</style></author><author><style face="normal" font="default" size="100%">Bacci, Marianna</style></author><author><style face="normal" font="default" size="100%">Kumar, Sanjiv</style></author><author><style face="normal" font="default" size="100%">Popovic, Dragoslav</style></author><author><style face="normal" font="default" size="100%">Tamburlini, Giorgio</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Progress towards the achievement of MDG4 in the Commonwealth of Independent States: uncertain data, clear priorities.</style></title><secondary-title><style face="normal" font="default" size="100%">Health Res Policy Syst</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Health Res Policy Syst</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">8</style></volume><pages><style face="normal" font="default" size="100%">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;Data on under five mortality in the twelve countries of the Commonwealth of Independent States show important fluctuations over time due to variations in quality of data, definitions of neonatal deaths and methods of mortality estimation. Despite the uncertainties regarding mortality trends, the analysis of health and social information from different sources offers clues to identify priority areas and key strategic directions for accelerating the achievement of the 4th Millennium Development Goal. Neonatal deaths represent from 40% to over 50% of under five deaths in all these countries. Maternal mortality was above 50 per 100,000 in 2005, despite the good coverage with antenatal care and births assisted by skilled birth attendants. The scanty information on quality of perinatal care indicates widespread substandard care at all levels. Stunting in children under five is above 10% in ten out of twelve countries and coexists with emerging overweight. Exclusivity and duration of breastfeeding fall short of what is recommended. There are important inequalities in child and maternal mortality, malnutrition and access and use of health services within countries. Taken as a whole, the available information clearly indicates that priority should be given to improvement of the health of women in reproductive age and of the quality of perinatal care, including the establishment of reliable data collection systems. To achieve this, action will need to focus on strengthening the capacity of the health system to improve the technical content of service provision, and on improving access and appropriate use of services by the most disadvantaged groups. The involvement of other sectors will be necessary to improve reproductive health and nutrition at community level and to tackle inequity. Comparisons between countries with similar socioeconomic background but different health policies seem to indicate that gradual progression towards universal coverage with essential health care through a national health insurance system is associated with larger reduction of child mortality than troubled transition towards a privatized and unregulated health system.&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/20205914?dopt=Abstract</style></custom1></record></records></xml>