<?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%">Poropat, Federico</style></author><author><style face="normal" font="default" size="100%">Cozzi, Giorgio</style></author><author><style face="normal" font="default" size="100%">Magnolato, Andrea</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Borrometi, Fabio</style></author><author><style face="normal" font="default" size="100%">Krauss, Baruch</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%">Teaching pain recognition through art: the Ramsay-Caravaggio sedation scale.</style></title><secondary-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Clinical Competence</style></keyword><keyword><style  face="normal" font="default" size="100%">Conscious Sedation</style></keyword><keyword><style  face="normal" font="default" size="100%">Deep Sedation</style></keyword><keyword><style  face="normal" font="default" size="100%">Education, Medical, Graduate</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Hospitals, University</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Internship and Residency</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%">Medicine in the Arts</style></keyword><keyword><style  face="normal" font="default" size="100%">Monitoring, Physiologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Pain Measurement</style></keyword><keyword><style  face="normal" font="default" size="100%">Paintings</style></keyword><keyword><style  face="normal" font="default" size="100%">Pediatrics</style></keyword><keyword><style  face="normal" font="default" size="100%">Video Recording</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 Jan 31</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">44</style></volume><pages><style face="normal" font="default" size="100%">20</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Clinical observation is a key component of medical ability, enabling immediate evaluation of the patient's emotional state and contributing to a clinical clue that leads to final decision making. In medical schools, the art of learning to look can be taught using medical humanities and especially visual arts. By presenting a Ramsay sedation score (RSS) integrated with Caravaggio's paintings during a procedural sedation conference for pediatric residents, we want to test the effectiveness of this approach to improve the quality of learning.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;In this preliminary study, we presented videos showing sedated pediatric patients in the setting of a procedural sedation lesson to two randomized groups of residents, one attending a lesson on RSS explained through the masterpieces of Caravaggio, the other without artistic support. A week later we tested their learning with ten multi-choice questions focused on theoretical questions about sedation monitoring and ten more questions focused on recognizing the appropriate RSS viewing the videos. The primary outcome was the comparison of the total number of RSS layers properly recognized in both groups. We also evaluated the appreciation of the residents of the use of works of art integrated with the lesson.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Eleven students were randomized to each group. Two residents in the standard lesson did not attend the test. The percentage of correct answers on the theoretical part was similar, 82% in the art group and 89% in the other (p &gt; 0.05). No difference was found in the video recognition part of the RSS recognition test. Residents exposed to paintings shown great appreciation for the integration of the lesson with the Caravaggio's masterpieces.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Adding artwork to a standard medical conference does not improve the performance of student tests, although this approach has been greatly appreciated by residents.&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/29386058?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%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Grasso, Antonio Giacomo</style></author><author><style face="normal" font="default" size="100%">Conversano, Ester</style></author><author><style face="normal" font="default" size="100%">Lucafò, Marianna</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Gregori, Massimo</style></author><author><style face="normal" font="default" size="100%">Conti, Francesca</style></author><author><style face="normal" font="default" size="100%">Cancrini, Caterina</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Theophylline as a precision therapy in a young girl with PIK3R1 immunodeficiency.</style></title><secondary-title><style face="normal" font="default" size="100%">J Allergy Clin Immunol Pract</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Allergy Clin Immunol Pract</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 Nov - Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">2165-2167</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/29510232?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%">Gregori, Massimo</style></author><author><style face="normal" font="default" size="100%">Simeone, Roberto</style></author><author><style face="normal" font="default" size="100%">Sonzogni, Aurelio</style></author><author><style face="normal" font="default" size="100%">Zanon, Davide</style></author><author><style face="normal" font="default" size="100%">Boz, Giulia</style></author><author><style face="normal" font="default" size="100%">D'Antiga, Lorenzo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Total body irradiation and iron chelation treatment are associated with pancreatic injury following pediatric hematopoietic stem cell transplantation.</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><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 Apr 13</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">9</style></volume><pages><style face="normal" font="default" size="100%">19543-19554</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Whereas many studies have addressed the risk of organ dysfunction following hematopoietic stem cell transplantation (HSCT), little is known about pancreatic susceptibility in this setting. We aimed to investigate the effect of iron overload (IO) and total body irradiation (TBI) on pancreatic function of children undergoing HSCT. We retrospectively evaluated children admitted between 2012-2016 fulfilling the following criteria: normal pancreatic iron concentration (PIC), regular pancreatic function before HSCT, availability of abdominal magnetic resonance imaging with gradient-recalled-echo sequences and a full set of biochemical markers of IO and pancreatic function performed before HSCT and at discharge. We divided the patients according to the use of TBI or myeloablative chemotherapy (MCHT) in the conditioning regimen. All patients with severe IO or moderate IO with a high risk of engraftment delay or transplantation-related complications underwent chelation therapy with deferoxamine (DFO) from the first day of conditioning to discharge. 63 patients had a HSCT in the study period, 13 did not fulfill the inclusion criteria; 50 (25 in each group) are included in the analysis, and did not show differences at baseline evaluation. At follow up testing the TBI group showed a significantly higher PIC (107,8±100,3 μmol/g vs 28,4±37,9 in MCHT group, p&lt;0,0001). In the TBI group the patients who had DFO treatment had higher PIC (223,2±48,8 μmol/g vs 55,7±10,5 without DFO treatment, p&lt;0,0001), and all patients having PIC &gt;100 μmol/g at follow up had DFO-based chelation therapy, versus 26% of those with lower PIC (p&lt;0,0001). The number of patients presenting exocrine pancreatic dysfunctions one month after transplantation was significantly higher in the TBI group (48% vs 4%; p&lt;0.0001). The mean pancreatic volume reduction was significantly greater in the TBI group (39,1% vs 0,9% in the MCHT group; p&lt;0,05), and was significantly worse on those who received DFO therapy. Based on our data, we suggest that TBI is detrimental for pancreatic functions, and speculate that DFO may contribute to the rapid pancreatic IO observed in these patients.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">28</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/29731964?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%">Castellano, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Divella, Chiara</style></author><author><style face="normal" font="default" size="100%">Sallustio, Fabio</style></author><author><style face="normal" font="default" size="100%">Montinaro, Vincenzo</style></author><author><style face="normal" font="default" size="100%">Curci, Claudia</style></author><author><style face="normal" font="default" size="100%">Zanichelli, Andrea</style></author><author><style face="normal" font="default" size="100%">Bonanni, Erika</style></author><author><style face="normal" font="default" size="100%">Suffritti, Chiara</style></author><author><style face="normal" font="default" size="100%">Caccia, Sonia</style></author><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Gallone, Anna</style></author><author><style face="normal" font="default" size="100%">Schena, Francesco Paolo</style></author><author><style face="normal" font="default" size="100%">Gesualdo, Loreto</style></author><author><style face="normal" font="default" size="100%">Cicardi, Marco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">A transcriptomics study of hereditary angioedema attacks.</style></title><secondary-title><style face="normal" font="default" size="100%">J Allergy Clin Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Allergy Clin. 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 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">142</style></volume><pages><style face="normal" font="default" size="100%">883-891</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;Hereditary angioedema (HAE) caused by C1-inhibitor deficiency is a lifelong illness characterized by recurrent acute attacks of localized skin or mucosal edema. Activation of the kallikrein/bradykinin pathway at the endothelial cell level has a relevant pathogenetic role in acute HAE attacks. Moreover, other pathways are involved given the variable clinical expression of the disease in different patients.&lt;/p&gt;&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;We sought to explore the involvement of other putative genes in edema formation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We performed a PBMC microarray gene expression analysis on RNA isolated from patients with HAE during an acute attack and compared them with the transcriptomic profile of the same patients in the remission phase.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Gene expression analysis identified 23 genes significantly modulated during acute attacks that are involved primarily in the natural killer cell signaling and leukocyte extravasation signaling pathways. Gene set enrichment analysis showed a significant activation of relevant biological processes, such as response to external stimuli and protein processing (q &lt; 0.05), suggesting involvement of PBMCs during acute HAE attacks. Upregulation of 2 genes, those encoding adrenomedullin and cellular receptor for urokinase plasminogen activator (uPAR), which occurs during an acute attack, was confirmed in PBMCs of 20 additional patients with HAE by using real-time PCR. Finally, in vitro studies demonstrated the involvement of uPAR in the generation of bradykinin and endothelial leakage.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Our study demonstrates the increase in levels of adrenomedullin and uPAR in PBMCs during an acute HAE attack. Activation of these genes usually involved in regulation of vascular tone and in inflammatory response might have a pathogenic role by amplifying bradykinin production and edema formation in patients with HAE.&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/29729940?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%">Alkowari, Moza K</style></author><author><style face="normal" font="default" size="100%">Vozzi, Diego</style></author><author><style face="normal" font="default" size="100%">Bhagat, Shruti</style></author><author><style face="normal" font="default" size="100%">Krishnamoorthy, Navaneethakrishnan</style></author><author><style face="normal" font="default" size="100%">Morgan, Anna</style></author><author><style face="normal" font="default" size="100%">Hayder, Yousra</style></author><author><style face="normal" font="default" size="100%">Logendra, Barathy</style></author><author><style face="normal" font="default" size="100%">Najjar, Nehal</style></author><author><style face="normal" font="default" size="100%">Gandin, Ilaria</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Badii, Ramin</style></author><author><style face="normal" font="default" size="100%">Girotto, Giorgia</style></author><author><style face="normal" font="default" size="100%">Abdulhadi, Khalid</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Targeted sequencing identifies novel variants involved in autosomal recessive hereditary hearing loss in Qatari families.</style></title><secondary-title><style face="normal" font="default" size="100%">Mutat Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mutat. Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">Cadherins</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%">Connexins</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">GPI-Linked Proteins</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%">Membrane Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Models, Molecular</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%">Pedigree</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Conformation</style></keyword><keyword><style  face="normal" font="default" size="100%">Qatar</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, DNA</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%">800-802</style></volume><pages><style face="normal" font="default" size="100%">29-36</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Hereditary hearing loss is characterized by a very high genetic heterogeneity. In the Qatari population the role of GJB2, the worldwide HHL major player, seems to be quite limited compared to Caucasian populations. In this study we analysed 18 Qatari families affected by non-syndromic hearing loss using a targeted sequencing approach that allowed us to analyse 81 genes simultaneously. Thanks to this approach, 50% of these families (9 out of 18) resulted positive for the presence of likely causative alleles in 6 different genes: CDH23, MYO6, GJB6, OTOF, TMC1 and OTOA. In particular, 4 novel alleles were detected while the remaining ones were already described to be associated to HHL in other ethnic groups. Molecular modelling has been used to further investigate the role of novel alleles identified in CDH23 and TMC1 genes demonstrating their crucial role in Ca2+ binding and therefore possible functional role in proteins. Present study showed that an accurate molecular diagnosis based on next generation sequencing technologies might largely improve molecular diagnostics outcome leading to benefits for both genetic counseling and definition of recurrence risk.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28501645?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%">Pellegrin, Maria Chiara</style></author><author><style face="normal" font="default" size="100%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">Cattaruzzi, Elisabetta</style></author><author><style face="normal" font="default" size="100%">Barbi, Egidio</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 Teenager with Sudden Unilateral Breast Enlargement.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Bullying</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Gynecomastia</style></keyword><keyword><style  face="normal" font="default" size="100%">Hematoma</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%">Wounds, Nonpenetrating</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 03</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">182</style></volume><pages><style face="normal" font="default" size="100%">394</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27956018?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">De Cunto, Angela</style></author><author><style face="normal" font="default" size="100%">Paviotti, Giulia</style></author><author><style face="normal" font="default" size="100%">Bua, Jenny</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%">Theophylline increases diaphragmatic contractility in mechanically ventilated newborns.</style></title><secondary-title><style face="normal" font="default" size="100%">J Crit Care</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Crit Care</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Diaphragm</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%">Muscle Contraction</style></keyword><keyword><style  face="normal" font="default" size="100%">Theophylline</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 02</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">37</style></volume><pages><style face="normal" font="default" size="100%">264-265</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28340998?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%">Simeone, Roberto</style></author><author><style face="normal" font="default" size="100%">Giacomello, Roberta</style></author><author><style face="normal" font="default" size="100%">Bruno, Germano</style></author><author><style face="normal" font="default" size="100%">Parco, Sergio</style></author><author><style face="normal" font="default" size="100%">Maximova, Natalia</style></author><author><style face="normal" font="default" size="100%">Martinelli, Monica</style></author><author><style face="normal" font="default" size="100%">Zito, Gabriella</style></author><author><style face="normal" font="default" size="100%">Luppi, Stefania</style></author><author><style face="normal" font="default" size="100%">Cervi, Gina</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%">Thrombogenesis in Thrombophilic Pregnancy: Evaluation of Low-Molecular-Weight Heparin Prophylaxis.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Haematol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Haematol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Anticoagulants</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Factor Xa Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Heparin, Low-Molecular-Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Nadroparin</style></keyword><keyword><style  face="normal" font="default" size="100%">Partial Thromboplastin Time</style></keyword><keyword><style  face="normal" font="default" size="100%">Peptide Fragments</style></keyword><keyword><style  face="normal" font="default" size="100%">Pilot Projects</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Complications, Hematologic</style></keyword><keyword><style  face="normal" font="default" size="100%">Prothrombin</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombophilia</style></keyword><keyword><style  face="normal" font="default" size="100%">Thrombosis</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">137</style></volume><pages><style face="normal" font="default" size="100%">201-206</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The aim of this study is to investigate thrombogenesis and the hypercoagulable changes in pregnant women affected by thrombophilia who received low-molecular-weight heparin (LWMH) prophylaxis. We included 21 pregnant women affected by thrombophilia treated with LWMH and 20 nontreated normal pregnant women as the control group. The sample group of thrombophilic pregnant women included different conditions (factor V Leiden mutation, protein C deficiency, protein S deficiency, antiphospholipid antibodies syndrome, and combined defects). Three blood samples were collected during pregnancy (i.e., at 16, 20, and 24 weeks) and tested for activated partial thromboplastin time and prothrombin fragment F1 + 2 (F1 + 2); anti-FXa activity was tested only in treated thrombophilic pregnant women. F1 + 2 levels progressively increased during pregnancy in both study groups. However, the F1 + 2 increase in women exposed to heparin prophylaxis was significantly lower than that in normal pregnant women in all 3 measurements carried out during gestation (p &lt; 0.05); a statistically significant inverse correlation between F1 + 2 levels and anti-Xa activity (R = -0.8575, p &lt; 0.05) was observed in treated women during pregnancy. Our findings suggest that F1 + 2 in addition to anti-Xa measurement could be used to adjust LWMH prophylaxis, at least in high-risk pregnant women.&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/28478442?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%">Magurano, Fabio</style></author><author><style face="normal" font="default" size="100%">Baggieri, Melissa</style></author><author><style face="normal" font="default" size="100%">Filia, Antonietta</style></author><author><style face="normal" font="default" size="100%">Del Manso, Martina</style></author><author><style face="normal" font="default" size="100%">Lazzarotto, Tiziana</style></author><author><style face="normal" font="default" size="100%">Amendola, Antonella</style></author><author><style face="normal" font="default" size="100%">D'Agaro, Pierlanfranco</style></author><author><style face="normal" font="default" size="100%">Chironna, Maria</style></author><author><style face="normal" font="default" size="100%">Ansaldi, Filippo</style></author><author><style face="normal" font="default" size="100%">Iannazzo, Stefania</style></author><author><style face="normal" font="default" size="100%">Bucci, Paola</style></author><author><style face="normal" font="default" size="100%">Marchi, Antonella</style></author><author><style face="normal" font="default" size="100%">Nicoletti, Loredana</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Measles Surveillance Group</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Towards measles elimination in Italy: Virological surveillance and genotypes trend (2013-2015).</style></title><secondary-title><style face="normal" font="default" size="100%">Virus Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Virus Res.</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%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Outbreaks</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%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Measles</style></keyword><keyword><style  face="normal" font="default" size="100%">Measles virus</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Molecular Epidemiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Sentinel Surveillance</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 05 15</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">236</style></volume><pages><style face="normal" font="default" size="100%">24-29</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;In accordance with the goal of the World Health Organization Regional Office for Europe, the Italian National Measles and Rubella Elimination Plan aimed to interrupt indigenous measles transmission in Italy by the end of 2015. However, from 2013 to 2015, Italy experienced high measles burden with 4902 measles cases (49.3% laboratory-confirmed) reported to the enhanced measles surveillance system (cumulative incidence in the triennium reference period: 2.4/100,000 population). The measles elimination goal was not reached. Laboratory surveillance of measles circulating genotypes is performed by the Measles and Rubella National Reference Laboratory (NRL) at the Italian National Institute of Health (Istituto Superiore di Sanità - ISS), in Rome. Samples received from 1 January 2013-31 December 2015 were analysed. Those positive for measles genome by molecular tests were sequenced and phylogenetically analysed. Phylogenetic analysis performed by NRL identified that genotypes D4 and D8 were endemic and co-circulated in 2011-2013: study results show that genotype D4 disappeared during 2013. Sporadic cases were associated to genotype B3 during 2011-2013, which became endemic in Italy during 2014 and co-circulated with D8 until 2015. Sporadic cases were found belonging to genotypes D9 and H1 all over the period in exam. Similar trend has been observed in European WHO Region.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28522332?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Cegolon, L</style></author><author><style face="normal" font="default" size="100%">Heymann, W C</style></author><author><style face="normal" font="default" size="100%">Xodo, C</style></author><author><style face="normal" font="default" size="100%">Lange, J H</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Training in Occupational Medicine: Jurisprudential Malfunctions in the Italian System and European Perspectives.</style></title><secondary-title><style face="normal" font="default" size="100%">Ann Ig</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ann Ig</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Certification</style></keyword><keyword><style  face="normal" font="default" size="100%">European Union</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Occupational Medicine</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2017</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2017 May-Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">29</style></volume><pages><style face="normal" font="default" size="100%">197-205</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;To practice occupational health in Europe, a medical doctor must qualify in occupational medicine. This requires a period of postgraduate specialist medical training lasting a minimum of four years, in conformity with European regulations, to obtain a certificate of completion of training which is then mutually recognized within the entire European Union.&lt;/p&gt;&lt;p&gt;&lt;b&gt;DISCUSSION: &lt;/b&gt;In 2002 an Italian law allowed doctors specialized in public health medicine and legal/forensic medicine to also practice as consultants in occupational medicine in the country. However a subsequent law in 2008 determined that only physicians specialized in occupational medicine could freely practice as consultants in this discipline. The other two categories (consultants in public health medicine and consultants in legal/forensic medicine) were required to undertake additional training (a Master course) to qualify as consultants in occupational medicine.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Doctors who entered postgraduate training in public health or legal/forensic medicine before 2008, with the option to practice also as consultants in occupational medicine upon completion of their training, suffered an unprecedented and legally questionable retroactive application of this new law which stripped them of previously acquired rights. Moreover, even after qualifying by undertaking this extra training in occupational medicine, the latter two categories of doctors do not have their training recognized in other member states of the European Union. To disallow the rights of doctors qualified in occupational medicine to work as consultants in the latter medical discipline elsewhere within the European Union seems a clear violation of professional rights and, as such, legal action could be taken to submit this issue to European attention.&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/28383611?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%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</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%">Thalidomide for inflammatory bowel disease: Systematic review.</style></title><secondary-title><style face="normal" font="default" size="100%">Medicine (Baltimore)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Medicine (Baltimore)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jul</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">95</style></volume><pages><style face="normal" font="default" size="100%">e4239</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;Thalidomide is an immunomodulatory drug used in the experimental treatment of refractory Crohn disease and ulcerative colitis. We aimed to review the existing evidence on the efficacy and safety of thalidomide in the treatment of inflammatory bowel diseases.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;CENTRAL, MEDLINE, LILACS, POPLINE, CINHAL, and Web of Science were searched in March 2016. Manual search included conference and reference lists. All types of studies, except single case reports, were included. Outcomes evaluated were: induction of remission; maintenance of remission; steroid reduction; effect on penetrating Crohn disease; endoscopic remission; adverse events.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The research strategies retrieved 722 papers. Two randomized controlled trials and 29 uncontrolled studies for a total of 489 patients matched the inclusion criteria. Thalidomide induced a clinical response in 296/427 (69.3%) patients. Clinical remission was achieved in 220/427 (51.5%) cases. Maintenance of remission was reported in 128/160 (80.0%) patients at 6 months and in 96/133 (72.2%) at 12 months. Reduction in steroid dosage was reported in 109/152 (71.7%) patients. Fistulas improved in 49/81 (60.5%) cases and closed in 28/81 (34.6%). Endoscopic improvement was observed in 46/66 (69.7%) and complete mucosal healing in 35/66 (53.0%) patients. Cumulative incidence of total adverse events and of those leading to drug suspension was 75.6 and 19.7/1000 patient-months, respectively. Neurological disturbances accounted for 341/530 (64.3%) adverse events and were the most frequent cause of drug withdrawal.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Existing evidence suggests that thalidomide may be a valid treatment option for patients with inflammatory bowel diseases refractory to other first- and second-line treatments.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">30</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27472695?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%">Pelin, Marco</style></author><author><style face="normal" font="default" size="100%">De Iudicibus, Sara</style></author><author><style face="normal" font="default" size="100%">Londero, Margherita</style></author><author><style face="normal" font="default" size="100%">Spizzo, Riccardo</style></author><author><style face="normal" font="default" size="100%">Dei Rossi, Sveva</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><author><style face="normal" font="default" size="100%">Stocco, Gabriele</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Thiopurine Biotransformation and Pharmacological Effects: Contribution of Oxidative Stress.</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%">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%">542-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Thiopurine antimetabolites are important agents for the treatment of severe diseases, such as acute lymphoblastic leukemia and inflammatory bowel disease. Their pharmacological actions depend on biotransformation into active thioguanine-nucleotides; intracellular metabolism is mediated by enzymes of the salvage pathway of nucleotide synthesis and relies on polymorphic enzymes involved in thiopurines' catabolism such as thiopurine-S-methyl transferase. Given the enzymes involved in thiopurines' metabolism, it is reasonable to hypothesize that these drugs are able to induce significant oxidative stress conditions, possibly altering their pharmacological activity.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;A systemic search of peer-reviewed scientific literature in bibliographic databases has been carried out. Both clinical and preclinical studies as well as mechanistic studies have been included to shed light on the role of oxidative stress in thiopurines' pharmacological effects.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Sixty-nine papers were included in our review, allowing us to review the contribution of oxidative stress in the pharmacological action of thiopurines. Thiopurines are catabolized in the liver by xanthine oxidase, with potential production of reactive oxidative species and azathioprine is converted into mercaptopurine by a reaction with reduced glutathione, that, in some tissues, may be facilitated by glutathione- S-transferase (GST). A clear role of GSTM1 in modulating azathioprine cytotoxicity, with a close dependency on superoxide anion production, has been recently demonstrated. Interestingly, recent genome-wide association studies have shown that, for both azathioprine in inflammatory bowel disease and mercaptopurine in acute lymphoblastic leukemia, treatment effects on patients' white blood cells are related to variants of a gene, NUDT15, involved in biotransformation of oxidated nucleotides.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Basing on previous evidences published in literature, oxidative stress may contribute to thiopurine effects in significant ways that, however, are still not completely elucidated.&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/26935390?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Parco, Sergio</style></author><author><style face="normal" font="default" size="100%">Vascotto, Fulvia</style></author><author><style face="normal" font="default" size="100%">Simeone, Roberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Thromboprophilaxis in neurological conditions in pregnancy. A clinical dilemma or a methods dilemma?</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><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%">68</style></volume><pages><style face="normal" font="default" size="100%">95-6</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/26990102?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%">Silano, Marco</style></author><author><style face="normal" font="default" size="100%">Paganin, Paola</style></author><author><style face="normal" font="default" size="100%">Davanzo, Riccardo</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Time for the 70°C water precautionary option in the home dilution of powdered infant formula.</style></title><secondary-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ital J Pediatr</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">17</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Powdered infant formulas (PIF) are usually not sterile and may frequently be contaminated by several bacteria strains. Among them, Cronobacter species, previously known as Enterobacter sakazakii, is one of the most harmful, since it might be the causative agent of sepsis and meningitis in newborns and preterm infants during the first weeks of life. The mortality rate of these infections is up to 80 %. Therefore, some precautions are required in the home handling and dilution of PIF. Whereas there is wide consensus about the need that a PIF should be used immediately after being diluted or, if not, stored at &lt; &quot;5 °C&quot;, still recently the optimal temperature of the water used to dilute PIF is controversial among scientific societies and health agencies. The current knowledge is reviewed in this paper and provides sufficient evidence to cautiously advise the use of hot water at a temperature of &quot;70 °C&quot; in the dilution of PIF in order to prevent the Cronobacter sp. contamination and growth.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26895705?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%">Ugwumadu, A</style></author><author><style face="normal" font="default" size="100%">Steer, P</style></author><author><style face="normal" font="default" size="100%">Parer, B</style></author><author><style face="normal" font="default" size="100%">Carbone, B</style></author><author><style face="normal" font="default" size="100%">Vayssiere, C</style></author><author><style face="normal" font="default" size="100%">Maso, G</style></author><author><style face="normal" font="default" size="100%">Arulkumaran, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Time to optimise and enforce training in interpretation of intrapartum cardiotocograph.</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><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">123</style></volume><pages><style face="normal" font="default" size="100%">866-9</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/26773808?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%">Pizzol, Antonio</style></author><author><style face="normal" font="default" size="100%">Bramuzzo, Matteo</style></author><author><style face="normal" font="default" size="100%">Pillon, Roberto</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%">Torticollis as the Presenting Sign of Cervical Spondylodiscitis.</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%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Feb 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;Acquired torticollis is a common clinical finding in children evaluated in the pediatric emergency department. It may be the presentation symptom of different illnesses, such as trauma, muscle contraction, infections, or malignancies, and an accurate differential diagnosis is required to correctly identify the cause and choose the right treatment. Spondylodiscitis is a low-grade bacterial infection that involves intervertebral disks and the adjacent vertebral bodies. Spondylodiscitis of the cervical spine is unusual and may be a rare cause of torticollis. We report the case of a 4-year-old male patient admitted to the emergency department for a 5-day history of painful torticollis. Blood tests showed an elevated erythrocyte sedimentation rate. The radiograph of the cervical spine showed a thin fifth cervical soma. The magnetic resonance imaging of cervical spine showed the alteration of cervical vertebral bodies and intervertebral disks, suggesting the diagnosis of cervical spondylodiscitis. The patient recovered after endovenous antibiotic treatment. We suggest that cervical spondylodiscitis should be suspected and investigated by means of an magnetic resonance imaging in every case of unexplained torticollis with persisting symptoms.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27248775?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%">Marta, Silvia Dalla</style></author><author><style face="normal" font="default" size="100%">Rabusin, Marco</style></author><author><style face="normal" font="default" size="100%">Bonifacio, Alois</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%">Toward SERS-based point-of-care approaches for therapeutic drug monitoring: the case of methotrexate.</style></title><secondary-title><style face="normal" font="default" size="100%">Faraday Discuss</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Faraday Discuss.</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 23</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">187</style></volume><pages><style face="normal" font="default" size="100%">485-99</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 date, in spite of their toxicity, the plasmatic concentration of most chemotherapeutic drugs is difficult to monitor in oncological patients, because their quantitative determination is expensive and time consuming. This contribution reports a first attempt for the direct quantitative determination of a chemotherapeutic drug in human serum samples by means of Surface Enhanced Raman Spectroscopy (SERS). In this study, SERS substrates constituted by Au nanoparticles deposited on paper by a simple dipping method have been used for rapid (few minutes) analysis of diluted human serum spiked with different concentrations of methotrexate, MTX. The drug concentrations were chosen in a range designed to cover typical therapeutic plasmatic values (from nanomolar to millimolar) in oncological patients, and the pertinent calibration was obtained by Partial Least-Squares Regression (PLSR). Stability selection was employed to evaluate the capability of the PLSR model to accurately predict and extract spectral variations correlated to MTX concentration. Such a quantitative determination is crucial for frequent, and hence adherent, therapeutic drug monitoring, TDM, of chemiotherapic drugs, given their heavy side effects. Its low cost, rapid response and the possibility of obtaining spectra with simple and compact instruments, make SERS particularly apt for implementing effective TDM. The promising results obtained in the analytical validation indicate which steps are to be taken on the way toward a clinical validation with real samples from oncological patients, for MTX as well as for other chemotherapeutic drugs.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27055173?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%">Cini, Giulia</style></author><author><style face="normal" font="default" size="100%">Mezzavilla, Massimo</style></author><author><style face="normal" font="default" size="100%">Della Puppa, Lara</style></author><author><style face="normal" font="default" size="100%">Cupelli, Elisa</style></author><author><style face="normal" font="default" size="100%">Fornasin, Alessio</style></author><author><style face="normal" font="default" size="100%">D'Elia, Angela Valentina</style></author><author><style face="normal" font="default" size="100%">Dolcetti, Riccardo</style></author><author><style face="normal" font="default" size="100%">Damante, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Bertok, Sara</style></author><author><style face="normal" font="default" size="100%">Miolo, Gianmaria</style></author><author><style face="normal" font="default" size="100%">Maestro, Roberta</style></author><author><style face="normal" font="default" size="100%">de Paoli, Paolo</style></author><author><style face="normal" font="default" size="100%">Amoroso, Antonio</style></author><author><style face="normal" font="default" size="100%">Viel, Alessandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Tracking of the origin of recurrent mutations of the BRCA1 and BRCA2 genes in the North-East of Italy and improved mutation analysis strategy.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Med Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Med. Genet.</style></alt-title></titles><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%">Alleles</style></keyword><keyword><style  face="normal" font="default" size="100%">BRCA1 Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">BRCA2 Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Breast Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Case-Control Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Mutational Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Founder Effect</style></keyword><keyword><style  face="normal" font="default" size="100%">Genetic Testing</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotyping Techniques</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%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Microsatellite Repeats</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Ovarian Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">17</style></volume><pages><style face="normal" font="default" size="100%">11</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;About 20 % of hereditary breast cancers are caused by mutations in BRCA1 and BRCA2 genes. Since BRCA1 and BRCA2 mutations may be spread throughout the gene, genetic testing is usually performed by direct sequencing of entire coding regions. In some populations, especially if relatively isolated, a few number of recurrent mutations is reported, sometimes caused by founder effect.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;BRCA1 and BRCA2 screening for mutations was carried out on 1114 breast and/or ovarian cancer patients complying with the eligibility criteria for BRCA testing. Haplotype analysis was performed on the probands carrying recurrent mutations and their relatives, using two sets of microsatellite markers covering the BRCA1 (D17S588, D17S806, D17S902, D17S1325, D17S855, D17S1328, D17S800, and D17S250) and BRCA2 (D13S220, D13S267, D13S171, D13S1701, D13S1698, D13S260, D13S290, D13S1246) loci. The DMLE + 2.2 software was used to estimate the age of BRCA1 c.676delT and BRCA2 c.7806-2A &gt; G. A multiplex PCR and two different primer extension assays were optimized and used for genotyping the recurrent mutations of the two genes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;In the time frame of almost 20 years of genetic testing, we have found that five BRCA1 and three BRCA2 mutations are recurrent in a substantial subset of carriers from North-East Italy and neighboring Istria, where they represent more than 50 % of all mutations. Microsatellite analyses identified a common haplotype of different length for each mutation. Age estimation of BRCA1 c.676delT and BRCA2 c.7806-2A &gt; G mutations revealed that they arose in the Friuli Venezia Giulia area about 86 and 94 generations ago, respectively. Suggestion of an association between BRCA2 c.7806-2A &gt; G and risk of breast cancer in males has emerged. Finally, we developed a simple and efficient pre-screening test, performing an in-house primer extension SNaPshot® assay for the rapid identification of the eight recurrent mutations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Proofs of common ancestry has been obtained for the eight recurrent mutations. The observed genotype-phenotype correlation and the proposed rapid mutation detection strategy could improve the clinical management of breast and ovarian patients in North-East of Italy and neighboring geographic areas.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26852130?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%">Amorim, Lidiane L B</style></author><author><style face="normal" font="default" size="100%">da Fonseca-Dos-Santos, Romulo</style></author><author><style face="normal" font="default" size="100%">Guida-Santos, Mauro</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%">Transcription factors involved in plant resistance to pathogens.</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 Jun 19</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;Phytopathogenic microorganisms have a significant influence on survival and productivity of several crop plants. Transcription factors (TFs) are important players in the response to biotic stresses, as insect attack and pathogen infection. In face of such adversities many TF families have been previously reported as differentially expressed in plants as a reaction to bacterial, fungal and viral infection. This review highlights recent progresses in understanding the structure, function, signal regulation and interaction of transcription factors with other proteins in response to pathogens. Hence, we focus on three families of transcription factors: ERF, bZIP and WRKY, due to their abundance, importance and the availability of functionally well-characterized members in response to pathogen attack. Their roles and the possibilities related to the use of this knowledge for engineering pathogen resistance in crop plants are also discussed.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27323805?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%">Lazzari, Elisa</style></author><author><style face="normal" font="default" size="100%">Meroni, Germana</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TRIM32 ubiquitin E3 ligase, one enzyme for several pathologies: From muscular dystrophy to tumours.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Biochem Cell Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int. J. Biochem. Cell Biol.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jul 22</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;TRIM32 is a member of the TRIpartite Motif family characterised by the presence of an N-terminal three-domain-module that includes a RING domain, which confers E3 ubiquitin ligase activity, one or two B-box domains and a Coiled-Coil region that mediates oligomerisation. Several TRIM32 substrates were identified including muscular proteins and proteins involved in cell cycle regulation and cell motility. As ubiquitination is a versatile post-translational modification that can affect target turnover, sub-cellular localisation or activity, it is likely that diverse substrates may be differentially affected by TRIM32-mediated ubiquitination, reflecting its multi-faceted roles in muscle physiology, cancer and immunity. With particular relevance for muscle physiology, mutations in TRIM32 are associated with autosomal recessive Limb-Girdle Muscular Dystrophy 2H, a muscle-wasting disease with variable clinical spectrum ranging from almost asymptomatic to wheelchair-bound patients. In this review, we will focus on the ability of TRIM32 to mark specific substrates for proteasomal degradation discussing how the TRIM32-proteasome axis may (i) be important for muscle homeostasis and for the pathogenesis of muscular dystrophy; and (ii) define either an oncogenic or tumour suppressive role for TRIM32 in the context of different types of cancer.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27458054?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Celerino da Silva, Ronaldo</style></author><author><style face="normal" font="default" size="100%">Coelho, Antônio Victor Campos</style></author><author><style face="normal" font="default" size="100%">Arraes, Luiz Claudio</style></author><author><style face="normal" font="default" size="100%">Brandão, Lucas André Cavalcanti</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Guimarães, Rafael Lima</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TRIM5 gene polymorphisms in HIV-1-infected patients and healthy controls from Northeastern Brazil.</style></title><secondary-title><style face="normal" font="default" size="100%">Immunol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Immunol. Res.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2016</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2016 Jul 8</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;Humans show heterogeneity in vulnerability to HIV-1 infection, partially under control of genes involved in host immunity and virus replication. TRIM5α protein has restriction activity against replication of many retroviruses. Human TRIM5 gene single nucleotide polymorphisms have been reported as involved in susceptibility to HIV-1 infection. We recruited 213 HIV-1-positive patients and 234 healthy uninfected controls from Northeast Brazil; two non-synonymous variants at exon 2, rs3740996 (H43Y) and rs10838525 (R136Q), and one regulatory polymorphism (rs16934386) at 5'UTR region of TRIM5 were analyzed. The R136Q variation presented significant differences between HIV-1-positive patients and healthy controls. The 136Q allele and the 136QQ genotype were more frequent in healthy controls (32.7 and 10.2 %, respectively) than in HIV-1-positive patients (136Q allele: 24.4 %; OR 0.66; CI 95 % 0.49-0.90; p value = 0.008/136QQ genotype: 4.2 %; OR 0.33; CI 95 % 0.13-0.79, p = 0.008) also after adjusting for age and sex. We also stratified our findings according to the presence of CCR5Δ32 variation, but the results remained the same. We observed that rs10838525 (R136Q) and rs3740996 (H43Y) were in linkage disequilibrium (D' = 0.71), forming four possible haplotypes. The H43-136Q haplotype was significantly more frequent in healthy controls (28.2 %) than in HIV-positive patients (21.4 %; OR 0.69; CI 95 % 0.50-0.96; p = 0.022). An increased frequency of allele (136Q) and genotype (136QQ) of the non-synonymous rs10838525 (R136Q) variant and the haplotype (43H-136Q) was observed among healthy controls individuals. Being aware of the limitation of this study (unavailability of exposed but uninfected individuals), we hypothesize a potential role for TRIM5 variations in the protection against HIV-1 infection.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/27388872?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%">Morgan, Anna</style></author><author><style face="normal" font="default" size="100%">Gandin, Ilaria</style></author><author><style face="normal" font="default" size="100%">Belcaro, Chiara</style></author><author><style face="normal" font="default" size="100%">Palumbo, Pietro</style></author><author><style face="normal" font="default" size="100%">Palumbo, Orazio</style></author><author><style face="normal" font="default" size="100%">Biamino, Elisa</style></author><author><style face="normal" font="default" size="100%">Dal Col, Valentina</style></author><author><style face="normal" font="default" size="100%">Laurini, Erik</style></author><author><style face="normal" font="default" size="100%">Pricl, Sabrina</style></author><author><style face="normal" font="default" size="100%">Bosco, Paolo</style></author><author><style face="normal" font="default" size="100%">Carella, Massimo</style></author><author><style face="normal" font="default" size="100%">Ferrero, Giovanni Battista</style></author><author><style face="normal" font="default" size="100%">Romano, Corrado</style></author><author><style face="normal" font="default" size="100%">d'Adamo, Adamo Pio</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</style></author><author><style face="normal" font="default" size="100%">Vozzi, Diego</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Target sequencing approach intended to discover new mutations in non-syndromic intellectual disability.</style></title><secondary-title><style face="normal" font="default" size="100%">Mutat Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mutat. Res.</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%">781</style></volume><pages><style face="normal" font="default" size="100%">32-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The technological improvements over the last years made considerable progresses in the knowledge of the etiology of intellectual Disability (ID). However, at present very little is known about the genetic heterogeneity underlying the non-syndromic form of ID (NS-ID). To investigate the genetic basis of NS-ID we analyzed 43 trios and 22 isolated NS-ID patients using a targeted sequencing (TS) approach. 71 NS-ID genes have been selected and sequenced in all subjects. We found putative pathogenic mutations in 7 out of 65 patients. The pathogenic role of mutations was evaluated through sequence comparison and structural analysis was performed to predict the effect of alterations in a 3D computational model through molecular dynamics simulations. Additionally, a deep patient clinical re-evaluation has been performed after the molecular results. This approach allowed us to find novel pathogenic mutations with a detection rate close to 11% in our cohort of patients. This result supports the hypothesis that many NS-ID related genes still remain to be discovered and that NS-ID is a more complex phenotype compared to syndromic form, likely caused by a complex and broad interaction between genes alterations and environment factors.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26411299?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%">Capolla, Sara</style></author><author><style face="normal" font="default" size="100%">Garrovo, Chiara</style></author><author><style face="normal" font="default" size="100%">Zorzet, Sonia</style></author><author><style face="normal" font="default" size="100%">Lorenzon, Andrea</style></author><author><style face="normal" font="default" size="100%">Rampazzo, Enrico</style></author><author><style face="normal" font="default" size="100%">Spretz, Ruben</style></author><author><style face="normal" font="default" size="100%">Pozzato, Gabriele</style></author><author><style face="normal" font="default" size="100%">Núñez, Luis</style></author><author><style face="normal" font="default" size="100%">Tripodo, Claudio</style></author><author><style face="normal" font="default" size="100%">Macor, Paolo</style></author><author><style face="normal" font="default" size="100%">Biffi, Stefania</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Targeted tumor imaging of anti-CD20-polymeric nanoparticles developed for the diagnosis of B-cell malignancies.</style></title><secondary-title><style face="normal" font="default" size="100%">Int J Nanomedicine</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Int J Nanomedicine</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%">10</style></volume><pages><style face="normal" font="default" size="100%">4099-109</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The expectations of nanoparticle (NP)-based targeted drug delivery systems in cancer, when compared with convectional therapeutic methods, are greater efficacy and reduced drug side effects due to specific cellular-level interactions. However, there are conflicting literature reports on enhanced tumor accumulation of targeted NPs, which is essential for translating their applications as improved drug-delivery systems and contrast agents in cancer imaging. In this study, we characterized biodegradable NPs conjugated with an anti-CD20 antibody for in vivo imaging and drug delivery onto tumor cells. NPs' binding specificity mediated by anti-CD20 antibody was evaluated on MEC1 cells and chronic lymphocytic leukemia patients' cells. The whole-body distribution of untargeted NPs and anti-CD20 NPs were compared by time-domain optical imaging in a localized human/mouse model of B-cell malignancy. These studies provided evidence that NPs' functionalization by an anti-CD20 antibody improves tumor pharmacokinetic profiles in vivo after systemic administration and increases in vivo imaging of tumor mass compared to non-targeted NPs. Together, drug delivery and imaging probe represents a promising theranostics tool for targeting B-cell malignancies.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26124662?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%">Magnolato, Andrea</style></author><author><style face="normal" font="default" size="100%">Pederiva, Federica</style></author><author><style face="normal" font="default" size="100%">Spagnut, Giulia</style></author><author><style face="normal" font="default" size="100%">Maschio, Massimo</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Taddio, Andrea</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Three cases of Bartonella quintana infection in children.</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><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">34</style></volume><pages><style face="normal" font="default" size="100%">540-2</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We present 3 children affected by B. quintana infection treated at the IRCCS Burlo Garofolo of Trieste between March and April 2013. B. quintana infection is rare but it should be suspected in patients with fever and lymphadenopathy who do not respond to conventional antibiotic treatment. All patients had a complete recovery without sequelae or relapses.&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/25647503?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%">Paloni, Giulia</style></author><author><style face="normal" font="default" size="100%">Valerio, Enrico</style></author><author><style face="normal" font="default" size="100%">Berti, Irene</style></author><author><style face="normal" font="default" size="100%">Cutrone, Mario</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Tinea Incognito.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">167</style></volume><pages><style face="normal" font="default" size="100%">1450-1450.e2</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/26423793?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%">Perri, Paolo</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Gonelli, Arianna</style></author><author><style face="normal" font="default" size="100%">Milani, Daniela</style></author><author><style face="normal" font="default" size="100%">Celeghini, Claudio</style></author><author><style face="normal" font="default" size="100%">Lamberti, Giuseppe</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%">TNF-related apoptosis inducing ligand in ocular cancers and ocular diabetic complications.</style></title><secondary-title><style face="normal" font="default" size="100%">Biomed Res Int</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Biomed Res Int</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Complications</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus</style></keyword><keyword><style  face="normal" font="default" size="100%">Eye Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, TNF-Related Apoptosis-Inducing Ligand</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%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">2015</style></volume><pages><style face="normal" font="default" size="100%">424019</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;TNF-related apoptosis inducing ligand (TRAIL) is an intensively studied cytokine, in particular for its anticancer activity. The discovery that conjunctival sac fluid contains extremely high levels of soluble TRAIL as compared to other body fluids suggested important implications in the context of the immunological surveillance of the eye, in particular of the anterior surface. In this review, we discuss the potential physiopathologic and therapeutic role of the TRAIL/TRAIL receptor system in a variety of ocular cancers. Moreover, since an increasing amount of data has indicated the important biological activities of the TRAIL/TRAIL receptor systems also in a completely different pathologic context such as diabetes mellitus, in the second part of this review we summarize the currently available data on the involvement of TRAIL in the ocular complications of diabetes mellitus as modulator of the inflammatory and angiogenic response in the eye.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25834817?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%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Valencic, Erica</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Vecchi Brumatti, Liza</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">To Extinguish the Fire from Outside the Cell or to Shutdown the Gas Valve Inside? Novel Trends in Anti-Inflammatory Therapies.</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%">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%">16</style></volume><pages><style face="normal" font="default" size="100%">21277-93</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cytokines are the most important soluble mediators of inflammation. Rare pediatric diseases provided exemplar conditions to study the anti-inflammatory efficacy of new generation therapies (biologics/biopharmaceuticals) selectively targeting single cytokines. Monoclonal antibodies and recombinant proteins have revolutionized anti-inflammatory therapies in the last two decades, allowing the specific targeting of single cytokines. They are very effective in extinguishing inflammation from outside the cell, even with the risk of an excessive and prolonged immunosuppression. Small molecules can enter the cell and shutdown the valve of inflammation by directly targeting signal proteins involved in cytokine release or in response to cytokines. They are orally-administrable drugs whose dosage can be easily adjusted to obtain the desired anti-inflammatory effect. This could make these drugs more suitable for a wide range of diseases as stroke, gout, or neurological impairment, where inflammatory activation plays a pivotal role as trigger. Autoinflammatory diseases, which have previously put anti-cytokine proteins in the limelight, can again provide a valuable model to measure the real potential of small inhibitors as anti-inflammatory agents.&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/26370962?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%">Rabelo, K C N</style></author><author><style face="normal" font="default" size="100%">Albuquerque, C M R</style></author><author><style face="normal" font="default" size="100%">Tavares, V B</style></author><author><style face="normal" font="default" size="100%">Santos, S M</style></author><author><style face="normal" font="default" size="100%">Souza, C A</style></author><author><style face="normal" font="default" size="100%">Oliveira, T C</style></author><author><style face="normal" font="default" size="100%">Oliveira, N C L</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Trace samples of human blood in mosquitoes as a forensic investigation tool.</style></title><secondary-title><style face="normal" font="default" size="100%">Genet Mol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genet. Mol. Res.</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%">14</style></volume><pages><style face="normal" font="default" size="100%">14847-56</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Investigations of any type of crime invariably starts at the crime scene by collecting evidence. Thus, the purpose of this research was to collect and analyze an entomological trace from an environment that is similar to those of indoor crime scenes. Hematophagous mosquitoes were collected from two residential units; saliva of volunteers that were residents in the units was also collected for genetic analysis as reference samples. We examined the allele frequencies of 15 short tandem repeat loci (D8S1179, D21S11, D7S820, CSF1PO, D3S1358, TH01, D13S317, D16S539, D2S1338, D19S433, vWA, TPOX, D18S51, D5S818, and FGA) and amelogenin. A total of 26 female hematophagous mosquitoes were identified as Aedes aegypti, Aedes albopictus, and Culex quinquefasciatus; we were able to obtain 11 forensically valid genetic profiles, with a minimum of 0.028203 ng/μL of human DNA. Thus, the results of this study showed that it was possible to correlate human genetic information from mosquitoes with the volunteer reference samples, which validates the use of this information as forensic evidence. Furthermore, we observed mixed genetic profiles from one mosquito. Therefore, it is clearly important to collect these insects indoors where crimes were committed, because it may be possible to find intact genetic profiles of suspects in the blood found in the digestive tract of hematophagous mosquitoes for later comparison to identify an offender and/or exclude suspects.&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/26600546?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bossi, Fleur</style></author><author><style face="normal" font="default" size="100%">Bernardi, Stella</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><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TRAIL modulates the immune system and protects against the development of diabetes.</style></title><secondary-title><style face="normal" font="default" size="100%">J Immunol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Immunol Res</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immune System</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, TNF-Related Apoptosis-Inducing Ligand</style></keyword><keyword><style  face="normal" font="default" size="100%">Signal Transduction</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">2015</style></volume><pages><style face="normal" font="default" size="100%">680749</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;TRAIL or tumor necrosis factor (TNF) related apoptosis-inducing ligand is a member of the TNF superfamily of proteins, whose best characterized function is the induction of apoptosis in tumor, infected, or transformed cells through activation of specific receptors. In nontransformed cells, however, the actions of TRAIL are less well characterized. Recent studies suggest that TRAIL may be implicated in the development and progression of diabetes. Here we review TRAIL biological actions, its effects on the immune system, and how and to what extent it has been shown to protect against diabetes.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25759846?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%">Bibalo, Cristina</style></author><author><style face="normal" font="default" size="100%">Longo, Giorgio</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%">Treatment of asthma based on symptoms.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Asthma</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%">Spirometry</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">166</style></volume><pages><style face="normal" font="default" size="100%">1324-5</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/25771387?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%">Cani, Alice</style></author><author><style face="normal" font="default" size="100%">Simioni, Carolina</style></author><author><style face="normal" font="default" size="100%">Martelli, Alberto M</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Tabellini, Giovanna</style></author><author><style face="normal" font="default" size="100%">Ultimo, Simona</style></author><author><style face="normal" font="default" size="100%">McCubrey, James A</style></author><author><style face="normal" font="default" size="100%">Capitani, Silvano</style></author><author><style face="normal" font="default" size="100%">Neri, Luca M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Triple Akt inhibition as a new therapeutic strategy in T-cell acute lymphoblastic leukemia.</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><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015 Mar 30</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">6</style></volume><pages><style face="normal" font="default" size="100%">6597-610</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;T-cell acute lymphoblastic leukemia (T-ALL) is an aggressive neoplastic disorder in which chemotherapy resistance and refractory relapses occur, with a poorer prognostic outcome.Constitutively active PI3K/Akt/mTOR pathway is a common feature of T-ALL upregulating cell proliferation, survival and drug resistance. This pathway is currently under clinical trials with small molecules inhibitors (SMI).To verify whether a multi-inhibition treatment against Akt protein could enhance the efficacy of individual drug administration and overcome drug resistance as well as to obtain a decrease in single drug concentration, we tested on T-ALL cell lines the effects of combined treatments with three Akt inhibitors with different mode of action, GSK690693, MK-2206 and Perifosine.In cells with hyperactivated Akt, combined administration of the drugs displayed a significant synergistic and cytotoxic effect and affected PI3K/Akt/mTOR pathway at much lower concentration than single drug use. Highest synergistic effect for full inhibition of Akt was also related to the timing of every drug administration. Furthermore the triple treatment had greater efficacy in inducing cell cycle arrest in G0/G1 phase and both apoptosis and autophagy.Targeting Akt as a key protein of PI3K/Akt/mTOR pathway with multiple drugs might represent a new and promising pharmacological strategy for treatment of T-ALL patients.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">9</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25788264?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%">Tavares, Mayara C Mansur</style></author><author><style face="normal" font="default" size="100%">de Lima Júnior, Sérgio F</style></author><author><style face="normal" font="default" size="100%">Coelho, Antonio V C</style></author><author><style face="normal" font="default" size="100%">Marques, Trícia Ruschelle N M</style></author><author><style face="normal" font="default" size="100%">de Araújo, Diêgo Henrique T</style></author><author><style face="normal" font="default" size="100%">Heráclio, Sandra de A</style></author><author><style face="normal" font="default" size="100%">Amorim, Melânia M Ramos</style></author><author><style face="normal" font="default" size="100%">de Souza, Paulo Roberto E</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%">Tumor necrosis factor (TNF) alpha and interleukin (IL) 18 genes polymorphisms are correlated with susceptibility to HPV infection in patients with and without cervical intraepithelial lesion.</style></title><secondary-title><style face="normal" font="default" size="100%">Ann Hum Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ann. Hum. Biol.</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 16</style></date></pub-dates></dates><pages><style face="normal" font="default" size="100%">1-8</style></pages><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;The Human Papillomavirus (HPV) predisposes 500 000 women to cervical cancer. Host genetic background may facilitate virus persistence in the uterine cervix. Polymorphisms in regulatory and coding regions of cytokine genes have been associated with susceptibility to some human diseases.&lt;/p&gt;&lt;p&gt;&lt;b&gt;AIM: &lt;/b&gt;This study aims at investigating whether TNFA -308 G/A and IL18 -137 G/C and -607 C/A polymorphisms are associated with susceptibility to HPV infection/progression to high-grade squamous intraepithelial lesion (HSIL).&lt;/p&gt;&lt;p&gt;&lt;b&gt;SUBJECTS AND METHODS: &lt;/b&gt;One hundred and twenty-two HPV infected and 132 HPV negative women (the latter used as healthy controls) were analysed. TNFA -308 G/A and IL18 (-137G/C and -607 C/A) polymorphisms were analysed using specific sequence polymorphism PCR (SSP-PCR). Univariate statistical analysis and a logistic regression were performed.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The TNFA -308A allele was associated with susceptibility to HPV infection (p = 0.0008), while the IL18 -607A allele conferred protection against HPV infection (p = 0.0043). TNFA -308 G/A and IL18 (-137G/C and -607 C/A) polymorphisms were not associated with development of cervical lesions (p &gt; 0.05). An association was also observed between smoking and susceptibility to the development of HSIL.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The findings suggest an association between two TNFA SNPs and susceptibility to HPV infection in women from Northeast Brazil. The results need to be functionally validated and replicated in other populations with different ethnic backgrounds.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/26079218?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 Albuquerque Maranhão, R M</style></author><author><style face="normal" font="default" size="100%">Martins Esteves, F A</style></author><author><style face="normal" font="default" size="100%">Crovella, S</style></author><author><style face="normal" font="default" size="100%">Segat, L</style></author><author><style face="normal" font="default" size="100%">Eleutério Souza, P R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Tumor necrosis factor-α and interleukin-6 gene polymorphism association with susceptibility to celiac disease in Italian patients.</style></title><secondary-title><style face="normal" font="default" size="100%">Genet Mol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Genet. Mol. Res.</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%">14</style></volume><pages><style face="normal" font="default" size="100%">16343-52</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 this research was to study polymorphisms in the genes encoding cytokines interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) in patients with celiac disease (CD) antigens DQ2 (DQ2-positive) or DQ8 (DQ8-positive). We compared the results with healthy controls to determine whether any of the polymorphisms have a role in susceptibility to CD. A case-control of 192 patients with CD (96 DQ2-positive and 96 DQ8-positive) and 96 healthy controls from northeast Italy were included in the study. Analysis of single nucleotide polymorphisms (SNPs) was carried out using the polymerase chain reaction-restriction fragment length polymorphism method. Significant differences for the TNF-α(-308 G&gt;A) polymorphism were observed when we compared the flowing groups: DQ2-positive with controls [odds ratio (OR) = 0.45, P = 0.0002]; DQ8-positive with controls (OR = 3.55, P &lt; 0.0001); and DQ2-positive with DQ8-positive (OR = 0.12, P &lt; 0.0001). We did not observe a statistically significant association between IL-6 (-174 G&gt;C) polymorphism and CD (P &gt; 0.05). Our results suggest that TNF-α(-308 G&gt;A) polymorphism may play a role in susceptibility to CD in Italian 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/26662429?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%">Zanconati, Fabrizio</style></author><author><style face="normal" font="default" size="100%">Arrigoni, Giorgio</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Romano, Andrea</style></author><author><style face="normal" font="default" size="100%">Banco, Rubina</style></author><author><style face="normal" font="default" size="100%">Zweyer, Marina</style></author><author><style face="normal" font="default" size="100%">Milani, Daniela</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%">Two-dimensional gel electrophoresis analysis of the leiomyoma interstitial fluid reveals altered protein expression with a possible involvement in pathogenesis.</style></title><secondary-title><style face="normal" font="default" size="100%">Oncol Rep</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Oncol. 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 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">33</style></volume><pages><style face="normal" font="default" size="100%">2219-26</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Uterine leiomyoma is the most common smooth benign neoplasm. In the present study, we analyzed the global interstitial fluid (IF) profile of leiomyoma vs. normal myometrium to identify protein dysregulation involved in leiomyoma pathogenesis. Two-dimensional gel electrophoresis and mass spectrometry were used to generate and compare the global interstitial fluid profiles of the leiomyoma and of the normal tissue. Two proteins were validated by immunohistochemistry. By comparing the interstitial fluid profile of the leiomyoma with that of the normal myometrium, the levels of seven proteins were found to be significantly different: four structural organization proteins (desmin, prelamin-A/C, transgelin and α-actinin-1), an inflammatory response (α1-antitrypsin), a response to oxidative stress (peroxiredoxin-2), and a folding protein (heat shock 70 kDa protein 1A/1B). Desmin, α1-antitrypsin and peroxiredoxin-2 were upregulated in the leiomyoma, whereas heat shock 70 kDa protein 1A/1B, α-actinin-1, prelamin-A/C and transgelin were downregulated. Desmin and α1-antitrypsin were further validated by immunohistochemistry. By identifying proteins with altered expression levels compared to the myometrium from several pathways of the leiomyoma pathogenesis, we found the leiomyoma interstitial fluid to have a characteristic proteomic profile. A better appreciation of the pathophysiology of the disease can be useful in the development of conservative treatments that serve as viable alternatives to hysterectomy.&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/25738828?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Bianco, Anna Monica</style></author><author><style face="normal" font="default" size="100%">Faletra, Flavio</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%">Knowles, Alessandra</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Zauli, Giorgio</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%">Two‑gene mutation in a single patient: Biochemical and functional analysis for a correct interpretation of exome results.</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%">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%">12</style></volume><pages><style face="normal" font="default" size="100%">6128-32</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Next-generation sequencing (NGS) has generated a large amount of sequence data with the requirement of frequent critical revisions of reported mutations. This innovative tool has proved to be effective in detecting pathogenic mutations; however, it requires a certain degree of experience to identify incidental findings. In the present study, whole exome sequencing analysis was performed for the molecular diagnosis and correct genotype/phenotype correlation between parents and a patient presenting with an atypical phenotype. In addition, mevalonic acid quantification and frequency analysis of detected variants in public databases and X‑chromosome inactivation (XCI) studies on the patient's mother were performed. V377I as well as the S135L mutations were identified on the mevalonate kinase deficiency gene and the levels of mevalonic acid in the patient were 5,496 µg/ml. A D59G variation, reported in ESP6500 in two healthy individuals, was found on the Martin Probst syndrome gene (RAB40AL). Based on XCI studies on the patient's mother, it is likely that RAB40AL escapes XCI, while still remaining balanced. In conclusion, the results of the present study indicated that the Martin Probst syndrome is an X‑linked condition, which is probably not caused by RAB40AL mutations. Although NGS is a powerful tool to identify pathogenic mutations, the analysis of genetic data requires expert critical revision of all detected variants.&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/26300074?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%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Grosso, Daniele</style></author><author><style face="normal" font="default" size="100%">Fascetta, Riccardo</style></author><author><style face="normal" font="default" size="100%">Marini, Marta</style></author><author><style face="normal" font="default" size="100%">Odoni, Luca</style></author><author><style face="normal" font="default" size="100%">Di Carlo, Valentina</style></author><author><style face="normal" font="default" size="100%">Dibello, Daniela</style></author><author><style face="normal" font="default" size="100%">Vittoria, Francesca</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%">Teleradiology for remote consultation using iPad improves the use of health system human resources for paediatric fractures: prospective controlled study in a tertiary care hospital in Italy.</style></title><secondary-title><style face="normal" font="default" size="100%">BMC Health Serv Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">BMC Health Serv Res</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%">Computers, Handheld</style></keyword><keyword><style  face="normal" font="default" size="100%">Decision Making</style></keyword><keyword><style  face="normal" font="default" size="100%">Fractures, Bone</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%">Remote Consultation</style></keyword><keyword><style  face="normal" font="default" size="100%">Teleradiology</style></keyword><keyword><style  face="normal" font="default" size="100%">Time 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%">327</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 growing cost of health care and lack of specialised staff have set e-Health high on the European political agenda. In a prospective study we evaluated the effect of providing images for remote consultation through an iPad on the number of in-hospital orthopaedic consultations for children with bone fractures.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;Children from 0 to 18 years diagnosed with a bone fracture by the radiologist during the hours when an orthopaedic service is provided only on-call were eligible for enrollment. Cases were enrolled prospectively during September and October 2013. A standard approach (verbal information only, no X-Ray provided remotely) was compared to an experimental approach (standard approach plus the provision of X-ray for remote consultation through an iPad). The primary outcome was the number of orthopaedic in-hospital consultations that occurred. Other outcomes included: immediate activation of other services; time needed for decision-making; technical difficulties; quality of images and diagnostic confidence (on a likert scale of 1 to 10).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Forty-two children were enrolled in the study. Number of in-hospital consultancies dropped from 32/42 (76.1%) when no X-ray was provided to 16/42 (38%) when the X-rays was provided (p &lt; 0.001). With remote X-ray consultation in 14/42 (33.3%) cases services such as surgery and plaster room could be immediately activated, compared to no service activated without teleradiology (p &lt; 0.001). Average time for decision making was 23.4 ± 21.8 minutes with remote X-ray consultation, compared to 56.2 ± 16.1 when the X-ray was not provided (p &lt; 0.001). The comparison between images on the iPad and on the standard system for X- Ray visualisation resulted in a non statistically significant difference in the quality of images (average score 9.89 ± 0.37 vs 9.91 ± 0.30; p = 0.79), and in non statistically significant difference in diagnostic confidence (average score 9.91 ± 0.32 vs 9.92 ± 0.31; p = 0.88).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Remote X-ray consultation through Aycan OsiriX PRO and iPad should be considered as a means for reducing the need of in-hospital orthopaedic consultation during on-call times, and potentially decrease the cost of care for the health system. In the future, alternative systems less expensive than Aycan OsiriX PRO should be further developed and tested.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25070705?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%">Franca, Raffaella</style></author><author><style face="normal" font="default" size="100%">Rebora, Paola</style></author><author><style face="normal" font="default" size="100%">Athanasakis, Emmanouil</style></author><author><style face="normal" font="default" size="100%">Favretto, Diego</style></author><author><style face="normal" font="default" size="100%">Verzegnassi, Federico</style></author><author><style face="normal" font="default" size="100%">Basso, Giuseppe</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Valsecchi, Maria Grazia</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Rabusin, Marco</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TNF-α SNP rs1800629 and risk of relapse in childhood acute lymphoblastic leukemia: relation to immunophenotype.</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacogenomics</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pharmacogenomics</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Antineoplastic Agents</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 Resistance, Neoplasm</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%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</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%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Precursor Cell Lymphoblastic Leukemia-Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Precursor T-Cell Lymphoblastic Leukemia-Lymphoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Risk Assessment</style></keyword><keyword><style  face="normal" font="default" size="100%">Steroids</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</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%">15</style></volume><pages><style face="normal" font="default" size="100%">619-27</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;In the AIEOP-BFM ALL (Associazione Italiana Ematologia Oncologia Pediatrica-Berlin Frankfurt Münster acute lymphoblastic leukemia) 2000 protocol, 70% of relapsed patients had favorable prognostic features and fell within less intensive polychemotherapeutic regimens, suggesting the need for better assessing lower risk stratification.&lt;/p&gt;&lt;p&gt;&lt;b&gt;MATERIALS &amp; METHODS: &lt;/b&gt;A novel two-phase study design selected 614 children to be genotyped for TNF-α SNP rs1800629 (-308G&gt;A). A weighted Cox model was applied to evaluate the SNP effect on hazard of relapse, adjusting for immunophenotype, risk group, age and gender and including interaction terms.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Significant interaction was found with immunophenotypes (p = 0.0007, with minor allele genotypes being adverse genetic markers in B-cell acute lymphoblastic leukemia and protective ones in T-cell acute lymphoblastic leukemia), and also with risk protocols (p = 0.0041, with minor allele genotypes as prognostic factor of relapse for standard risk patients [only one T-cell acute lymphoblastic leukemia in the subgroup analyzed]).&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;The presence of at least one A allele in TNF-α SNP rs1800629 should suggest a closer monitoring in B-cell acute lymphoblastic leukemia standard risk patients.&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/24798719?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%">Calligaris, Lorenzo</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%">Tramadol can selectively manage moderate pain in children following European advice limiting codeine use.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Paediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Paediatr.</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2014</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2014 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">103</style></volume><pages><style face="normal" font="default" size="100%">1110-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;UNLABELLED: &lt;/b&gt;The European Medicine Agency recommendations limiting codeine use in children have created a void in managing moderate pain. We review the evidence on the pharmacokinetic, pharmacodynamic and safety profile of tramadol, a possible substitute for codeine.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Tramadol appears to be safe in both paediatric inpatients and outpatients. It may be appropriate to limit the current use of tramadol to monitored settings in children with risk factors for respiratory depression, subject to further safety evidence.&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/25041277?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%">Keller, Margaux F</style></author><author><style face="normal" font="default" size="100%">Reiner, Alexander P</style></author><author><style face="normal" font="default" size="100%">Okada, Yukinori</style></author><author><style face="normal" font="default" size="100%">van Rooij, Frank J A</style></author><author><style face="normal" font="default" size="100%">Johnson, Andrew D</style></author><author><style face="normal" font="default" size="100%">Chen, Ming-Huei</style></author><author><style face="normal" font="default" size="100%">Smith, Albert V</style></author><author><style face="normal" font="default" size="100%">Morris, Andrew P</style></author><author><style face="normal" font="default" size="100%">Tanaka, Toshiko</style></author><author><style face="normal" font="default" size="100%">Ferrucci, Luigi</style></author><author><style face="normal" font="default" size="100%">Zonderman, Alan B</style></author><author><style face="normal" font="default" size="100%">Lettre, Guillaume</style></author><author><style face="normal" font="default" size="100%">Harris, Tamara</style></author><author><style face="normal" font="default" size="100%">Garcia, Melissa</style></author><author><style face="normal" font="default" size="100%">Bandinelli, Stefania</style></author><author><style face="normal" font="default" size="100%">Qayyum, Rehan</style></author><author><style face="normal" font="default" size="100%">Yanek, Lisa R</style></author><author><style face="normal" font="default" size="100%">Becker, Diane M</style></author><author><style face="normal" font="default" size="100%">Becker, Lewis C</style></author><author><style face="normal" font="default" size="100%">Kooperberg, Charles</style></author><author><style face="normal" font="default" size="100%">Keating, Brendan</style></author><author><style face="normal" font="default" size="100%">Reis, Jared</style></author><author><style face="normal" font="default" size="100%">Tang, Hua</style></author><author><style face="normal" font="default" size="100%">Boerwinkle, Eric</style></author><author><style face="normal" font="default" size="100%">Kamatani, Yoichiro</style></author><author><style face="normal" font="default" size="100%">Matsuda, Koichi</style></author><author><style face="normal" font="default" size="100%">Kamatani, Naoyuki</style></author><author><style face="normal" font="default" size="100%">Nakamura, Yusuke</style></author><author><style face="normal" font="default" size="100%">Kubo, Michiaki</style></author><author><style face="normal" font="default" size="100%">Liu, Simin</style></author><author><style face="normal" font="default" size="100%">Dehghan, Abbas</style></author><author><style face="normal" font="default" size="100%">Felix, Janine F</style></author><author><style face="normal" font="default" size="100%">Hofman, Albert</style></author><author><style face="normal" font="default" size="100%">Uitterlinden, André G</style></author><author><style face="normal" font="default" size="100%">van Duijn, Cornelia M</style></author><author><style face="normal" font="default" size="100%">Franco, Oscar H</style></author><author><style face="normal" font="default" size="100%">Longo, Dan L</style></author><author><style face="normal" font="default" size="100%">Singleton, Andrew B</style></author><author><style face="normal" font="default" size="100%">Psaty, Bruce M</style></author><author><style face="normal" font="default" size="100%">Evans, Michelle K</style></author><author><style face="normal" font="default" size="100%">Cupples, L Adrienne</style></author><author><style face="normal" font="default" size="100%">Rotter, Jerome I</style></author><author><style face="normal" font="default" size="100%">O'Donnell, Christopher J</style></author><author><style face="normal" font="default" size="100%">Takahashi, Atsushi</style></author><author><style face="normal" font="default" size="100%">Wilson, James G</style></author><author><style face="normal" font="default" size="100%">Ganesh, Santhi K</style></author><author><style face="normal" font="default" size="100%">Nalls, Mike A</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">CHARGE Hematology</style></author><author><style face="normal" font="default" size="100%">COGENT</style></author><author><style face="normal" font="default" size="100%">BioBank Japan Project (RIKEN) Working Groups</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Trans-ethnic meta-analysis of white blood cell phenotypes.</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%">African Americans</style></keyword><keyword><style  face="normal" font="default" size="100%">Asian Continental Ancestry Group</style></keyword><keyword><style  face="normal" font="default" size="100%">Bayes Theorem</style></keyword><keyword><style  face="normal" font="default" size="100%">European Continental Ancestry Group</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Genome-Wide Association Study</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocyte Count</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Linkage Disequilibrium</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Quantitative Trait Loci</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 20</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">23</style></volume><pages><style face="normal" font="default" size="100%">6944-60</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;White blood cell (WBC) count is a common clinical measure used as a predictor of certain aspects of human health, including immunity and infection status. WBC count is also a complex trait that varies among individuals and ancestry groups. Differences in linkage disequilibrium structure and heterogeneity in allelic effects are expected to play a role in the associations observed between populations. Prior genome-wide association study (GWAS) meta-analyses have identified genomic loci associated with WBC and its subtypes, but much of the heritability of these phenotypes remains unexplained. Using GWAS summary statistics for over 50 000 individuals from three diverse populations (Japanese, African-American and European ancestry), a Bayesian model methodology was employed to account for heterogeneity between ancestry groups. This approach was used to perform a trans-ethnic meta-analysis of total WBC, neutrophil and monocyte counts. Ten previously known associations were replicated and six new loci were identified, including several regions harboring genes related to inflammation and immune cell function. Ninety-five percent credible interval regions were calculated to narrow the association signals and fine-map the putatively causal variants within loci. Finally, a conditional analysis was performed on the most significant SNPs identified by the trans-ethnic meta-analysis (MA), and nine secondary signals within loci previously associated with WBC or its subtypes were identified. This work illustrates the potential of trans-ethnic analysis and ascribes a critical role to multi-ethnic cohorts and consortia in exploring complex phenotypes with respect to variants that lie outside the European-biased GWAS pool.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">25</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25096241?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 Lorenzo, Giovanni</style></author><author><style face="normal" font="default" size="100%">Monasta, Lorenzo</style></author><author><style face="normal" font="default" size="100%">Ceccarello, Matteo</style></author><author><style face="normal" font="default" size="100%">Cecotti, Vera</style></author><author><style face="normal" font="default" size="100%">D'Ottavio, Giuseppina</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Third trimester abdominal circumference, estimated fetal weight and uterine artery doppler for the identification of newborns small and large for gestational age.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Obstet Gynecol Reprod Biol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur. J. Obstet. Gynecol. Reprod. Biol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Anthropometry</style></keyword><keyword><style  face="normal" font="default" size="100%">Birth Weight</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes, Gestational</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Growth Retardation</style></keyword><keyword><style  face="normal" font="default" size="100%">Fetal Weight</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%">Hypertension, Pregnancy-Induced</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Small for Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy Trimester, Third</style></keyword><keyword><style  face="normal" font="default" size="100%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Sensitivity and Specificity</style></keyword><keyword><style  face="normal" font="default" size="100%">Ultrasonography, Prenatal</style></keyword><keyword><style  face="normal" font="default" size="100%">Uterine Artery</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 Feb</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">166</style></volume><pages><style face="normal" font="default" size="100%">133-8</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;OBJECTIVE: &lt;/b&gt;To understand if ultrasound biometric evaluation at 30-32 weeks of gestation is a valuable screening tool for the detection of small-for-gestational-age (SGA) and large-for-gestational-age (LGA) infants at birth in a low risk population.&lt;/p&gt;&lt;p&gt;&lt;b&gt;STUDY DESIGN: &lt;/b&gt;We enrolled 1848 pregnant women with singleton pregnancy undergoing routine fetal biometry. We divided the infants into four groups: moderate SGA, severe SGA, moderate LGA and severe LGA. We considered third-trimester estimated fetal weight (EFW), abdominal circumference (AC), EFW centile (EFWc), AC centile (ACc) and compared their prediction toward SGA and LGA to determine which of these parameters was the best estimator for fetal size. Then we took the strongest predictive value and added all history-related and ultrasound factors to run a stepdown multivariate logistic regression. All the variables were then dichotomized and sensitivity models only for statistically significant parameters were calculated.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;We identified the following predictive factors for each outcome: for severe SGA: EFWc with p&lt;0.001, uterine artery pulsatility index (UtA PI) with p&lt;0.002. For moderate SGA: EFWc with p&lt;0.001, UtA PI with p&lt;0.004, maternal preeclampsia p&lt;0.002. For moderate and severe LGA: EFWc with p&lt;0.001.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;We can detect in a low-risk population a group at risk of growth deviations. Adding Doppler velocimetry to 30-32 weeks EFWc improves the specificity (84%) regarding SGA newborns, maintaining a good sensitivity (71%), and reducing the population to be re-screened from 27 to 17%. An ultrasound examination at 34-36 weeks or the clinical assessment of maternal risk factors remain the best tools for LGA newborns.&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/23122032?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%">Rabach, Ingrid</style></author><author><style face="normal" font="default" size="100%">Poli, Furio</style></author><author><style face="normal" font="default" size="100%">Zennaro, Floriana</style></author><author><style face="normal" font="default" size="100%">Germani, Claudio</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%">Is treatment with hydroxychloroquine effective in surfactant protein C deficiency?</style></title><secondary-title><style face="normal" font="default" size="100%">Arch Bronconeumol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arch. Bronconeumol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Disease Progression</style></keyword><keyword><style  face="normal" font="default" size="100%">Diseases in Twins</style></keyword><keyword><style  face="normal" font="default" size="100%">Dyspnea</style></keyword><keyword><style  face="normal" font="default" size="100%">Failure to Thrive</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hydroxychloroquine</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%">Pulmonary Alveolar Proteinosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Pulmonary Surfactant-Associated Protein C</style></keyword><keyword><style  face="normal" font="default" size="100%">Respiratory Insufficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Tomography, X-Ray Computed</style></keyword><keyword><style  face="normal" font="default" size="100%">Twins, Monozygotic</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 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">49</style></volume><pages><style face="normal" font="default" size="100%">213-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;We present the case of two twin brothers with surfactant protein C deficiency who were treated with hydroxychloroquine for three years, with apparent success. The exact physiopathology of this disease is not known and there is no specific treatment for it. There is merely news from a few previous descriptions in the literature about the use of hydroxychloroquine for surfactant protein C deficiency with satisfactory results. Two years after the treatment was withdrawn, the twins were evaluated once again: they presented no new infections, growth and general state were normal and chest CT showed a notable additional reduction in the interstitial pneumopathy. These data seem to cast some doubt on the efficacy of hydroxychloroquine, and they suggest that the clinical improvement was simply the natural evolution of the disease.&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/23137777?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, Paola</style></author><author><style face="normal" font="default" size="100%">Faleschini, Elena</style></author><author><style face="normal" font="default" size="100%">Tonini, Giorgio</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%">Type 1 diabetes mellitus and celiac disease: usefulness of gluten-free diet.</style></title><secondary-title><style face="normal" font="default" size="100%">Acta Diabetol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Acta Diabetol</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2013</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2013 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">50</style></volume><pages><style face="normal" font="default" size="100%">821-2</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/21833778?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%">Codrich, Daniela</style></author><author><style face="normal" font="default" size="100%">Lembo, Maria Antonietta</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%">Thoracoscopic removal of a bulky cystic mediastinal mature teratoma in a 4-year-old child: report of one case and few surgical tricks.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Pediatr Surg</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur J Pediatr Surg</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Mediastinal Neoplasms</style></keyword><keyword><style  face="normal" font="default" size="100%">Teratoma</style></keyword><keyword><style  face="normal" font="default" size="100%">Thoracoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Tomography, X-Ray Computed</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">22</style></volume><pages><style face="normal" font="default" size="100%">318-20</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/22576302?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%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Tikellis, Christos</style></author><author><style face="normal" font="default" size="100%">Candido, Riccardo</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</style></author><author><style face="normal" font="default" size="100%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Cooper, Mark E</style></author><author><style face="normal" font="default" size="100%">Thomas, Merlin C</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TNF-related apoptosis-inducing ligand significantly attenuates metabolic abnormalities in high-fat-fed mice reducing adiposity and systemic inflammation.</style></title><secondary-title><style face="normal" font="default" size="100%">Clin Sci (Lond)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Clin. Sci.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adiposity</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%">Calorimetry</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Dietary Fats</style></keyword><keyword><style  face="normal" font="default" size="100%">Energy Intake</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucose Tolerance Test</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperglycemia</style></keyword><keyword><style  face="normal" font="default" size="100%">Hyperinsulinism</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred C57BL</style></keyword><keyword><style  face="normal" font="default" size="100%">Oxidation-Reduction</style></keyword><keyword><style  face="normal" font="default" size="100%">Palmitic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Real-Time Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">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 Nov</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">123</style></volume><pages><style face="normal" font="default" size="100%">547-55</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;TRAIL [TNF (tumour necrosis factor)-related apoptosis-inducing ligand] has recently been shown to ameliorate the natural history of DM (diabetes mellitus). It has not been determined yet whether systemic TRAIL delivery would prevent the metabolic abnormalities due to an HFD [HF (high-fat) diet]. For this purpose, 27 male C57bl6 mice aged 8 weeks were randomly fed on a standard diet, HFD or HFD+TRAIL for 12 weeks. TRAIL was delivered weekly by intraperitoneal injection. Body composition was evaluated; indirect calorimetry studies, GTT (glucose tolerance test) and ITT (insulin tolerance test) were performed. Pro-inflammatory cytokines, together with adipose tissue gene expression and apoptosis, were measured. TRAIL treatment reduced significantly the increased adiposity associated with an HFD. Moreover, it reduced significantly hyperglycaemia and hyperinsulinaemia during a GTT and it improved significantly the peripheral response to insulin. TRAIL reversed the changes in substrate utilization induced by the HFD and ameliorated skeletal muscle non-esterified fatty acids oxidation rate. This was associated with a significant reduction of pro-inflammatory cytokines together with a modulation of adipose tissue gene expression and apoptosis. These findings shed light on the possible anti-adipogenic and anti-inflammatory effects of TRAIL and open new therapeutic possibilities against obesity, systemic inflammation and T2DM (Type 2 DM).&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/22616837?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%">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%">TRAIL, a new weapon against neointimal hyperplasia.</style></title><secondary-title><style face="normal" font="default" size="100%">Cardiology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Cardiology</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Coronary Restenosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug-Eluting Stents</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%">Neointima</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%">123</style></volume><pages><style face="normal" font="default" size="100%">94-6</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/23018637?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%">Secchiero, Paola</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</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%">TRAIL administration down-modulated the acute systemic inflammatory response induced in a mouse model by muramyldipeptide or lipopolysaccharide.</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%">Acetylmuramyl-Alanyl-Isoglutamine</style></keyword><keyword><style  face="normal" font="default" size="100%">Acute Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Chemokine CCL2</style></keyword><keyword><style  face="normal" font="default" size="100%">Cytokines</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Models, Animal</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulocyte Colony-Stimulating Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Immunoassay</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammation Mediators</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-1alpha</style></keyword><keyword><style  face="normal" font="default" size="100%">Interleukin-6</style></keyword><keyword><style  face="normal" font="default" size="100%">Lipopolysaccharides</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred BALB C</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Serum Amyloid A Protein</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 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">60</style></volume><pages><style face="normal" font="default" size="100%">43-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The potent inducer of apoptosis TRAIL/Apo2 ligand is now under considerations in clinical trials for the treatment of different types of cancer. Since the natural history of cancer is often characterized by microbial infections, we have investigated the effect of recombinant human TRAIL in a mouse model of systemic acute inflammation of microbial origin represented by BALB/c mice treated with either bacterial muramyldipeptide (MDP) or lipopolysaccharide (LPS). When administered intraperitoneally (i.p.), these inflammatory bacterial compounds triggered a severe systemic inflammatory response within 2h, represented by body temperature elevation, increase of circulating serum amyloid-A (SAA) and of the number of leukocytes in the peritoneal cavity. Moreover, both MDP and LPS induced a significant elevation of the circulating levels of several inflammatory cytokines and chemokines. Noteworthy, pre-treatment with recombinant human TRAIL 48 and 72 h before administration of either MDP or LPS, significantly counteracted all acute inflammatory responses, including the elevation of key pro-inflammatory cytokines/chemokines such as IL-1α, IL-6, G-CSF, MCP-1. These data demonstrate for the first time that TRAIL has a potent anti-inflammatory activity, which might be beneficial for the anti-tumoral activity of TRAIL.&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/22727903?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%">Milani, Daniela</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</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%">TRAIL as biomarker and potential therapeutic tool for cardiovascular diseases.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Drug Targets</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr Drug Targets</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Biological Markers</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiovascular Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Prognosis</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 Aug</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">13</style></volume><pages><style face="normal" font="default" size="100%">1215-21</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 review focuses on TNF-related apoptosis-inducing ligand (TRAIL), also called Apo2 ligand, a protein belonging to the TNF superfamily. TRAIL can be found either in its transmembrane or circulating form, and its mostly studied peripheral effect is the induction of cellular apoptosis. Here, we discuss the evidences supporting the use of TRAIL as biomarker of cardiovascular diseases as well as the evidences showing the potential beneficial therapeutic effects of TRAIL on cardiovascular diseases and diabetes.&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/22676911?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%">Toffoli, Barbara</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%">Zacchigna, Serena</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</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%">TRAIL shows potential cardioprotective activity.</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%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Apolipoproteins E</style></keyword><keyword><style  face="normal" font="default" size="100%">Apoptosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Cardiotonic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Experimental</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Type 1</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetic Cardiomyopathies</style></keyword><keyword><style  face="normal" font="default" size="100%">Fibrosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Knockout</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</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 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%">1257-60</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 clinical trials carried out in patients with advanced cancer have shown that recombinant TRAIL administration is usually safe and well tolerated when used either alone or in association with chemotherapeutic drugs. Notably, anticancer chemotherapy can be associated to cardiomiopathy. We have here demonstrated that TRAIL (administrated as either recombinant soluble TRAIL or as AAV-TRAIL expression viral vector) reduced the development of cardiomyopathy in the ApoE(-/-) diabetic mouse model. These data suggest, for the first time, that therapeutically administration of TRAIL might have a cardioprotective effect.&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/21197620?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, S</style></author><author><style face="normal" font="default" size="100%">Londero, M</style></author><author><style face="normal" font="default" size="100%">Barbieri, F</style></author><author><style face="normal" font="default" size="100%">Di Leo, G</style></author><author><style face="normal" font="default" size="100%">Paparazzo, R</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Treatment with pamidronate for osteoporosis complicating long-term intestinal failure.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr Gastroenterol Nutr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr. Gastroenterol. Nutr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Absorptiometry, Photon</style></keyword><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Density</style></keyword><keyword><style  face="normal" font="default" size="100%">Bone Density Conservation Agents</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%">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%">Intestinal Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoporosis</style></keyword><keyword><style  face="normal" font="default" size="100%">Parenteral Nutrition, Home</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%">55</style></volume><pages><style face="normal" font="default" size="100%">615-8</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Long-term home parenteral nutrition (PN) is a potential risk for developing osteoporosis. Various attempts have been made to treat bone disease both by modifying the composition of PN and by administering hormones, such as calcitonin, parathyroid hormone, and sexual hormones. Bisphosphonates are recognized as a medication useful for the treatment of several bone disorders associated with excessive reabsorption. Nevertheless, there have been no paediatric studies on bisphosphonates use for intestinal failure-associated bone disease. Our study includes 6 paediatric patients receiving extremely long-term home PN (at least 3 years) who showed radiological and clinical signs of osteoporosis. Diagnosis of bone disease was made after a median period of 127.5 PN months. Treatment consisted in 2 cycles of intravenous pamidronate, 30 mg/m once per month for 6 months consecutively. They all showed a significant improvement in bone mineral density, evaluated after 6 and 12 months of pamidronate treatment. In our sample anthropometrical variables (weight, height, and body mass index) are not related with the z-score trend. Our patients had normal levels of calcium, phosphorus, and vitamin D, and proper nutrient intake. At the last follow-up, dual-energy x-ray absorptiometry scan showed that no patients had a z-score lower than -2.5; moreover, nobody developed bone fractures during the 108-month follow-up. The patients did not have any prominent adverse effect. Finally, in our experience, pamidronate is effective for improving bone mineral density and safe in patients with intestinal failure-associated bone disease.&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/22614111?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, E</style></author><author><style face="normal" font="default" size="100%">Fabretto, A</style></author><author><style face="normal" font="default" size="100%">Faletra, F</style></author><author><style face="normal" font="default" size="100%">Mocenigo, M</style></author><author><style face="normal" font="default" size="100%">Morgan, A</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%">Two Novel COH1 Mutations in an Italian Patient with Cohen Syndrome.</style></title><secondary-title><style face="normal" font="default" size="100%">Mol Syndromol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Mol Syndromol</style></alt-title></titles><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%">3</style></volume><pages><style face="normal" font="default" size="100%">30-33</style></pages><language><style face="normal" font="default" size="100%">ENG</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Cohen syndrome (CS) is an autosomal recessive disease caused by mutations in the COH1 gene. It is characterized by intellectual disability, hypotonia, joint hyperlaxity, severe myopia, characteristic facial dysmorphisms and, in some cases, intermittent isolated neutropenia. We investigated an Italian patient with CS together with his family. Genetic analysis disclosed 2 novel mutations: the first is an intronic mutation (c.8697-9A&gt;G) creating a new splice site 8 nucleotides upstream, and the second is a duplication of 1 base (c.10156dupA) generating a premature stop codon. The compound heterozygous mutations explain the proband's phenotype and improved the knowledge of genotype-phenotype correlation.&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/22855652?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%">Vatta, Serena</style></author><author><style face="normal" font="default" size="100%">Fabris, Annalisa</style></author><author><style face="normal" font="default" size="100%">Segat, Ludovica</style></author><author><style face="normal" font="default" size="100%">Not, Tarcisio</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%">Tag-single nucleotide polymorphism-based human leukocyte antigen genotyping in celiac disease patients from northeastern Italy.</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%">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%">Celiac Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">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%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mass Screening</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</style></keyword><keyword><style  face="normal" font="default" size="100%">Reverse Transcriptase Polymerase Chain Reaction</style></keyword><keyword><style  face="normal" font="default" size="100%">Sensitivity and Specificity</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 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">72</style></volume><pages><style face="normal" font="default" size="100%">499-502</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 genotyped celiac disease (CD)-associated haplotypes DQ2.5, DQ8, DQ2.2, and DQ7 in 1005 CD patients from North Eastern Italy using a Tag-single nucleotide polymorphism (SNPs) approach and real time PCR platform, checking the accuracy and reliability of the method and comparing it to traditional PCR-SSP. Only 14 of 2010 chromosomes analyzed (0.7%) showed discrepancies between the Tag-SNPs real-time polymerase chain reaction (PCR) method and the PCR-single-strand polymorphism (SSP) technique, indicating a high sensitivity and specificity (ranging from 0.987 to 1 and from 0.998 to 0.999, respectively) for tagging with respect to corresponding human leukocyte antigen (HLA) alleles identified by PCR-SSP. Moreover, the overall cost of the Tag-SNPs HLA typing method was low (3 to 4 €/sample instead of 35 to 70 €/sample with commercial kits), making it suitable for mass screenings. Hence, we believe that the Tag-SNPs HLA typing could be used to complement or replace classic HLA typing in at high-risk groups, for research purposes and eventually in population screening programs.&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/21513759?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%">Hasija, Rachana</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%">Demirkaya, Erkan</style></author><author><style face="normal" font="default" size="100%">Khubchandani, Raju</style></author><author><style face="normal" font="default" size="100%">Guseinova, Dinara</style></author><author><style face="normal" font="default" size="100%">Malattia, Clara</style></author><author><style face="normal" font="default" size="100%">Canhao, Helena</style></author><author><style face="normal" font="default" size="100%">Harel, Liora</style></author><author><style face="normal" font="default" size="100%">Foell, Dirk</style></author><author><style face="normal" font="default" size="100%">Wouters, Carine</style></author><author><style face="normal" font="default" size="100%">De Cunto, Carmen</style></author><author><style face="normal" font="default" size="100%">Huemer, Christian</style></author><author><style face="normal" font="default" size="100%">Kimura, Yukiko</style></author><author><style face="normal" font="default" size="100%">Mangge, Harald</style></author><author><style face="normal" font="default" size="100%">Minetti, Carlo</style></author><author><style face="normal" font="default" size="100%">Nordal, Ellen Berit</style></author><author><style face="normal" font="default" size="100%">Philippet, Pierre</style></author><author><style face="normal" font="default" size="100%">Garozzo, Rosaria</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 Organization</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Therapeutic approaches in the treatment of juvenile dermatomyositis in patients with recent-onset disease and in those experiencing disease flare: an international multicenter PRINTO study.</style></title><secondary-title><style face="normal" font="default" size="100%">Arthritis Rheum</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Arthritis Rheum.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Adrenal Cortex Hormones</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Dermatologic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Dermatomyositis</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%">Longitudinal Studies</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%">Prospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</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 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">63</style></volume><pages><style face="normal" font="default" size="100%">3142-52</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 evaluate response to therapy over a 24-month period in a large prospective international cohort of patients with juvenile dermatomyositis (DM).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The study included 145 patients with recent-onset juvenile DM and 130 juvenile DM patients experiencing disease flare, all of whom were &lt;18 years old. Disease activity parameters and therapeutic approaches in 4 geographic areas were analyzed at baseline and at 6, 12, and 24 months. Response was assessed according to the Pediatric Rheumatology International Trials Organization (PRINTO) juvenile DM response criteria, and data were reported &quot;as observed&quot; and in the intent-to-treat (ITT) population.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Patients with recent-onset juvenile DM at baseline had higher baseline disease activity and greater improvement over 24 months when compared to juvenile DM patients experiencing disease flare at baseline. Methotrexate (MTX) or high-dose corticosteroids were administered more frequently to patients with recent-onset juvenile DM, compared to juvenile DM patients experiencing disease flare, who were more likely to receive cyclosporine. Compared to patients from Western and Eastern Europe, a higher proportion of patients from South and Central America and North America received pulse steroids, and the average steroid dosage was higher in the North American and South and Central American patients. The use of MTX was similar in all 4 regions, while cyclosporin A was more frequently used in Western Europe. In the &quot;as observed&quot; analysis, 57.9% of the patients with recent-onset juvenile DM and 36.4% of the patients experiencing disease flare (P&lt;0.001) reached at least a 70% response by PRINTO criteria at 6 months; these proportions had increased at month 24 to 78.4% and 51.2%, respectively (P&lt;0.001). Corresponding results of the ITT analysis were much lower, with only one-third of the patients able to maintain the initial assigned therapy over 24 months.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Patients with recent-onset juvenile DM are more likely to achieve significant clinical improvement over 24 months, when compared to patients experiencing flares of juvenile DM. Internationally, various therapeutic approaches are used to treat this disease.&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/21647864?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%">Lazzerini, Marzia</style></author><author><style face="normal" font="default" size="100%">Bramuzzo, Matteo</style></author><author><style face="normal" font="default" size="100%">Maschio, Massimo</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></authors></contributors><titles><title><style face="normal" font="default" size="100%">Thromboembolism in pediatric inflammatory bowel disease: systematic review.</style></title><secondary-title><style face="normal" font="default" size="100%">Inflamm Bowel Dis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Inflamm. Bowel Dis.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</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%">Risk Factors</style></keyword><keyword><style  face="normal" font="default" size="100%">Thromboembolism</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 Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">17</style></volume><pages><style face="normal" font="default" size="100%">2174-83</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;BACKGROUND: &lt;/b&gt;Several studies suggest an increased risk of venous and arterial thromboembolism (TE) in adults with inflammatory bowel disease (IBD) compared to the general population. We performed a systematic review of studies on incidence and characteristic of TE in children with IBD.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;We searched Medline, LILACS, EMBASE, POPLINE, CINHAL, and reference lists of identified articles, without language restrictions, in August 2010.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;Population studies suggest that there is an increased risk of TE in children with IBD compared to controls. TE occurred in children with IBD in all age ranges, mostly (82.8%) during active disease, and more frequently in children with ulcerative colitis (odds ratio [OR] 3.7, 95% confidence interval [CI] 1.8-7.6). At least one specific risk factor for TE was recognized in 50% of cases; two risk factors were present in 24%. Out of 92 published cases of TE in children with IBD, 54.3% occurred in cerebral site, 26% in the limbs, 13% in the abdominal vessels, and the remaining in the retina and lungs. After a first episode of TE, an early recurrence was observed in 11.4% of children, a late recurrence in 10%. A number of different therapeutic schemes were used. Overall mortality was 5.7% and was mostly associated with cerebral TE.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Population studies are needed to clarify the risk of TE in children with IBD, the relative weight of other risk factors, the characteristics of the events, and to define guidelines of therapy and prophylaxis.&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/21910180?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Corallini, Federica</style></author><author><style face="normal" font="default" size="100%">Celeghini, Claudio</style></author><author><style face="normal" font="default" size="100%">Rimondi, Erika</style></author><author><style face="normal" font="default" size="100%">di Iasio, Maria Grazia</style></author><author><style face="normal" font="default" size="100%">Gonelli, Arianna</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%">Trail down-regulates the release of osteoprotegerin (OPG) by primary stromal cells.</style></title><secondary-title><style face="normal" font="default" size="100%">J Cell Physiol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Cell. Physiol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Bone Marrow Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Death</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Coculture Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Down-Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Endothelial Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme Activation</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme-Linked Immunosorbent Assay</style></keyword><keyword><style  face="normal" font="default" size="100%">Fibroblasts</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">MAP Kinase Signaling System</style></keyword><keyword><style  face="normal" font="default" size="100%">Mesenchymal Stromal Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">Osteoprotegerin</style></keyword><keyword><style  face="normal" font="default" size="100%">p38 Mitogen-Activated Protein Kinases</style></keyword><keyword><style  face="normal" font="default" size="100%">Protein Binding</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Stromal Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">TNF-Related Apoptosis-Inducing Ligand</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor-alpha</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 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">226</style></volume><pages><style face="normal" font="default" size="100%">2279-86</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The soluble member of the TNF-R superfamily osteoprotegerin (OPG) is abundantly released under basal conditions by both mesenchymal stem cells (MSC) and fibroblasts and by endothelial cells upon stimulation with inflammatory cytokines. Since MSC, fibroblasts and endothelial cells represent key elements of the normal and tumor microenvironment and express detectable levels of surface TRAIL receptors, we investigated the effect of TRAIL on OPG release. Unexpectedly, recombinant TRAIL decreased the spontaneous OPG release in all cell types examined. Moreover, TRAIL decreased OPG release also in stromal cells co-cultured with lymphoma cells and counteracted the OPG induction by TN-alpha in HUVEC and MSC. Such down-regulation was not due to a masking effect in the ELISA quantification of the OPG released in the culture supernatants due to binding of OPG to its ligands (TRAIL and RANKL), as demonstrated by competition experiments with recombinant TRAIL and by the lack of RANKL release/induction. In addition, OPG down-regulation was not due to induction of cytotoxic effects by TRAIL, since the degree of apoptosis in response to TRAIL was negligible in all primary cell types. With regards to the possible molecular mechanism accounting for the down-regulation of OPG release by TRAIL, we found that treatment of MSC with TRAIL significantly decreased the phosphorylation levels of p38/MAPK. There is a suggestion that this pathway is involved in the stabilization of OPG mRNA. In this respect, the ability of TRAIL to decrease the release of OPG, in the absence of cell cytotoxicity, was mimicked by the p38/MAPK inhibitor SB203580.&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/21660951?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%">Sancilio, S</style></author><author><style face="normal" font="default" size="100%">Di Giacomo, V</style></author><author><style face="normal" font="default" size="100%">Quaglietta, A M</style></author><author><style face="normal" font="default" size="100%">Iacone, A</style></author><author><style face="normal" font="default" size="100%">Angelucci, D</style></author><author><style face="normal" font="default" size="100%">Tatasciore, U</style></author><author><style face="normal" font="default" size="100%">Rana, R A</style></author><author><style face="normal" font="default" size="100%">Cataldi, A</style></author><author><style face="normal" font="default" size="100%">Zauli, G</style></author><author><style face="normal" font="default" size="100%">Di Pietro, R</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">TRAIL promotes a pro-survival signal in erythropoietin-deprived human erythroblasts through the activation of an NF-kB/IkBalpha pathway.</style></title><secondary-title><style face="normal" font="default" size="100%">J Biol Regul Homeost Agents</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Biol. Regul. Homeost. Agents</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Cell Survival</style></keyword><keyword><style  face="normal" font="default" size="100%">Erythroblasts</style></keyword><keyword><style  face="normal" font="default" size="100%">Erythropoietin</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">I-kappa B Kinase</style></keyword><keyword><style  face="normal" font="default" size="100%">Jurkat Cells</style></keyword><keyword><style  face="normal" font="default" size="100%">NF-kappa B</style></keyword><keyword><style  face="normal" font="default" size="100%">Peptides</style></keyword><keyword><style  face="normal" font="default" size="100%">TNF-Related Apoptosis-Inducing Ligand</style></keyword><keyword><style  face="normal" font="default" size="100%">Tumor Necrosis Factor Decoy Receptors</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 Jul-Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">25</style></volume><pages><style face="normal" font="default" size="100%">375-86</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;The biological activity of TNF-related apoptosis inducing ligand (TRAIL) was analyzed in primary human erythroblasts derived from mononuclear cells of blood donors, kept in culture in the presence of 20 percent foetal calf serum, growth factors (EPO, SCF, IL-3) and glucocorticoids (10-6 M dexamethasone, 10-6 M oestradiol) or under growth factor and serum starvation. In the presence of growth factors and serum, primary erythroblasts showed a differential expression of TRAIL-Receptors (Rs) at various degrees of maturation and responded to TRAIL treatment with a mild cytotoxicity. On the other hand, in the absence of serum and growth factors, TRAIL treatment unexpectedly up-regulated TRAIL-R4 decoy receptor and promoted erythroblast survival. The concomitant activation of NF-kB/IkB survival pathway was detected with Western blotting and immunofluorescence procedures and confirmed by experiments performed with SN50, a pharmacological inhibitor of the NF-kB/IkB pathway. Our study indicates that TRAIL has a twofold activity on erythroid lineages: it induces a mild erythroid cell cytotoxicity in the presence of serum and growth factors, while it promotes erythroid cell survival through the activation of the NF-kB/IkB pathway under starvation conditions.&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/22023762?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%">Maschio, Massimo</style></author><author><style face="normal" font="default" size="100%">Di Leo, Grazia</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%">Two lumens, one diagnosis.</style></title><secondary-title><style face="normal" font="default" size="100%">J Pediatr</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Pediatr.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Capsule Endoscopy</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Gastrointestinal Hemorrhage</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%">Meckel Diverticulum</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</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 Sep</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">159</style></volume><pages><style face="normal" font="default" size="100%">511</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><issue><style face="normal" font="default" size="100%">3</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/21645910?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 Leo, Luigina</style></author><author><style face="normal" font="default" size="100%">Marcuzzi, Annalisa</style></author><author><style face="normal" font="default" size="100%">Decorti, Giuliana</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Crovella, Sergio</style></author><author><style face="normal" font="default" size="100%">Pontillo, Alessandra</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Targeting farnesyl-transferase as a novel therapeutic strategy for mevalonate kinase deficiency: in vitro and in vivo approaches.</style></title><secondary-title><style face="normal" font="default" size="100%">Pharmacol Res</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Pharmacol. Res.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Inflammatory Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Enzyme Inhibitors</style></keyword><keyword><style  face="normal" font="default" size="100%">Farnesyltranstransferase</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%">Mevalonate Kinase Deficiency</style></keyword><keyword><style  face="normal" font="default" size="100%">Mevalonic Acid</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice, Inbred BALB C</style></keyword><keyword><style  face="normal" font="default" size="100%">Monocytes</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyenes</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyisoprenyl Phosphates</style></keyword><keyword><style  face="normal" font="default" size="100%">Polyunsaturated Alkamides</style></keyword><keyword><style  face="normal" font="default" size="100%">Young Adult</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">61</style></volume><pages><style face="normal" font="default" size="100%">506-10</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Mevalonate kinase deficiency (MKD) is a rare inborn auto-inflammatory disease due to the impairment of the pathway for the biosynthesis of cholesterol and non-sterol isoprenoids. The shortage of isoprenoids compounds and in particular of geranylgeranylpyrophosphate (GGPP) was recently associated to the MKD characteristic inflammatory attacks. The aim of this study is to demonstrate that the normalization of the mevalonate pathway intermediates levels and in particular of GGPP, through the specific inhibition of farnesyl-transferase (FT) with Manumycin A could ameliorate the inflammatory phenotype of MKD patients. The effect of Manumycin A was first evaluated in MKD mouse and cellular models, chemically obtained using the aminobisphosphonate alendronate (ALD), and then in monocytes isolated from 2 MKD patients. Our findings were compared to those obtained by using natural exogenous isoprenoids (NEIs). Manumycin A was able to significantly reduce the inflammatory marker serum amyloid A in ALD-treated Balb/c mice, as well as IL-1 beta secretion in ALD-monocytes and in MKD patients. These results clearly showed that, through the inhibition of FT, an increased number of mevalonate pathway intermediates could be redirected towards the synthesis of GGPP diminishing the inflammatory response. The importance in limiting the shortage of GGPP was emphasized by the anti-inflammatory effect of NEIs that, due to their biochemical structure, can enter the MKD pathway. In conclusion, manumycin A, as well as NEIs, showed anti-inflammatory effect in MKD models and especially in MKD-monocytes, suggesting novel approaches in the treatment of MKD, an orphan disease without any efficacious treatment currently available.&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/20206266?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%">Freudenberg, Folke</style></author><author><style face="normal" font="default" size="100%">Wintergerst, Uwe</style></author><author><style face="normal" font="default" size="100%">Roesen-Wolff, Angela</style></author><author><style face="normal" font="default" size="100%">Albert, Michael H</style></author><author><style face="normal" font="default" size="100%">Prell, Christine</style></author><author><style face="normal" font="default" size="100%">Strahm, Brigitte</style></author><author><style face="normal" font="default" size="100%">Koletzko, Sibylle</style></author><author><style face="normal" font="default" size="100%">Ehl, Stephan</style></author><author><style face="normal" font="default" size="100%">Roos, Dirk</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Ventura, Alessandro</style></author><author><style face="normal" font="default" size="100%">Belohradsky, Bernd H</style></author><author><style face="normal" font="default" size="100%">Seger, Reinhard</style></author><author><style face="normal" font="default" size="100%">Roesler, Joachim</style></author><author><style face="normal" font="default" size="100%">Güngör, Tayfun</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Therapeutic strategy in p47-phox deficient chronic granulomatous disease presenting as inflammatory bowel disease.</style></title><secondary-title><style face="normal" font="default" size="100%">J Allergy Clin Immunol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J. Allergy Clin. Immunol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Age of Onset</style></keyword><keyword><style  face="normal" font="default" size="100%">Anti-Bacterial Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Antibodies, Monoclonal</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug Therapy, Combination</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Deletion</style></keyword><keyword><style  face="normal" font="default" size="100%">Granulomatous Disease, Chronic</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%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">NADPH Oxidase</style></keyword><keyword><style  face="normal" font="default" size="100%">Steroids</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Vidarabine</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 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">125</style></volume><pages><style face="normal" font="default" size="100%">943-946.e1</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/20371400?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%">Elks, Cathy E</style></author><author><style face="normal" font="default" size="100%">Perry, John R B</style></author><author><style face="normal" font="default" size="100%">Sulem, Patrick</style></author><author><style face="normal" font="default" size="100%">Chasman, Daniel I</style></author><author><style face="normal" font="default" size="100%">Franceschini, Nora</style></author><author><style face="normal" font="default" size="100%">He, Chunyan</style></author><author><style face="normal" font="default" size="100%">Lunetta, Kathryn L</style></author><author><style face="normal" font="default" size="100%">Visser, Jenny A</style></author><author><style face="normal" font="default" size="100%">Byrne, Enda M</style></author><author><style face="normal" font="default" size="100%">Cousminer, Diana L</style></author><author><style face="normal" font="default" size="100%">Gudbjartsson, Daniel F</style></author><author><style face="normal" font="default" size="100%">Esko, Tõnu</style></author><author><style face="normal" font="default" size="100%">Feenstra, Bjarke</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%">Kutalik, Zoltán</style></author><author><style face="normal" font="default" size="100%">Lin, Peng</style></author><author><style face="normal" font="default" size="100%">Mangino, Massimo</style></author><author><style face="normal" font="default" size="100%">Marongiu, Mara</style></author><author><style face="normal" font="default" size="100%">McArdle, Patrick F</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%">van Wingerden, Sophie H</style></author><author><style face="normal" font="default" size="100%">Zhao, Jing Hua</style></author><author><style face="normal" font="default" size="100%">Albrecht, Eva</style></author><author><style face="normal" font="default" size="100%">Corre, Tanguy</style></author><author><style face="normal" font="default" size="100%">Ingelsson, Erik</style></author><author><style face="normal" font="default" size="100%">Hayward, Caroline</style></author><author><style face="normal" font="default" size="100%">Magnusson, Patrik K E</style></author><author><style face="normal" font="default" size="100%">Smith, Erin N</style></author><author><style face="normal" font="default" size="100%">Ulivi, Shelia</style></author><author><style face="normal" font="default" size="100%">Warrington, Nicole M</style></author><author><style face="normal" font="default" size="100%">Zgaga, Lina</style></author><author><style face="normal" font="default" size="100%">Alavere, Helen</style></author><author><style face="normal" font="default" size="100%">Amin, Najaf</style></author><author><style face="normal" font="default" size="100%">Aspelund, Thor</style></author><author><style face="normal" font="default" size="100%">Bandinelli, Stefania</style></author><author><style face="normal" font="default" size="100%">Barroso, Inês</style></author><author><style face="normal" font="default" size="100%">Berenson, Gerald S</style></author><author><style face="normal" font="default" size="100%">Bergmann, Sven</style></author><author><style face="normal" font="default" size="100%">Blackburn, Hannah</style></author><author><style face="normal" font="default" size="100%">Boerwinkle, Eric</style></author><author><style face="normal" font="default" size="100%">Buring, Julie E</style></author><author><style face="normal" font="default" size="100%">Busonero, Fabio</style></author><author><style face="normal" font="default" size="100%">Campbell, Harry</style></author><author><style face="normal" font="default" size="100%">Chanock, Stephen J</style></author><author><style face="normal" font="default" size="100%">Chen, Wei</style></author><author><style face="normal" font="default" size="100%">Cornelis, Marilyn C</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%">d'Adamo, Pio</style></author><author><style face="normal" font="default" size="100%">de Faire, Ulf</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%">Deloukas, Panos</style></author><author><style face="normal" font="default" size="100%">Döring, Angela</style></author><author><style face="normal" font="default" size="100%">Smith, George Davey</style></author><author><style face="normal" font="default" size="100%">Easton, Douglas F</style></author><author><style face="normal" font="default" size="100%">Eiriksdottir, Gudny</style></author><author><style face="normal" font="default" size="100%">Emilsson, Valur</style></author><author><style face="normal" font="default" size="100%">Eriksson, Johan</style></author><author><style face="normal" font="default" size="100%">Ferrucci, Luigi</style></author><author><style face="normal" font="default" size="100%">Folsom, Aaron R</style></author><author><style face="normal" font="default" size="100%">Foroud, Tatiana</style></author><author><style face="normal" font="default" size="100%">Garcia, 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face="normal" font="default" size="100%">Nelis, Mari</style></author><author><style face="normal" font="default" size="100%">Ness, Andrew R</style></author><author><style face="normal" font="default" size="100%">Northstone, Kate</style></author><author><style face="normal" font="default" size="100%">Oostra, Ben A</style></author><author><style face="normal" font="default" size="100%">Peacock, Munro</style></author><author><style face="normal" font="default" size="100%">Palmer, Lyle J</style></author><author><style face="normal" font="default" size="100%">Palotie, Aarno</style></author><author><style face="normal" font="default" size="100%">Paré, Guillaume</style></author><author><style face="normal" font="default" size="100%">Parker, Alex N</style></author><author><style face="normal" font="default" size="100%">Pedersen, Nancy L</style></author><author><style face="normal" font="default" size="100%">Peltonen, Leena</style></author><author><style face="normal" font="default" size="100%">Pennell, Craig E</style></author><author><style face="normal" font="default" size="100%">Pharoah, Paul</style></author><author><style face="normal" font="default" size="100%">Polasek, Ozren</style></author><author><style face="normal" font="default" size="100%">Plump, Andrew S</style></author><author><style face="normal" font="default" size="100%">Pouta, Anneli</style></author><author><style face="normal" font="default" size="100%">Porcu, Eleonora</style></author><author><style face="normal" font="default" size="100%">Rafnar, Thorunn</style></author><author><style face="normal" font="default" size="100%">Rice, John P</style></author><author><style face="normal" font="default" size="100%">Ring, Susan M</style></author><author><style face="normal" font="default" size="100%">Rivadeneira, Fernando</style></author><author><style face="normal" font="default" size="100%">Rudan, Igor</style></author><author><style face="normal" font="default" size="100%">Sala, 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Gerard</style></author><author><style face="normal" font="default" size="100%">Wareham, Nicholas J</style></author><author><style face="normal" font="default" size="100%">Waterworth, Dawn M</style></author><author><style face="normal" font="default" size="100%">Weedon, Michael N</style></author><author><style face="normal" font="default" size="100%">Wichmann, H Erich</style></author><author><style face="normal" font="default" size="100%">Willemsen, Gonneke</style></author><author><style face="normal" font="default" size="100%">Wilson, James F</style></author><author><style face="normal" font="default" size="100%">Wright, Alan F</style></author><author><style face="normal" font="default" size="100%">Young, Lauren</style></author><author><style face="normal" font="default" size="100%">Zhai, Guangju</style></author><author><style face="normal" font="default" size="100%">Zhuang, Wei Vivian</style></author><author><style face="normal" font="default" size="100%">Bierut, Laura J</style></author><author><style face="normal" font="default" size="100%">Boomsma, Dorret I</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%">Demerath, Ellen W</style></author><author><style face="normal" font="default" size="100%">van Duijn, Cornelia M</style></author><author><style face="normal" font="default" size="100%">Econs, Michael J</style></author><author><style face="normal" font="default" size="100%">Harris, Tamara B</style></author><author><style face="normal" font="default" size="100%">Hunter, David 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%">Metspalu, Andres</style></author><author><style face="normal" font="default" size="100%">Montgomery, Grant W</style></author><author><style face="normal" font="default" size="100%">Ridker, Paul M</style></author><author><style face="normal" font="default" size="100%">Spector, Tim D</style></author><author><style face="normal" font="default" size="100%">Streeten, Elizabeth A</style></author><author><style face="normal" font="default" size="100%">Stefansson, Kari</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%">Widen, Elisabeth</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><author><style face="normal" font="default" size="100%">Murray, Anna</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">GIANT Consortium</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Thirty new loci for age at menarche identified by a meta-analysis of genome-wide association studies.</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><keywords><keyword><style  face="normal" font="default" size="100%">Adolescent</style></keyword><keyword><style  face="normal" font="default" size="100%">Aging</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Height</style></keyword><keyword><style  face="normal" font="default" size="100%">Body Size</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">DNA Copy Number Variations</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%">Genetic Predisposition to Disease</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%">Inheritance Patterns</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%">Polymorphism, Single Nucleotide</style></keyword><keyword><style  face="normal" font="default" size="100%">Quantitative Trait Loci</style></keyword><keyword><style  face="normal" font="default" size="100%">Reproducibility of Results</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 Dec</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">42</style></volume><pages><style face="normal" font="default" size="100%">1077-85</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 identify loci for age at menarche, we performed a meta-analysis of 32 genome-wide association studies in 87,802 women of European descent, with replication in up to 14,731 women. In addition to the known loci at LIN28B (P = 5.4 × 10⁻⁶⁰) and 9q31.2 (P = 2.2 × 10⁻³³), we identified 30 new menarche loci (all P &lt; 5 × 10⁻⁸) and found suggestive evidence for a further 10 loci (P &lt; 1.9 × 10⁻⁶). The new loci included four previously associated with body mass index (in or near FTO, SEC16B, TRA2B and TMEM18), three in or near other genes implicated in energy homeostasis (BSX, CRTC1 and MCHR2) and three in or near genes implicated in hormonal regulation (INHBA, PCSK2 and RXRG). Ingenuity and gene-set enrichment pathway analyses identified coenzyme A and fatty acid biosynthesis as biological processes related to menarche timing.&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/21102462?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%">Nazzi, F</style></author><author><style face="normal" font="default" size="100%">Martinelli, E</style></author><author><style face="normal" font="default" size="100%">Del Fabbro, S</style></author><author><style face="normal" font="default" size="100%">Bernardinelli, I</style></author><author><style face="normal" font="default" size="100%">Milani, N</style></author><author><style face="normal" font="default" size="100%">Iob, A</style></author><author><style face="normal" font="default" size="100%">Pischiutti, P</style></author><author><style face="normal" font="default" size="100%">Campello, C</style></author><author><style face="normal" font="default" size="100%">D'Agaro, P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Ticks and Lyme borreliosis in an alpine area in northeast Italy.</style></title><secondary-title><style face="normal" font="default" size="100%">Med Vet Entomol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Med. Vet. Entomol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Borrelia burgdorferi</style></keyword><keyword><style  face="normal" font="default" size="100%">Climate</style></keyword><keyword><style  face="normal" font="default" size="100%">Ecology</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Incidence</style></keyword><keyword><style  face="normal" font="default" size="100%">Italy</style></keyword><keyword><style  face="normal" font="default" size="100%">Ixodes</style></keyword><keyword><style  face="normal" font="default" size="100%">Lyme Disease</style></keyword><keyword><style  face="normal" font="default" size="100%">Nymph</style></keyword><keyword><style  face="normal" font="default" size="100%">Population Density</style></keyword><keyword><style  face="normal" font="default" size="100%">Prevalence</style></keyword><keyword><style  face="normal" font="default" size="100%">Seasons</style></keyword><keyword><style  face="normal" font="default" size="100%">Ticks</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%">24</style></volume><pages><style face="normal" font="default" size="100%">220-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A 2-year study was conducted in a mountainous area of northeast Italy to evaluate the occurrence and distribution of ticks, as well as to assess the prevalence of the spirochaete Borrelia burgdorferi sensu lato. All ticks collected were Ixodes ricinus L. (Parasitiformes: Ixodidae). In general, most nymphs and adult ticks were collected from April to July. Tick density was highly variable among sites; however, two areas with different infestation levels were recognized. Prevalences of B. burgdorferi s.l. in nymphal stages were rather variable between sites; overall the prevalence of infected nymphs in the whole area was slightly higher than 20%. The prevalence of B. burgdorferi s.l. in nymphs does not seem to be correlated with nymph density. The correlation between the incidence of Lyme borreliosis (reported human cases/1000 inhabitants/year) and Borrelia prevalence in nymphs was not significant, although a significant correlation was found between borreliosis incidence and nymph density.&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/20534008?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%">Swanson, Robert C</style></author><author><style face="normal" font="default" size="100%">Bongiovanni, Annette</style></author><author><style face="normal" font="default" size="100%">Bradley, Elizabeth</style></author><author><style face="normal" font="default" size="100%">Murugan, Varnee</style></author><author><style face="normal" font="default" size="100%">Sundewall, Jesper</style></author><author><style face="normal" font="default" size="100%">Betigeri, Arvind</style></author><author><style face="normal" font="default" size="100%">Nyonator, Frank</style></author><author><style face="normal" font="default" size="100%">Cattaneo, Adriano</style></author><author><style face="normal" font="default" size="100%">Harless, Brandi</style></author><author><style face="normal" font="default" size="100%">Ostrovsky, Andrey</style></author><author><style face="normal" font="default" size="100%">Labonté, Ronald</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Toward a consensus on guiding principles for health systems strengthening.</style></title><secondary-title><style face="normal" font="default" size="100%">PLoS Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">PLoS Med.</style></alt-title></titles><keywords><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%">Public Health</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">7</style></volume><pages><style face="normal" font="default" size="100%">e1000385</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><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/21203584?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%">Nyqvist, K H</style></author><author><style face="normal" font="default" size="100%">Anderson, G C</style></author><author><style face="normal" font="default" size="100%">Bergman, N</style></author><author><style face="normal" font="default" size="100%">Cattaneo, A</style></author><author><style face="normal" font="default" size="100%">Charpak, N</style></author><author><style face="normal" font="default" size="100%">Davanzo, R</style></author><author><style face="normal" font="default" size="100%">Ewald, U</style></author><author><style face="normal" font="default" size="100%">Ibe, O</style></author><author><style face="normal" font="default" size="100%">Ludington-Hoe, S</style></author><author><style face="normal" font="default" size="100%">Mendoza, S</style></author><author><style face="normal" font="default" size="100%">Pallás-Allonso, C</style></author><author><style face="normal" font="default" size="100%">Ruiz Peláez, J G</style></author><author><style face="normal" font="default" size="100%">Sizun, J</style></author><author><style face="normal" font="default" size="100%">Widström, A-M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Towards universal Kangaroo Mother Care: recommendations and report from the First European conference and Seventh International Workshop on Kangaroo Mother Care.</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><keywords><keyword><style  face="normal" font="default" size="100%">Congresses as Topic</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</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 Care</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%">Parent-Child Relations</style></keyword><keyword><style  face="normal" font="default" size="100%">Practice Guidelines as Topic</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%">Skin</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 Jun</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">99</style></volume><pages><style face="normal" font="default" size="100%">820-6</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;UNLABELLED: &lt;/b&gt;The hallmark of Kangaroo Mother Care (KMC) is the kangaroo position: the infant is cared for skin-to-skin vertically between the mother's breasts and below her clothes, 24 h/day, with father/substitute(s) participating as KMC providers. Intermittent KMC (for short periods once or a few times per day, for a variable number of days) is commonly employed in high-tech neonatal intensive care units. These two modalities should be regarded as a progressive adaptation of the mother-infant dyad, ideally towards continuous KMC, starting gradually and progressively with intermittent KMC. The other components in KMC are exclusive breastfeeding (ideally) and early discharge in kangaroo position with strict follow-up. Current evidence allows the following general statements about KMC in affluent and low-income settings: KMC enhances bonding and attachment; reduces maternal postpartum depression symptoms; enhances infant physiologic stability and reduces pain, increases parental sensitivity to infant cues; contributes to the establishment and longer duration of breastfeeding and has positive effects on infant development and infant/parent interaction. Therefore, intrapartum and postnatal care in all types of settings should adhere to a paradigm of nonseparation of infants and their mothers/families. Preterm/low-birth-weight infants should be regarded as extero-gestational foetuses needing skin-to-skin contact to promote maturation.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Kangaroo Mother Care should begin as soon as possible after birth, be applied as continuous skin-to-skin contact to the extent that this is possible and appropriate and continue for as long as appropriate.&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/20219044?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%">Puzelli, Simona</style></author><author><style face="normal" font="default" size="100%">Facchini, Marzia</style></author><author><style face="normal" font="default" size="100%">Spagnolo, Domenico</style></author><author><style face="normal" font="default" size="100%">De Marco, Maria A</style></author><author><style face="normal" font="default" size="100%">Calzoletti, Laura</style></author><author><style face="normal" font="default" size="100%">Zanetti, Alessandro</style></author><author><style face="normal" font="default" size="100%">Fumagalli, Roberto</style></author><author><style face="normal" font="default" size="100%">Tanzi, Maria L</style></author><author><style face="normal" font="default" size="100%">Cassone, Antonio</style></author><author><style face="normal" font="default" size="100%">Rezza, Giovanni</style></author><author><style face="normal" font="default" size="100%">Donatelli, Isabella</style></author></authors><translated-authors><author><style face="normal" font="default" size="100%">Surveillance Group for Pandemic A H1N1 2009 Influenza Virus in Italy</style></author></translated-authors></contributors><titles><title><style face="normal" font="default" size="100%">Transmission of hemagglutinin D222G mutant strain of pandemic (H1N1) 2009 virus.</style></title><secondary-title><style face="normal" font="default" size="100%">Emerg Infect Dis</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Emerging Infect. Dis.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Amino Acid Substitution</style></keyword><keyword><style  face="normal" font="default" size="100%">Disease Outbreaks</style></keyword><keyword><style  face="normal" font="default" size="100%">Hemagglutinin Glycoproteins, Influenza Virus</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza A Virus, H1N1 Subtype</style></keyword><keyword><style  face="normal" font="default" size="100%">Influenza, Human</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation, Missense</style></keyword><keyword><style  face="normal" font="default" size="100%">Phylogeny</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Viral</style></keyword><keyword><style  face="normal" font="default" size="100%">Sequence Analysis, RNA</style></keyword><keyword><style  face="normal" font="default" size="100%">Severity of Illness Index</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 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">16</style></volume><pages><style face="normal" font="default" size="100%">863-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;A pandemic (H1N1) 2009 virus strain carrying the D222G mutation was identified in a severely ill man and was transmitted to a household contact. Only mild illness developed in the contact, despite his obesity and diabetes. The isolated virus reacted fully with an antiserum against the pandemic vaccine strain.&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/20409386?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Zauli, Giorgio</style></author><author><style face="normal" font="default" size="100%">Toffoli, Barbara</style></author><author><style face="normal" font="default" size="100%">di Iasio, Maria Grazia</style></author><author><style face="normal" font="default" size="100%">Celeghini, Claudio</style></author><author><style face="normal" font="default" size="100%">Fabris, Bruno</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%">Treatment with recombinant tumor necrosis factor-related apoptosis-inducing ligand alleviates the severity of streptozotocin-induced diabetes.</style></title><secondary-title><style face="normal" font="default" size="100%">Diabetes</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Diabetes</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Animals</style></keyword><keyword><style  face="normal" font="default" size="100%">Cells, Cultured</style></keyword><keyword><style  face="normal" font="default" size="100%">Diabetes Mellitus, Experimental</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Islets of Langerhans</style></keyword><keyword><style  face="normal" font="default" size="100%">Leukocytes, Mononuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Mice</style></keyword><keyword><style  face="normal" font="default" size="100%">Recombinant Proteins</style></keyword><keyword><style  face="normal" font="default" size="100%">Suppressor of Cytokine Signaling Proteins</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%">2010</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2010 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">59</style></volume><pages><style face="normal" font="default" size="100%">1261-5</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To evaluate the potential therapeutic effect of recombinant human tumor necrosis factor (TNF)-related apoptosis-inducing ligand (TRAIL) treatment in a model of type 1 diabetes.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESEARCH DESIGN AND METHODS: &lt;/b&gt;Recombinant TRAIL was added in vitro to primary human and mouse peripheral blood mononuclear cells (PBMCs) and isolated human islets to evaluate the expression of the immunoregulatory gene SOCS1. Diabetes was induced by five consecutive daily injections of low-concentration (50 mg/kg) streptozotocin (STZ) in C57 black mice (n = 24). A group of these mice (n = 12) was co-injected with recombinant TRAIL (20 microg/day) for 5 days, and the diabetic status (glycemia and body weight) was followed over time. After 6 weeks, circulating levels of insulin, TNF-alpha, and osteoprotegerin (OPG) were measured, and animals were killed to perform the histological analysis of the pancreas.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The in vitro exposure of both PBMCs and human islets to recombinant TRAIL significantly upregulated the expression of SOCS1. With respect to STZ-treated animals, mice co-injected with STZ+TRAIL were characterized by 1) lower levels of hyperglycemia, 2) higher levels of body weight and insulinemia, 3) a partial preservation of pancreatic islets with normal morphology, and 4) a lower expression of both systemic (TNF-alpha and OPG) and pancreatic (vascular cell adhesion molecule [VCAM]-1) inflammatory markers.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;Overall, these data demonstrate that the administration of recombinant TRAIL ameliorates the severity of STZ-induced type 1 diabetes, and this effect was accompanied by the upregulation of SOCS1 expression.&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/20185810?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Fabretto, Antonella</style></author><author><style face="normal" font="default" size="100%">Kutsche, Kerstin</style></author><author><style face="normal" font="default" size="100%">Harmsen, May-Britt</style></author><author><style face="normal" font="default" size="100%">Demarini, Sergio</style></author><author><style face="normal" font="default" size="100%">Gasparini, Paolo</style></author><author><style face="normal" font="default" size="100%">Fertz, Maria Cristina</style></author><author><style face="normal" font="default" size="100%">Zenker, Martin</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Two cases of Noonan syndrome with severe respiratory and gastroenteral involvement and the SOS1 mutation F623I.</style></title><secondary-title><style face="normal" font="default" size="100%">Eur J Med Genet</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Eur J Med Genet</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Child, Preschool</style></keyword><keyword><style  face="normal" font="default" size="100%">Genes, ras</style></keyword><keyword><style  face="normal" font="default" size="100%">Germ-Line Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Heterozygote</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</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%">Noonan Syndrome</style></keyword><keyword><style  face="normal" font="default" size="100%">Phenotype</style></keyword><keyword><style  face="normal" font="default" size="100%">SOS1 Protein</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-Oct</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">53</style></volume><pages><style face="normal" font="default" size="100%">322-4</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Noonan syndrome (NS) is an autosomal dominant, inherited disorder characterized by facial dysmorphism, congenital heart defects, and reduced postnatal growth. Dysregulated RAS-MAPK signalling is the common molecular basis for NS, a genetically heterogeneous disease. Germline mutations in genes encoding small GTPases of the RAS family (KRAS and NRAS), modulators of RAS function (PTPN11, SOS1 and SHOC2) or downstream signal transducers (RAF1) are causative for NS. SOS1 is the second major gene for NS after PTPN11. Compared to patients with mutations in other genes, SOS1 mutation-positive individuals in general tend to have a more favorable outcome, with less short stature and cognitive impairment. We describe two unrelated patients with NS carrying the same heterozygous SOS1 missense mutation (c.1867T &gt; A/p.F623I). The phenotype of both patients is remarkable as they show uncommon clinical features such as pulmonary lymphangiectasis, congenital pleural effusions, severe feeding problems, and laryngomalacia. These findings may be related to the specific mutation present in our two patients, or be part of the SOS1 phenotype. Detailed clinical assessment of large cohorts of patients with NS and SOS1 mutation is required to clarify this initial observation.&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/20673819?dopt=Abstract</style></custom1></record></records></xml>