<?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%">Lucafò, Marianna</style></author><author><style face="normal" font="default" size="100%">Di Silvestre, Alessia</style></author><author><style face="normal" font="default" size="100%">Romano, Maurizio</style></author><author><style face="normal" font="default" size="100%">Avian, Alice</style></author><author><style face="normal" font="default" size="100%">Antonelli, Roberta</style></author><author><style face="normal" font="default" size="100%">Martelossi, Stefano</style></author><author><style face="normal" font="default" size="100%">Naviglio, Samuele</style></author><author><style face="normal" font="default" size="100%">Tommasini, Alberto</style></author><author><style face="normal" font="default" size="100%">Stocco, Gabriele</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%">De Iudicibus, Sara</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Role of the Long Non-Coding RNA Growth Arrest-Specific 5 in Glucocorticoid Response in Children with Inflammatory Bowel Disease.</style></title><secondary-title><style face="normal" font="default" size="100%">Basic Clin Pharmacol Toxicol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Basic Clin. Pharmacol. Toxicol.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Biomarkers</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Line, Tumor</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Child</style></keyword><keyword><style  face="normal" font="default" size="100%">Drug Resistance</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Knockdown Techniques</style></keyword><keyword><style  face="normal" font="default" size="100%">Glucocorticoids</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Inflammatory Bowel Diseases</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Patient Selection</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharmacogenomic Testing</style></keyword><keyword><style  face="normal" font="default" size="100%">Precision Medicine</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Long Noncoding</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Small Interfering</style></keyword><keyword><style  face="normal" font="default" size="100%">Treatment Outcome</style></keyword><keyword><style  face="normal" font="default" size="100%">Up-Regulation</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</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">122</style></volume><pages><style face="normal" font="default" size="100%">87-93</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Glucocorticoids (GCs) are widely employed in inflammatory, autoimmune and neoplastic diseases, and, despite the introduction of novel therapies, remain the first-line treatment for inducing remission in inflammatory bowel disease (IBD). Given the high incidence of suboptimal response, associated with a significant number of side-effects, that are particularly severe in paediatric patients, the identification of subjects that are most likely to respond poorly to GCs is extremely important. Recent evidence suggests that the long non-coding RNA (lncRNA) GAS5 could be a potential marker of GC resistance. To address this issue, we evaluated the association between the lncRNA GAS5 and the efficacy of steroids, in terms of inhibition of proliferation, in two cell lines derived from colon and ovarian cancers, to confirm the sensitivity and specificity of these lncRNAs. These cells showed a different sensitivity to GCs and revealed differential expression of GAS5 after treatment. GAS5 was up-regulated in GC-resistant cells and accumulated more in the cytoplasm compared to the nucleus in response to the drug. The functions of GAS5 were assessed by silencing, and we found that GAS5 knock-down reduced the proliferation during GC treatment. Furthermore, for the first time, we measured GAS5 levels in 19 paediatric IBD patients at diagnosis and after the first cycle of GCs, and we demonstrated an up-regulation of the lncRNA in patients with unfavourable steroid response. Our preliminary results indicate that GAS5 could be considered a novel pharmacogenomic marker useful for the personalization of GC therapy.&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/28722800?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Celsi, Fulvio</style></author><author><style face="normal" font="default" size="100%">Piscianz, Elisa</style></author><author><style face="normal" font="default" size="100%">Romano, Maurizio</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%">Knockdown of MVK does not lead to changes in NALP3 expression or activation.</style></title><secondary-title><style face="normal" font="default" size="100%">J Inflamm (Lond)</style></secondary-title><alt-title><style face="normal" font="default" size="100%">J Inflamm (Lond)</style></alt-title></titles><dates><year><style  face="normal" font="default" size="100%">2015</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2015</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">12</style></volume><pages><style face="normal" font="default" size="100%">7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;BACKGROUND: &lt;/b&gt;Mutations in the Mevalonate Kinase gene (MVK) are causes of a rare autoinflammatory disease: Mevalonate Kinase Deficiency and its more acute manifestation, Mevalonic Aciduria. The latter is characterized, among other features, by neuroinflammation, developmental delay and ataxia, due to failed cerebellar development or neuronal death through chronic inflammation. Pathogenesis of neuroinflammation in Mevalonate Kinase Deficiency and Mevalonic Aciduria has not yet been completely clarified, however different research groups have been suggesting the inflammasome complex as the key factor in the disease development. A strategy to mimic this disease is blocking the mevalonate pathway, using HMG-CoA reductase inhibitors (Statins), while knock-out mice for Mevalonate Kinase are non-vital and their hemyzygous (i.e only one copy of gene preserved) littermate display almost no pathological features.&lt;/p&gt;&lt;p&gt;&lt;b&gt;FINDINGS: &lt;/b&gt;We sought to generate a murine cellular model closely resembling the pathogenic conditions found in vivo, by direct silencing of Mevalonate Kinase gene. Knockdown of Mevalonate Kinase in a murine microglial cellular model (BV-2 cells) results in neither augmented NALP3 expression nor increase of apoptosis. On the contrary, statin treatment of BV-2 cells produces an increase both in Mevalonate Kinase and NALP3 expression.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSIONS: &lt;/b&gt;MKD deficiency could be due or affected by protein accumulation leading to NALP3 activation, opening novel questions about strategies to tackle this disease.&lt;/p&gt;</style></abstract><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/25663823?dopt=Abstract</style></custom1></record></records></xml>