<?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%">Fichera, A</style></author><author><style face="normal" font="default" size="100%">Pagani, G</style></author><author><style face="normal" font="default" size="100%">Stagnati, V</style></author><author><style face="normal" font="default" size="100%">Cascella, S</style></author><author><style face="normal" font="default" size="100%">Faiola, S</style></author><author><style face="normal" font="default" size="100%">Gaini, C</style></author><author><style face="normal" font="default" size="100%">Lanna, M</style></author><author><style face="normal" font="default" size="100%">Pasquini, L</style></author><author><style face="normal" font="default" size="100%">Raffaelli, R</style></author><author><style face="normal" font="default" size="100%">Stampalija, T</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Prefumo, F</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Cervical-length measurement in mid-gestation to predict spontaneous preterm birth in asymptomatic triplet pregnancy.</style></title><secondary-title><style face="normal" font="default" size="100%">Ultrasound Obstet Gynecol</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Ultrasound Obstet Gynecol</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Cervical Length Measurement</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gestational Age</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Infant, Newborn</style></keyword><keyword><style  face="normal" font="default" size="100%">Logistic Models</style></keyword><keyword><style  face="normal" font="default" size="100%">Predictive Value of Tests</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy</style></keyword><keyword><style  face="normal" font="default" size="100%">Pregnancy, Triplet</style></keyword><keyword><style  face="normal" font="default" size="100%">Premature Birth</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2018</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2018 May</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">51</style></volume><pages><style face="normal" font="default" size="100%">614-620</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;&lt;b&gt;OBJECTIVE: &lt;/b&gt;To assess the predictive value of sonographic cervical-length (CL) measurement in mid-gestation for spontaneous preterm birth (PTB) in asymptomatic triplet pregnancy.&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;This was a retrospective study of asymptomatic triplet pregnancies followed at five Italian tertiary referral centers, between 2002 and 2015. CL was measured transvaginally between 18 and 24 weeks' gestation. Pregnancies with medically indicated PTB were excluded. Demographic and pregnancy characteristics of pregnancies complicated by PTB were analyzed and the distributions of CL measurements in these patients were calculated. Logistic regression analysis was performed to assess the association between CL and PTB, adjusted for confounders. Performance of CL measurement in prediction of PTB &lt; 28, &lt; 30 and &lt; 32 weeks of gestation was assessed.&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;A total of 120 triplet pregnancies were included in the final analysis. Median CL was 35 (interquartile range (IQR), 29-40) mm measured at a median gestational age of 20 + 2 (IQR, 20 + 0 to 23 + 4) weeks. Overall, 23 (19.2%), 17 (14.2%) and eight (6.7%) patients had a CL &lt; 25, &lt; 20 and &lt; 15 mm, respectively. Spontaneous PTB &lt; 32 weeks occurred in 41 (34.2%) cases, &lt; 30 weeks in 23 (19.2%) and &lt; 28 weeks in 12 (10%) cases. CL &lt; 15 mm was significantly more frequent in the group of patients who delivered &lt; 28 (P = 0.03) and &lt; 30 (P = 0.01) weeks' gestation, compared with those who delivered after 28 and after 30 weeks, respectively, while CL &lt; 20 mm was more common in triplet pregnancies with delivery &lt; 32 weeks compared with those delivered ≥ 32 weeks (P = 0.03). Logistic regression analysis was possible only for PTB &lt; 32 weeks due to the small number of cases that delivered &lt; 30 and &lt; 28 weeks. After adjustment for confounders, CL was not significantly associated with PTB &lt; 32 weeks (adjusted odds ratio, 0.97; 95% CI, 0.94-1.01). CL measurement had an area under the receiver-operating characteristics curve of 0.41 (95% CI, 0.20-0.62), 0.41 (95% CI, 0.26-0.56) and 0.42 (95% CI, 0.31-0.54) for the prediction of spontaneous PTB &lt; 28, &lt; 30 and &lt; 32 weeks, respectively.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;CL assessed in mid-gestation is a poor predictor of PTB &lt; 28, &lt; 30 and &lt; 32 weeks' gestation in asymptomatic triplet pregnancy. Copyright © 2017 ISUOG. Published by John Wiley &amp; Sons Ltd.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">5</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/28295801?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Lucafo, M</style></author><author><style face="normal" font="default" size="100%">De Iudicibus, S</style></author><author><style face="normal" font="default" size="100%">Di Silvestre, A</style></author><author><style face="normal" font="default" size="100%">Pelin, M</style></author><author><style face="normal" font="default" size="100%">Candussio, L</style></author><author><style face="normal" font="default" size="100%">Martelossi, S</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Piscianz, E</style></author><author><style face="normal" font="default" size="100%">Ventura, A</style></author><author><style face="normal" font="default" size="100%">Decorti, G</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Long noncoding RNA GAS5: a novel marker involved in glucocorticoid response.</style></title><secondary-title><style face="normal" font="default" size="100%">Curr Mol Med</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Curr. Mol. Med.</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Adult</style></keyword><keyword><style  face="normal" font="default" size="100%">Cell Proliferation</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Gene Expression Regulation</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%">Leukocytes, Mononuclear</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Methylprednisolone</style></keyword><keyword><style  face="normal" font="default" size="100%">Middle Aged</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Glucocorticoid</style></keyword><keyword><style  face="normal" font="default" size="100%">RNA, Long Noncoding</style></keyword><keyword><style  face="normal" font="default" size="100%">Transcription, Genetic</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%">15</style></volume><pages><style face="normal" font="default" size="100%">94-9</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Glucocorticoids (GCs) exert their effects through regulation of gene expression after activation in the cytoplasm of the glucocorticoid receptor (GR) encoded by NR3C1 gene. A negative feedback mechanism resulting in GR autoregulation has been demonstrated through the binding of the activated receptor to intragenic sequences called GRE-like elements, contained in GR gene. The long noncoding RNA growth arrest-specific transcript 5 (GAS5) interacts with the activated GR suppressing its transcriptional activity. The aim of this study was to evaluate the possible role of GAS5 and NR3C1 gene expression in the antiproliferative effect of methylprednisolone in peripheral blood mononuclear cells and to correlate the expression with individual sensitivity to GCs. Subjects being poor responders to GCs presented higher levels of GAS5 and NR3C1 in comparison with good responders. We suggest that abnormal levels of GAS5 may alter GC effectiveness, probably interfering with the mechanism of GR autoregulation.&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/25601472?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Faletra, F</style></author><author><style face="normal" font="default" size="100%">Berti, I</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Pecile, V</style></author><author><style face="normal" font="default" size="100%">Cleva, L</style></author><author><style face="normal" font="default" size="100%">Alberini, E</style></author><author><style face="normal" font="default" size="100%">Bruno, I</style></author><author><style face="normal" font="default" size="100%">Gasparini, P</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Phylloid pattern of hypomelanosis closely related to chromosomal abnormalities in the 13q detected by SNP array analysis.</style></title><secondary-title><style face="normal" font="default" size="100%">Dermatology</style></secondary-title><alt-title><style face="normal" font="default" size="100%">Dermatology (Basel)</style></alt-title></titles><keywords><keyword><style  face="normal" font="default" size="100%">Chromosomes, Human, Pair 13</style></keyword><keyword><style  face="normal" font="default" size="100%">Humans</style></keyword><keyword><style  face="normal" font="default" size="100%">Hypopigmentation</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mosaicism</style></keyword><keyword><style  face="normal" font="default" size="100%">Oligonucleotide Array Sequence Analysis</style></keyword><keyword><style  face="normal" font="default" size="100%">Polymorphism, Single Nucleotide</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2012</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2012</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">225</style></volume><pages><style face="normal" font="default" size="100%">294-7</style></pages><language><style face="normal" font="default" size="100%">eng</style></language><abstract><style face="normal" font="default" size="100%">&lt;p&gt;Phylloid hypomelanosis is a distinct type of pigmentary mosaicism characterized by congenital hypochromic macules resembling a floral ornament with various elements such as round or oval patches, asymmetrical macules similar to begonia leaves, or oblong lesions. It has been found to be predominantly associated with abnormalities in chromosome 13 and sometimes as-sociated with different extracutaneous abnormalities. Here, we report 2 new cases of phylloid hypomelanosis due to mosaicism involving chromosome 13. The first one is a mosaicism for a supernumerary marker belonging to chromosome 13 and the second one is the first report of phylloid hypomelanosis associated with a mosaic deletion of 13q. Because of the extremely low level of mosaicism in these 2 cases, SNP array analysis on skin fibroblasts was carried out, showing a 13q21.33-q34 duplication (71,024,411-115,103,529) and a 13q13.3-q34 (38,368,012-115,103,529) deletion. Both cases underline on the one hand the strict connection between phylloid hypomelanosis and anomalies of chromosome 13, and on the other hand the relevance of the SNP array analysis on skin fibroblasts in the detection of low-level mosaicism.&lt;/p&gt;</style></abstract><issue><style face="normal" font="default" size="100%">4</style></issue><custom1><style face="normal" font="default" size="100%">http://www.ncbi.nlm.nih.gov/pubmed/23095783?dopt=Abstract</style></custom1></record><record><source-app name="Biblio" version="7.x">Drupal-Biblio</source-app><ref-type>17</ref-type><contributors><authors><author><style face="normal" font="default" size="100%">Pelagatti, M A</style></author><author><style face="normal" font="default" size="100%">Meini, A</style></author><author><style face="normal" font="default" size="100%">Caorsi, R</style></author><author><style face="normal" font="default" size="100%">Cattalini, M</style></author><author><style face="normal" font="default" size="100%">Federici, S</style></author><author><style face="normal" font="default" size="100%">Zulian, F</style></author><author><style face="normal" font="default" size="100%">Calcagno, G</style></author><author><style face="normal" font="default" size="100%">Tommasini, A</style></author><author><style face="normal" font="default" size="100%">Bossi, G</style></author><author><style face="normal" font="default" size="100%">Sormani, M P</style></author><author><style face="normal" font="default" size="100%">Caroli, F</style></author><author><style face="normal" font="default" size="100%">Plebani, A</style></author><author><style face="normal" font="default" size="100%">Ceccherini, I</style></author><author><style face="normal" font="default" size="100%">Martini, A</style></author><author><style face="normal" font="default" size="100%">Gattorno, M</style></author></authors></contributors><titles><title><style face="normal" font="default" size="100%">Long-term clinical profile of children with the low-penetrance R92Q mutation of the TNFRSF1A gene.</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%">Antirheumatic Agents</style></keyword><keyword><style  face="normal" font="default" size="100%">Biological Therapy</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%">Familial Mediterranean Fever</style></keyword><keyword><style  face="normal" font="default" size="100%">Female</style></keyword><keyword><style  face="normal" font="default" size="100%">Fever</style></keyword><keyword><style  face="normal" font="default" size="100%">Follow-Up Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Genotype</style></keyword><keyword><style  face="normal" font="default" size="100%">Health Surveys</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%">Interleukin 1 Receptor Antagonist Protein</style></keyword><keyword><style  face="normal" font="default" size="100%">Longitudinal Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Lymphadenitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Male</style></keyword><keyword><style  face="normal" font="default" size="100%">Mutation</style></keyword><keyword><style  face="normal" font="default" size="100%">Pharyngitis</style></keyword><keyword><style  face="normal" font="default" size="100%">Quality of Life</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Tumor Necrosis Factor</style></keyword><keyword><style  face="normal" font="default" size="100%">Receptors, Tumor Necrosis Factor, Type I</style></keyword><keyword><style  face="normal" font="default" size="100%">Recurrence</style></keyword><keyword><style  face="normal" font="default" size="100%">Retrospective Studies</style></keyword><keyword><style  face="normal" font="default" size="100%">Steroids</style></keyword><keyword><style  face="normal" font="default" size="100%">Syndrome</style></keyword></keywords><dates><year><style  face="normal" font="default" size="100%">2011</style></year><pub-dates><date><style  face="normal" font="default" size="100%">2011 Apr</style></date></pub-dates></dates><volume><style face="normal" font="default" size="100%">63</style></volume><pages><style face="normal" font="default" size="100%">1141-50</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 analyze the long-term impact of the R92Q mutation of TNFRSF1A in children with periodic fever, in comparison with children with tumor necrosis factor receptor-associated periodic syndrome (TRAPS) with TNFRSF1A structural mutations and children with periodic fever of unknown origin fulfilling the criteria for periodic fever, aphthosis, pharyngitis, and adenitis syndrome (PFAPA).&lt;/p&gt;&lt;p&gt;&lt;b&gt;METHODS: &lt;/b&gt;The extracellular region of TNFRSF1A was analyzed in 720 consecutive children with periodic fever, using denaturing high-performance liquid chromatography and DNA sequencing. Followup data on 11 pediatric patients with TNFRSF1A structural mutations (cysteine or T50M), 23 pediatric patients with an R92Q substitution, and 64 pediatric patients with PFAPA were collected during routine clinic visits. The 50-item Child Health Questionnaire was used to assess health-related quality of life (HRQOL).&lt;/p&gt;&lt;p&gt;&lt;b&gt;RESULTS: &lt;/b&gt;The frequency of typical TRAPS-related clinical manifestations was significantly lower and the impact of the disease on HRQOL was significantly reduced in patients with the R92Q mutation compared with TRAPS patients carrying structural mutations of TNFRSF1A. Followup data on 11 TRAPS patients with TNFRSF1A structural mutations (mean followup 7.9 years), 16 patients with theR92Q substitution (mean followup 7.3 years), and 64 patients with PFAPA (mean followup 5.2 years) were available. Patients with R92Q mutations and patients with PFAPA displayed a higher rate of self-resolution or amelioration of the fever episodes than did TRAPS patients with structural mutations.&lt;/p&gt;&lt;p&gt;&lt;b&gt;CONCLUSION: &lt;/b&gt;Although some cases may progress to a more chronic disease course, the majority of children with an R92Q mutation of the TNFRSFA1 gene show a milder disease course than that in children with TNFRSFA1 structural mutations and have a high rate of spontaneous resolution and amelioration of the recurrent fever episodes.&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/21225694?dopt=Abstract</style></custom1></record></records></xml>