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10.1038/pr.2016.189 http://scihub22266oqcxt.onion/10.1038/pr.2016.189 C5235988!5235988!27656771     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27656771&cmd=llinks): Failed to open stream: HTTP request failed! 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Trinitrobenzene Sulfonic Acid-induced Intestinal Injury in Neonatal Mice Activates Transcriptional Networks Similar to those seen in Human Necrotizing Enterocolitis |pdf=|usr=}}{{27656771}} gab.com Text Trinitrobenzene Sulfonic Acid-induced Intestinal Injury in Neonatal Mice Activates Transcriptional Networks Similar to those seen in Human Necrotizing Enterocolitis JO: Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=27656771 #FOAvip Background: We have shown previously that enteral administration of 2, 4, 6-trinitrobenzene sulfonic acid in 10-day-old C57BL/6 pups produces an acute necrotizing enterocolitis with histopathological and inflammatory changes similar to human necrotizing enterocolitis (NEC). To determine whether murine neonatal TNBS-mediated intestinal injury could be used as a NEC model, we compared gene expression profiles of TNBS-mediated intestinal injury and NEC. Methods: Whole genome microarray analysis was performed on proximal colon from control and TNBS-treated pups (n=8/group). For comparison, we downloaded human microarray data of NEC (n=5) and surgical control (n=4) from a public database. Data were analyzed using the software programs Partek Genomics Suite and Ingenuity Pathway Analysis. Results: We detected extensive changes in gene expression in murine TNBS-mediated intestinal injury and human NEC. Using fold-change cut-offs of ±1.5, we identified 4440 differentially-expressed genes (DEGs) in murine TNBS-mediated injury and 1377 in NEC. Murine TNBS-mediated injury and NEC produced similar changes in expression of orthologous genes (r = 0.611, p<0.001), and also activated nearly-identical biological processes and pathways. Lipopolysaccharide was top predicted upstream regulator in both the murine and human datasets. Conclusions: Murine neonatal TNBS-mediated enterocolitis and human NEC activate nearly-identical biological processes, signaling pathways, and transcriptional networks. Twit Text FOAVip Trinitrobenzene Sulfonic Acid-induced Intestinal Injury in Neonatal Mice Activates Transcriptional Networks Similar to those seen in Human Necrotizing Enterocolitis ????Pediatr Res http://www.kidney.de/pget.php?&tw=1&pmid=27656771 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27656771 #FOAvip English Wikipedia <ref>{{Cite pmid|27656771}}</ref> Trinitrobenzene Sulfonic Acid-induced Intestinal Injury in Neonatal Mice Activates Transcriptional Networks Similar to those seen in Human Necrotizing Enterocolitis #MMPMID27656771 MohanKumar K; Namachivayam K; Cheng F; Jiang RHY; Flores-Torres J; Torres BA; Maheshwari A Pediatr Res 2017[Jan]; 81 (1-1): 99-112 PMID27656771show ga Background: We have shown previously that enteral administration of 2, 4, 6-trinitrobenzene sulfonic acid in 10-day-old C57BL/6 pups produces an acute necrotizing enterocolitis with histopathological and inflammatory changes similar to human necrotizing enterocolitis (NEC). To determine whether murine neonatal TNBS-mediated intestinal injury could be used as a NEC model, we compared gene expression profiles of TNBS-mediated intestinal injury and NEC. Methods: Whole genome microarray analysis was performed on proximal colon from control and TNBS-treated pups (n=8/group). For comparison, we downloaded human microarray data of NEC (n=5) and surgical control (n=4) from a public database. Data were analyzed using the software programs Partek Genomics Suite and Ingenuity Pathway Analysis. Results: We detected extensive changes in gene expression in murine TNBS-mediated intestinal injury and human NEC. Using fold-change cut-offs of ±1.5, we identified 4440 differentially-expressed genes (DEGs) in murine TNBS-mediated injury and 1377 in NEC. Murine TNBS-mediated injury and NEC produced similar changes in expression of orthologous genes (r = 0.611, p<0.001), and also activated nearly-identical biological processes and pathways. Lipopolysaccharide was top predicted upstream regulator in both the murine and human datasets. Conclusions: Murine neonatal TNBS-mediated enterocolitis and human NEC activate nearly-identical biological processes, signaling pathways, and transcriptional networks. äTrinitrobenzene Sulfonic Acid-induced Intestinal Injury in Neonatal Mi(epmc).pdf DeepDyve Pubget Overpricing