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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-d-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 2, 4, 6-trinitrobenzene sulfonic acid (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 4,440 differentially-expressed genes (DEGs) in murine TNBS-mediated injury and 1,377 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. CONCLUSION: 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 RH ; Flores-Torres J ; Torres BA ; Maheshwari A Pediatr Res 2017[Jan]; 81 (1-1 ): 99-112 PMID27656771 show ga BACKGROUND: We have shown previously that enteral administration of 2, 4, 6-trinitrobenzene sulfonic acid in 10-d-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 2, 4, 6-trinitrobenzene sulfonic acid (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 4,440 differentially-expressed genes (DEGs) in murine TNBS-mediated injury and 1,377 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. CONCLUSION: Murine neonatal TNBS-mediated enterocolitis and human NEC activate nearly-identical biological processes, signaling pathways, and transcriptional networks. |Animals [MESH] |Animals, Newborn [MESH] |Disease Models, Animal [MESH] |Enterocolitis, Necrotizing/etiology/*genetics [MESH] |Gene Expression Profiling [MESH] |Gene Regulatory Networks/*drug effects [MESH] |Humans [MESH] |Intestinal Mucosa/*metabolism [MESH] |Intestines/drug effects/*injuries [MESH] |Lipopolysaccharides/toxicity [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Species Specificity [MESH]Trinitrobenzene sulfonic acid-induced intestinal injury in neonatal mi(epmc).pdf DeepDyve Pubget Overpricing