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| 1 | Comparison of the chloride channel activator lubiprostone and the oral laxative Polyethylene Glycol 3350 on mucosal barrier repair in ischemic-injured porcine intestine显示文摘AIM: To investigate the effects of lubiprostone and Polyethylene Glycol 3350 (PEG) on mucosal barrier repair in ischemic-injured porcine intestine. METHODS: Ileum from 6 piglets (approximately 15 kg body weight) was subjected to ischemic conditions by occluding the local mesenteric circulation for 45 min in vivo. Ileal tissues from each pig were then harvested and mounted in Ussing chambers and bathed in oxygenated Ringer's solution in vitro. Intestinal barrier function was assessed by measuring transepithelial electrical resistance (TER) and mucosal-to-serosal fluxes of 3H-mannitol and 14C-inulin. Statistical analyses of data collected over a 120-min time course included 2-way ANOVA for the effects of time and treatment on indices of barrier function. RESULTS: Application of 1 μmol/L lubiprostone to the mucosal surface of ischemic-injured ileum in vitro induced significant elevations in TER compared to non-treated tissue. Lubiprostone also reduced mucosal-to-serosal fluxes of 3H-mannitol and 14C-inulin. Alternatively,application of a polyethylene laxative (PEG,20 mmol/L) to the mucosal surface of ischemic tissues significantly increased flux of 3H-mannitol and 14C-inulin. CONCLUSION: This experiment demonstrates that lubiprostone stimulates recovery of barrier function in ischemic intestinal tissues whereas the PEG laxative had deleterious effects on mucosal repair. These results suggest that,unlike osmotic laxatives,lubiprostone stimulates repair of the injured intestinal barrier. | Adam J Moeser Prashant K Nighot Birgit Roerig Ryuji Ueno Anthony T Blikslager | 2008 | World Journal of Gastroenterology2008，14，39： | 2 |
| 2 | Incorporating Station-related Outages in Composite System Reliability Analysis显示文摘 | BILLINTON R NIGHOT R | | 0，，02： | 1 |
| 3 | Reliability Evaluation of the IEEERTS Incorporating Station Related Outages显示文摘 | NIGHOT R BILLINTON R | | 0，，： | 1 |
| 4 | Emergence of a nephropathogenic avian infectious bronchitis virus with a novel genotype in India显示文摘 | Bayry J Goudar M S Nighot P K | 2005 | J Clin Microbiol2005，43，2： | 1 |
| 5 | Emergence of a nephropatbogenic avian infectious bronchitis virus with a novel genotype in India显示文摘 | BAYRY J GOUDAR M S NIGHOT P K | 2005 | J Clin Microbiol2005，43，2： | 1 |
| 6 | Emergence of a nephropathogenic avian Infectious Bronchitis virus with a novel genotype in India 显示文摘 | Bayry J Goudar M S Nighot P K et aI | 2005 | J Clin Microbiol2005，43，2： | 1 |
| 7 | Gas- trointestinal dysfunction induced by early weaning is attenuated by delayed weaning and mast cell blockade in pigs 显示文摘 | MOESER A J RYAN K A NIGHOT P K | 2007 | American Journal of Physiology : Gastroin- testinal and Liver Physiology2007，293，2： | 1 |
| 8 | Gastrointestinal dysfunction induced by early weaning is attenuated by de?layed weaning and mast cell blockade in pigs显示文摘 | Moeser AJ K A Ryan P K Nighot | 2007 | AmericanJournal of Physiology - Gastrointestinal and Liver Physiolo?gy2007，293，2： | 1 |
| 9 | Physiopathology of avian respiratory disease显示文摘 | Nighot P K | 2002 | Poultry International2002，8，： | 1 |
| 10 | Gastrointestinal dys- function induced by early weaning is attenuated by delayed wean- ing and mast cell blockade in pigs 显示文摘 | Moeser A J Ryan K A Nighot P K | 2007 | Am J Physiol-Gastr L2007，293，： | 1 |
| 11 | ClC-2 is required for rapid restoration of epit helial tight junctions in ischemicinjured murine jejunum显示文摘 | Nighot PK Moeser AJ Ryan KA | 2009 | Exp Cell Res2009，315，1： | 1 |
| 12 | Emergence of a Nephropathogenic Avian Infectious Bronchitis Virus with a Novel Genotype in India显示文摘 | Jagadeesh Bayry Mallikarjun S Goudar Prashant K Nighot | 2004 | Journal of clinical microbiology2004，43，： | 1 |
| 13 | Emergence of a nephropathogenic avian infectious bronchitis virus with a novel genotype in India 显示文摘 | Bayry J Goudar M S Nighot P K Kshirsagar S G Lad- man B S Gelb J Jr Ghalsasi G R Kohe G N | 2005 | Journal of Clinical Microbiology2005，43，： | 1 |
| 14 | Chloride channel ClC-2 modulates tight junction barrier function via intracellular trafficking of occludin 显示文摘 | Nighot PK Blikslager AT | 2012 | Am J Physiol Cell Physiol2012，302，1： | 1 |
| 15 | TGF-beta-activated kinase 1 signaling maintains intestinal integrity by preventing accumu- lation of reactive oxygen species in the intestinal epithelium 显示文摘 | Kajino-Sakamoto R Omori E Nighot PK | 2010 | J Immunol2010，185，8： | 1 |
| 16 | Gastrointestinal dys- function induced by early weaning is attenuated by delayed wean-ing and mast cell blockade in pigs 显示文摘 | Moeser A J Ryan K A Nighot P K et ol | 2007 | Am J Physiol Gastrointest Liver Physiol2007，293，： | 1 |
| 17 | Gastrointestinal dys function induced by early weaningis attenuated by delayed wea ning and mast cell blockade in pigs显示文摘 | Moeser A J Ryan K A Nighot P K | 2007 | J Physiol Gastrointest Liver Physiol2007，293，2： | 1 |
| 18 | Diclofenac poisoning is widespread in declining vulture populations across the Indian subcontinent显示文摘 | Shultz S Baral HS Charman S Cunningham AA Das D Ghalsasi GR Goudar MS Green RE Jones A Nighot P Pain DJ Prakash V | | 0，，6： | 1 |
| 19 | Emergence ofa ne- phrupathogenic avian infectious bronchitis virus with a novel geno- type in India显示文摘 | BAYRY J GOUDAR M S NIGHOT P K | | J Clin Micrubiol0，43，2： | 1 |
| 20 | Gastro protective properties of the novel prostone SPI-8811 against acid-injured porcine mucosa显示文摘AIM:To evaluate the protective properties of novel prostone ClC-2 agonist SPI-8811 in porcine model of gastric acid injury. METHODS:Porcine gastric mucosa was mounted in Ussing chambers and injured by bathing mucosal tissues in an HCl Ringer's solution (pH = 1.5) with or without SP1-8811 (1 μmol/L), cystic fibrosis transmem-brane conductance regulator (CFTR) inhibitor (inhibitor 172, 10 μmol/L, apical) and ClC-2 inhibitor ZnCl 2 , 300 μmol/L, apical), on the apical surface of tissues. Transepithelial resistance and mucosal-to-serosal 3 H-mannitol fluxes were measured over a 90-min period. Tissues were analyzed by morph metric techniques, Immunofluorescence and by western blots. RESULTS:Compared with control tissues, acid exposure decreased transepithelial electrical resistance (TER) and increased 3 H-mannitol flux. Pretreatment of gastric mucosa with SPI-8811 was protective against acid-induced decreases in TER (TER, 50 Ω . cm 2 vs 100 Ω . cm 2 ) and abolished increases in flux ( 3 H-mannitol flux, 0.10 μmol/L . cm 2 vs 0.04 μmol/L . cm 2 ). Evidence of histological damage in the presence of acid was markedly at- tenuated by SPI-0811. Immunofluorescence and western analysis for occludin revealed enhanced localization to the region of the tight junction (TJ) after treatment with SPI-8811. Pretreatment with the ClC-2 inhibitor ZnCl 2 , but not the selective CFTR inhibitor 172, attenuated SPI-8811-mediated mucosal protection, suggesting a role for ClC-2. Prostone may serve both protective and reparative roles in injured tissues. CONCLUSION: ClC-2 agonist SPI-8811 stimulated enhancement of mucosal barrier function by protecting TJ protein occludin in porcine gastric mucosa and thus protected the gastric acid injury in porcine stomach. | Meghali Nighot Adam Moeser Ryuji Ueno Anthony Blikslager | 2012 | World Journal of Gastroenterology2012，18，34： | 0 |
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