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Because hepatic steatosis has recently been associated with a lysosomal pathway of apoptosis, our aim was to determine whether this cell-death pathway contributes to CI\u002FWR injury of steatotic livers. Wild-type and cathepsin B-knockout ( Ctsb\u003Cjats:sup> −\u002F−\u003C\u002Fjats:sup>) mice were fed the methionine\u002Fcholine-deficient (MCD) diet for 2 wk to induce hepatic steatosis. Mouse livers were stored in the University of Wisconsin solution for 24 h at 4°C and reperfused for 1 h at 37°C in vitro. Immunofluorescence analysis of the lysosomal enzymes cathepsin B and D showed a punctated intracellular pattern consistent with lysosomal localization in wild-type mice fed a standard diet after CI\u002FWR injury. In contrast, cathepsin B and D fluorescence became diffuse in livers from wild-type mice fed MCD diet after CI\u002FWR, indicating that lysosomal permeabilization had occurred. Hepatocyte apoptosis was rare in both normal and steatotic livers in the absence of CI\u002FWR injury but increased in wild-type mice fed an MCD diet and subjected to CI\u002FWR injury. In contrast, hepatocyte apoptosis and liver damage were reduced in Ctsb\u003Cjats:sup> −\u002F−\u003C\u002Fjats:sup> and cathepsin B inhibitor-treated mice fed the MCD diet following CI\u002FWR injury. In conclusion, these findings support a prominent role for the lysosomal pathway of apoptosis in steatotic livers following CI\u002FWR injury. \u003C\u002Fjats:p>",{"EN":857},"Cathepsin B inactivation attenuates hepatocyte apoptosis and liver damage in steatotic livers after cold ischemia-warm reperfusion injury",{"VOID":859},"15472011",{"VOID":861},"10.1152\u002Fajpgi.00316.2004",[154],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpgi.00316.2004",[865,885,902,919,936,951,966],{"id":866,"sortIndex":329,"researcher":24,"roles":867,"affiliations":868,"properties":880},"6d2ee51b-7fd9-4e9b-af84-9fafd2f292e1",[],[869],{"id":870,"sortIndex":25,"affiliation":871,"properties":24},"2d078199-1973-4ee0-ba3c-905fa3d77d56",{"id":872,"createTime":873,"updateTime":874,"relativeEntities":875,"slug":876,"properties":877,"entityType":69,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"06ab9428-ad2e-42b7-88b7-f0bf8ff5c662","2024-02-13T17:32:12.199+00:00","2025-06-11T19:43:55.603+00:00",[],"Mayo-Clinic-College-of-Medicine-Rochester-Minnesota",{"title":878},{"VI":879},"Mayo Clinic, College of Medicine, Rochester, Minnesota",{"openalex":881,"title":883},{"VOID":882},"A5081293248",{"EN":884},"Steven F. 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The rapid induction of liver cell death in rats fed a choline-deficient methionine low diet. Am J Pathol 113: 309–314, 1983.",{},{"id":24,"text":1056,"url":24,"identifiers":1057},"10.1002\u002Fhep.1840060331",{"doi":1056},{"id":24,"text":1059,"url":24,"identifiers":1060},"10.1172\u002FJCI9914",{"doi":1059},{"id":24,"text":1062,"url":24,"identifiers":1063},"10.1038\u002Fsj.onc.1207512",{"doi":1062},{"id":24,"text":1065,"url":24,"identifiers":1066},"10.1016\u002FS0002-9440(10)63056-8",{"doi":1065},{"id":24,"text":1068,"url":24,"identifiers":1069},"10.3109\u002F10520298109067302",{"doi":1068},{"id":24,"text":1071,"url":24,"identifiers":1072},"10.1007\u002Fs005340050064",{"doi":1071},{"id":24,"text":1074,"url":24,"identifiers":1075},"10.1080\u002F08941930390205773",{"doi":1074},{"id":24,"text":1077,"url":24,"identifiers":1078},"Kagedal K, Johansson U, and Ollinger K. The lysosomal protease cathepsin D mediates apoptosis induced by oxidative stress. 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In this study, we investigate whether the antigenic or bacterial content of the gut, after Hp eradication, influences the changes in gut function induced by chronic Hp infection. Mice were infected with Hp for 4 mo and then treated with antibiotics or placebo for 2 wk. Gastric emptying was measured using videofluoroscopy, feeding behavior using a 24-h feeding system, and intestinal permeability using an isolated jejunal segment arterially perfused with an artificial oxygen carrier, hemoglobin vesicles. Immune responses were assessed by CD3\u003Cjats:sup>+\u003C\u002Fjats:sup>cell counts and anti- Hp antibodies using ELISA. To determine the role of luminal factors in host physiology posteradication, groups of mice received the probiotics containing Lactobacillus rhamnosus R0011 and L. helveticus R0052 or placebo for 2 wk or crude Hp antigen weekly for 2 mo. Chronic Hp infection was associated with delayed gastric emptying, increased intestinal permeability, and increased gastric CD3\u003Cjats:sup>+\u003C\u002Fjats:sup>cell counts. Hp-induced altered feeding patterns did not reverse after eradication. Probiotics accelerated the recovery of paracellular permeability and delayed gastric emptying, improved the CD3\u003Cjats:sup>+\u003C\u002Fjats:sup>cell counts, and normalized altered feeding patterns posteradication. Hp antigen resulted in increased anti- Hp antibodies and increased CD3\u003Cjats:sup>+\u003C\u002Fjats:sup>cell counts in the stomach and delayed recovery of gastric function. Our results suggest that the bacterial content of the gut, as well as the presence of relevant antigens, influences the rate of recovery of host pathophysiology induced by chronic Hp infection. These changes do not seem to occur in association with modulation of intestinal permeability.\u003C\u002Fjats:p>",{"EN":1125},"The role of luminal factors in the recovery of gastric function and behavioral changes after chronic\u003Ci>Helicobacter pylori\u003C\u002Fi>infection",{"VOID":1127},"18653723",{"VOID":1129},"10.1152\u002Fajpgi.90316.2008","2024-10-14T23:27:52.041+00:00","Author affiliation is blank",[154],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpgi.90316.2008",[1135,1146,1157,1168,1177,1186,1195,1216,1225,1236,1247],{"id":1136,"sortIndex":347,"researcher":24,"roles":1137,"affiliations":1138,"properties":1139},"d0dfc3b1-f7aa-4f25-98d7-15a60ce2a276",[],[],{"openalex":1140,"orcid":1142,"title":1144},{"VOID":1141},"A5078805860",{"VOID":1143},"https:\u002F\u002Forcid.org\u002F0000-0002-0681-3032",{"EN":1145},"Hiromi Sakai",{"id":1147,"sortIndex":275,"researcher":24,"roles":1148,"affiliations":1149,"properties":1150},"4d8d7e12-8540-4b17-b55c-992af6241b77",[],[],{"openalex":1151,"orcid":1153,"title":1155},{"VOID":1152},"A5009882164",{"VOID":1154},"https:\u002F\u002Forcid.org\u002F0000-0003-2726-7613",{"EN":1156},"Jun Lü",{"id":1158,"sortIndex":407,"researcher":24,"roles":1159,"affiliations":1160,"properties":1161},"fdcd9746-1a41-48a9-abc8-81c3e09ecd66",[],[],{"openalex":1162,"orcid":1164,"title":1166},{"VOID":1163},"A5090507970",{"VOID":1165},"https:\u002F\u002Forcid.org\u002F0000-0003-1613-3732",{"EN":1167},"Stephen M. 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(Abstract)",{"doi":1331},"10.1016\u002FS0016-5085(00)83873-1",{"id":24,"text":1333,"url":24,"identifiers":1334},"10.1053\u002Fj.gastro.2006.05.053",{"doi":1333},{"id":24,"text":1336,"url":24,"identifiers":1337},"Marshall BJ, Warren JR.Unidentified curved bacilli in the stomach of patients with gastritis and peptic ulceration.Lancet16: 1311–1315, 1984.",{"doi":1338},"10.1016\u002FS0140-6736(84)91816-6",{"id":24,"text":1340,"url":24,"identifiers":1341},"10.1097\u002F00042737-199912000-00006",{"doi":1340},{"id":24,"text":1343,"url":24,"identifiers":1344},"Matysiak-Budnik T, Terpend K, Alain S, Sanson le Pors MJ, Desjeux JF, Mégraud F, Heyman M.Helicobacter pylorialters exogenous antigen absorption and processing in a digestive tract epithelial cell line model.Infect Immun66: 5785–5791, 1998.",{"doi":1345},"10.1128\u002FIAI.66.12.5785-5791.1998",{"id":24,"text":1347,"url":24,"identifiers":1348},"10.1056\u002FNEJM199812243392601",{"doi":1347},{"id":24,"text":1350,"url":24,"identifiers":1351},"10.1053\u002Fj.gastro.2005.04.012",{"doi":1350},{"id":24,"text":1353,"url":24,"identifiers":1354},"Sakai H, Sou K, Horinouchi H, Kobayashi K, Tsuchida E.Hemoglobin vesicles as artificial oxygen carriers: present situation and future visions.J Intern Med263: 4–15, 2008.",{},{"id":24,"text":1356,"url":24,"identifiers":1357},"10.1136\u002Fgut.47.6.804",{"doi":1356},{"id":24,"text":1359,"url":24,"identifiers":1360},"10.1053\u002Fgast.2002.33663",{"doi":1359},{"id":24,"text":1362,"url":24,"identifiers":1363},"10.1136\u002Fbmj.318.7187.833",{"doi":1362},{"id":24,"text":1365,"url":24,"identifiers":1366},"10.1056\u002FNEJM199910073411502",{"doi":1365},{"id":24,"text":1368,"url":24,"identifiers":1369},"10.1053\u002Fj.gastro.2006.02.007",{"doi":1368},{"id":24,"text":1371,"url":24,"identifiers":1372},"10.1136\u002Fgut.2003.021154",{"doi":1371},{"id":24,"text":1374,"url":24,"identifiers":1375},"10.1136\u002Fgut.2005.080739",{"doi":1374},{"id":1377,"createTime":1378,"updateTime":1378,"relativeEntities":1379,"slug":1380,"properties":1381,"entityType":150,"verifyStatus":151,"verifyTime":1378,"verifyNote":152,"syncStatus":23,"languages":1395,"translateLanguages":24,"viewCount":25,"primaryUrl":1396,"fullTextUrl":24,"authors":1397,"publicationType":369,"publisherRelationship":1502,"citationCount":1535,"citationInfo":1536,"publishDate":1538,"publishYear":1539,"citationAnalyzeStatus":23,"lastCitationAnalyze":24,"indexDatabases":24,"openAccess":24,"references":1540,"isForceReanalyzing":544},"ca07b75d-0845-43c7-9662-87c04154791c","2024-09-21T23:13:26.179+00:00",[],"A-novel-ultrasound-technique-to-study-the-biomechanics-of-the-human-esophagus-in-vivo",{"mag":1382,"keywords":1384,"openalex":1385,"abstract":1387,"title":1389,"pm":1391,"doi":1393},{"VOID":1383},"2164251152",{},{"VOID":1386},"W2164251152",{"EN":1388},"\u003Cjats:p> The objectives of this study were to validate a novel ultrasound technique and to use it to study the circumferential stress-strain properties of the human esophagus in vivo. A manometric catheter equipped with a high-compliance bag and a high-frequency intraluminal ultrasonography probe was used to record esophageal pressure and images. Validation studies were performed in vitro followed by in vivo studies in healthy human subjects. Esophageal distensions were performed with either an isovolumic (5–20 ml of water) or with an isobaric (10–60 mmHg) technique. Sustained distension was also performed for 3 min in each subject. The circumferential wall stress and strain were calculated. In vitro studies indicate that the ultrasound technique can make measurements of the esophageal wall with an accuracy of 0.01 mm. The in vivo studies provide the necessary data to compute the Kirchhoff's stress, Green's strain, and Young's elastic modulus during esophageal distensions. The stress-strain relationship revealed a linear shape, the slope of which corresponds to the Young's modulus. During sustained distensions, we found dynamic changes of stress and strain during the period of distension. 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Distension of the esophagus can cause heartburn and chest pain; however, none of the available techniques to study the esophagus measure esophageal distension. We evaluated the technique of high-frequency intraluminal ultrasound probe (HFIUS) to measure the esophageal cross-sectional area (CSA) during gastroesophageal reflux (GER). The following methods were used: 1) the CSA of agarose gel tubes of known dimensions were measured using ultrasound probes; 2) seven normal subjects were studied to evaluate the esophageal CSA during different bolus volumes (1, 5, 10, 15, and 20 ml) of water swallows (WS); and 3) simultaneous pressures, pH, and ultrasound images of the esophagus were recorded in healthy subjects. In vitro studies showed that the HFIUS measured the CSA of the tubes accurately. The maximal CSA of the distal esophagus during WS with boluses of 1, 5, 10, 15, and 20 ml were 54, 101, 175, 235, and 246 mm\u003Cjats:sup>2\u003C\u002Fjats:sup>, respectively. Esophageal contents during 62 episodes of transient lower esophageal sphincter relaxations, 29 pH positive, and 33 pH negative GER episodes revealed that reflux of air into the esophagus occurred more frequently than liquid. The median CSA and estimated diameter of the esophagus during liquid GER was 44.1 mm\u003Cjats:sup>2\u003C\u002Fjats:sup> and 7.5 mm, respectively. We conclude that HFIUS is a valid technique to measure the CSA of the esophagus in vivo during GER. Distension of the esophagus during physiological GER is relatively small. \u003C\u002Fjats:p>",{"EN":1637},"Measuring esophageal distension by high-frequency  intraluminal ultrasound 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is thought to exert anti-inflammatory effects by inhibiting vascular cell adhesion molecule-1 (VCAM-1)-dependent leukocyte migration and by suppressing the expression of inducible nitric oxide synthase (iNOS). As VCAM-1 and iNOS are important mediators of tissue injury in the dextran sodium sulfate (DSS) murine model of inflammatory colitis, we examined whether bilirubin prevents colonic injury in DSS-treated mice. Male C57BL\u002F6 mice were administered 2.5% DSS in the drinking water for 7 days, while simultaneously receiving intraperitoneal injections of bilirubin (30 mg\u002Fkg) or potassium phosphate vehicle. Disease activity was monitored, peripheral blood counts and serum nitrate levels were determined, and intestinal specimens were analyzed for histological injury, leukocyte infiltration, and iNOS expression. The effect of bilirubin on IL-5 production by HSB-2 cells and on Jurkat cell transendothelial migration also was determined. DSS-treated mice that simultaneously received bilirubin lost less body weight, had lower serum nitrate levels, and exhibited reduced disease severity than vehicle-treated animals. Concordantly, histopathological analyses revealed that bilirubin-treated mice manifested significantly less colonic injury, including reduced infiltration of eosinophils, lymphocytes, and monocytes, and diminished iNOS expression. Bilirubin administration also was associated with decreased eosinophil and monocyte infiltration into the small intestine, with a corresponding increase in peripheral blood eosinophilia. Bilirubin prevented Jurkat migration but did not alter IL-5 production. In conclusion, bilirubin prevents DSS-induced colitis by inhibiting the migration of leukocytes across the vascular endothelium and by suppressing iNOS expression.\u003C\u002Fjats:p>",{"EN":1830},"Bilirubin prevents acute DSS-induced colitis by inhibiting leukocyte infiltration and suppressing upregulation of inducible nitric oxide synthase",{"VOID":1832},"26381705",{"VOID":1834},"10.1152\u002Fajpgi.00149.2014",[154],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpgi.00149.2014",[1838,1858,1875,1890,1907,1922,1937,1954],{"id":1839,"sortIndex":181,"researcher":24,"roles":1840,"affiliations":1841,"properties":1853},"6f1a5aaf-bd10-47b7-967c-18f0cbd00d95",[],[1842],{"id":1843,"sortIndex":25,"affiliation":1844,"properties":24},"0155b258-7864-4d4e-8dfd-7ed5623cbe04",{"id":1845,"createTime":1846,"updateTime":1847,"relativeEntities":1848,"slug":1849,"properties":1850,"entityType":69,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"f3631c8f-c696-4e64-8541-bfcebd5d8ef8","2023-12-28T10:26:18.470+00:00","2024-09-01T22:43:57.048+00:00",[],"Division-of-Digestive-Diseases-University-of-Cincinnati-Cincinnati-Ohio",{"title":1851},{"VI":1852},"Division of Digestive Diseases, University of Cincinnati, Cincinnati, Ohio",{"openalex":1854,"title":1856},{"VOID":1855},"A5012427930",{"EN":1857},"Ganesh V. 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be impossible to culture epithelial cells from the gastrointestinal tract of adult animals. Researchers have had to use either cell lines derived from newborn rat small intestine or colon carcinoma cell lines that have retained some of the properties of the gastrointestinal mucosa. We have described a method for establishing conditionally immortalized cell lines from the stomach, small intestine, colon, pancreas, and liver from tissue obtained from a transgenic mouse strain carrying a temperature-sensitive mutant of the SV40 large T gene (the “Immortomouse”). This immortalizing gene has proved to be useful for establishing cell lines from a number of transgenic mice following crossbreeding of the Immortomouse with the transgenic mouse of interest. These cell lines are being used in numerous studies. In this review we describe the methods for developing such lines and list the range of cell lines that have been developed from colon, small intestine, stomach, liver, and pancreas of a number of transgenic mice. \u003C\u002Fjats:p>",{"EN":2265},"Establishment of conditionally immortalized epithelial cell lines from the intestinal tissue of adult normal and transgenic mice",{"VOID":2267},"19109407",{"VOID":2269},"10.1152\u002Fajpgi.90381.2008",[154],"https:\u002F\u002Fwww.physiology.org\u002Fdoi\u002F10.1152\u002Fajpgi.90381.2008",[2273,2293],{"id":2274,"sortIndex":196,"researcher":24,"roles":2275,"affiliations":2276,"properties":2288},"afb8b9d3-f845-4d24-aa7a-c5f762622a45",[],[2277],{"id":2278,"sortIndex":25,"affiliation":2279,"properties":24},"0e34cd6c-4eb9-4d9e-ace9-dbeb367eaaf1",{"id":2280,"createTime":2281,"updateTime":2282,"relativeEntities":2283,"slug":2284,"properties":2285,"entityType":69,"verifyStatus":23,"verifyTime":24,"verifyNote":24,"syncStatus":23,"languages":24,"translateLanguages":24,"viewCount":25},"2838554c-0fca-4c73-b82e-60ab5168d152","2024-04-18T09:39:22.613+00:00","2025-02-01T14:14:40.198+00:00",[],"Vanderbilt-University",{"title":2286},{"EN":2287},"Vanderbilt University",{"openalex":2289,"title":2291},{"VOID":2290},"A5041860950",{"EN":2292},"Pamela S. 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We assessed the role of cationic amino acid transporter 2 (CAT2), the inducible transporter of l-Arg, in DSS colitis. Expression of CAT2 was upregulated in tissues from colitic mice and localized predominantly to colonic macrophages. CAT2-deficient (CAT2\u003Cjats:sup>−\u002F−\u003C\u002Fjats:sup>) mice exposed to DSS exhibited worsening of survival, body weight loss, colon weight, and histological injury. These effects were associated with increased serum l-Arg and decreased tissue l-Arg uptake and inducible nitric oxide synthase protein expression. Clinical benefits of l-Arg supplementation in wild-type mice were lost in CAT2\u003Cjats:sup>−\u002F−\u003C\u002Fjats:sup>mice. There was increased infiltration of macrophages, dendritic cells, granulocytes, and T cells in colitic CAT2\u003Cjats:sup>−\u002F−\u003C\u002Fjats:sup>compared with wild-type mice. Cytokine profiling revealed increases in proinflammatory granulocyte colony-stimulating factor, macrophage inflammatory protein-1α, IL-15, and regulated and normal T cell-expressed and -secreted and a shift from an IFN-γ- to an IL-17-predominant T cell response, as well as an increase in IL-13, in tissues from colitic CAT2\u003Cjats:sup>−\u002F−\u003C\u002Fjats:sup>mice. However, there were no increases in other T helper cell type 2 cytokines, nor was there a global increase in macrophage-derived proinflammatory cytokines. The increase in IL-17 derived from both CD4 and γδ T cells and was associated with colonic IL-6 expression. 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