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Effect of hepatic iron concentration reduction on hepatic fibrosis and damage in rats with cholestatic liver disease

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World Journal of Gastroenterology 2006年第2期12卷 240-245页

作者： Gil Peretz Gabriela Link Orit Pappo rafael bruck Zvi Ackerman Department of Internal Medicine Hebrew University- Hadassah Medical CenterMount Scopus CampusJerusalemIsrael Department of Human Nutrition and Metabolism Hebrew University Hadassah Medical SchoolJerusalemIsrael Department of Pathology Hebrew University-Hadassah Medical CenterJerusalemIsrael Department of Gastroenterology and Hepatology The EWolfson Medical CenterHolonand Sackler School of MedicineTel Aviv UniversityTel AvivIsrael

AIM： TO assess the effect of iron reduction after phlebotomy in rats with ＂normal＂ hepatic iron concentration （HIC） on the progression of hepatic fibrosis, as a result of bile duct ligation （BDL）. METHODS： Rats underwent phlebotomy before or after sham operation or BDL. Animals undergone only BDL or sham operation served as controls. Two weeks after surgery, indices of hepatic damage and fibrosis were evaluated. RESULTS： Phlebotomy lowered HIC. Phlebotomy after BDL was associated with body weight increase, lower hepatic weight, less portal hypertension, less periportal necrosis, less portal inflammation, lower hepatic activity index score and higher albumin levels. On the other hand, phlebotomy before BDL was associated with body weight decrease and hepatic activity index score increase. Phlebotomy after sham operation was not associated with any hepatic or systemic adverse effects. CONCLUSION： Reduction of HIC after induction of liver damage may have beneficial effects in BDL rats. However, iron deficiency could induce impairment of liver function and may make the liver more susceptible to insults like BDL.

关键词： Iron Phlebotomy Bile duct ligation Hepatic activity index Rat.

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Atorvastatin and rosuvastatin do not prevent thioacetamide induced liver cirrhosis in rats

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World Journal of Gastroenterology 2013年第2期19卷 241-248页

作者： Haim Shirin Efrat Sharvit Hussein Aeed Dov Gavish rafael bruck Gastroenterology Institute Assaf Harofeh Medical CenterZerifin 70300Israel Sackler School of Medicine Tel-Aviv University Tel-Aviv 69975Israel Department of Gastroenterology TelAviv Sourasky Medical CenterTelAviv 64239Israel Department of Gastroenterology The E.Wolfson Medical CenterHolon 58100Israel Department of Internal Medicine "A" The E.Wolfson Medical CenterHolon 58100Israel

AIM:To examine whether the administration of atorvastatin and rosuvastatin would prevent experimentallyinduced hepatic cirrhosis in ***:Liver cirrhosis was induced by injections of thioacetamide(TAA).Rats were treated concurrently with TAA alone or TAA and either atorvastatin(1,10 and 20 mg/kg) or rosuvastatin(1,2.5,5,10 and 20 mg/kg) given daily by nasogastric ***:Liver fibrosis and hepatic hydroxyproline content,in the TAA-treated group was significantly higher than those of the controls [11.5 ± 3.2 vs 2.6 ± 0.6 mg/g protein(P = 0.02)].There were no differences in serum aminotransferase levels in the TAA controls compared to all the groups treated concomitantly by *** statins used in our study did not prevent liver fibrosis or reduce portal hypertension,and had no effect on hepatic oxidative ***,the hepatic level of malondialdehyde was not lower in those groups treated by TAA + statins compared to TAA *** vitro studies,using the BrdU method have shown that atorvastatin had no effect of hepatic stellate cells ***,statin treatment was not associated with worsening of liver damage,portal hypertension or survival ***:Atorvastatin or rosuvastatin did not inhibit TAA-induced liver cirrhosis or oxidative stress in *** statins may have therapeutic applications in hepatic fibrosis due to other etiologies deserve further investigation.

关键词： Liver cirrhosis Statins Thioacetamide

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Daclatasvir vs telaprevir plus peginterferon alfa/ribavirin for hepatitis C virus genotype 1

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World Journal of Gastroenterology 2016年第12期22卷 3418-3431页

作者： Ira Jacobson Stefan Zeuzem Robert Flisiak Brygida Knysz Stefan Lueth Dorota Zarebska-Michaluk Ewa Janczewska Peter Ferenci Moises Diago Anna Linda Zignego Rifaat Safadi Yaacov Baruch Dzhamal Abdurakhmanov Stephen Shafran Dominique Thabut rafael bruck Adrian Gadano Alexander James Thompson Justin Kopit Fiona Mc Phee Tracy Michener Eric A Hughes Philip D Yin Stephanie Noviello Weill Cornell Medical College New YorkNY 10029United States Icahn School of Medicine at Mount Sinai New YorkNY 10029United States JW Goethe University Hospital 60323 FrankfurtGermany Uniwersytet Medyczny w Bialymstoku 15-089 BialystokPoland EMC and Medical University 50-220 WroclawPoland Universitatsklinikum Hamburg-Eppendorf 20246 HamburgGermany Wojewodzki Szpital Zespolony w Kielcach 25-736 KielcePoland ID Clinic 41-400 MyslowicePoland Medizinische Universitat Wien 1090 ViennaAustria Clinica Quiron 46010 ValenciaSpain Universita degli Studi di Firenze 50121 FlorenceItaly Holy Family Hospital Nazareth 6004Israel Rambam Medical Center Haifa 31096Israel 1st Moscow State Medical University N.A.I.M.Sechenov 119991 MoscowRussia University of Alberta Hospital EdmontonAlberta T6G 2B7Canada Groupe Hospitalier Pitie-Salpetriere 75013 ParisFrance Tel Aviv Sourasky Medical Center and Tel Aviv University Tel Aviv 64239Israel Hospital Italiano de Buenos Aires Buenos Aires C1181ACHArgentina St.Vincents Hospital and the University of Melbourne Melbourne 3065Australia Fiona McPhee Bristol-Myers Squibb Research and DevelopmentWallingfordCT 06492United States Bristol-Myers Squibb Research and Development PrincetonNJ 08450United States

AIM: To evaluate daclatasvir vs telaprevir, each combined with peginterferon alfa-2a/ribavirin(peg IFN/RBV), in treatment-naive hepatitis C virus(HCV) genotype(GT) 1-infected ***: In this phase 3, randomized, open-label, noninferiority study, 602 patients were randomly assigned(2:1) to daclatasvir vs telaprevir, stratified by IL28 B rs12979860 host genotype(CC vs non-CC), cirrhosis status(compensated cirrhosis vs no cirrhosis), and HCV GT1 subtype(GT1a vs GT1b). Patients were selected by study inclusion criteria from a total of 793 enrolled patients. Patients received daclatasvir 60 mg once daily or telaprevir 750 mg 3 times daily plus peg IFN/RBV. Daclatasvir recipients received 24 wk of daclatasvir plus peg IFN/RBV; those without an extended rapid virologic response(e RVR; undetectable HCV-RNA at weeks 4 and 12) received an additional 24 wk of peg IFN/RBV. Telaprevir-treated patients received 12 wk of telaprevir plus peg IFN/RBV followed by 12(with e RVR) or 36(no e RVR) wk of peg IFN/RBV. The primary objective was to compare for noninferiority of sustained virologic response rates at posttreatment week 12(SVR12) in GT1b-infected patients. Key secondary objectives were to demonstrate that the rates of anemia(hemoglobin < 10 g/d L) and rashrelated events, through week 12, were lower with daclatasvir + peg IFN/RBV than with telaprevir + peg IFN/RBV among GT1b-infected patients. Resistance testing was performed using population-based sequencing of the NS5 A region for all patients at baseline, and for patients with virologic failure or relapse and HCV-RNA ≥ 1000 IU/m L, to investigate any link between NS5 A polymorphisms associated with daclatasvir resistance and virologic outcome. RESULTS: Patient demographics and disease characteristics were generally balanced across treatment arms; however, there was a higher proportion of black/African Americans in the daclatasvir groups(6.0% and 8.2% in the GT1 b and GT1 a groups, respectively) than in the telaprevi

关键词： Direct-acting antiviral Chronic hepatitis C Daclatasvir Genotype 1b NS5A inhibitor Liver disease

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