Ali Canbay

ORCID: 0000-0001-6069-7899
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About
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Research Areas
  • Liver Disease Diagnosis and Treatment
  • Liver Disease and Transplantation
  • Diet, Metabolism, and Disease
  • Organ Transplantation Techniques and Outcomes
  • Drug-Induced Hepatotoxicity and Protection
  • Liver physiology and pathology
  • Hepatitis B Virus Studies
  • Hepatitis C virus research
  • Liver Diseases and Immunity
  • Hepatocellular Carcinoma Treatment and Prognosis
  • Diet and metabolism studies
  • Pancreatitis Pathology and Treatment
  • Endoplasmic Reticulum Stress and Disease
  • Cholangiocarcinoma and Gallbladder Cancer Studies
  • Pediatric Hepatobiliary Diseases and Treatments
  • Drug Transport and Resistance Mechanisms
  • Lipid metabolism and disorders
  • Gallbladder and Bile Duct Disorders
  • Alcohol Consumption and Health Effects
  • Metabolism and Genetic Disorders
  • Atrial Fibrillation Management and Outcomes
  • Peroxisome Proliferator-Activated Receptors
  • Pancreatic and Hepatic Oncology Research
  • Cardiac Arrhythmias and Treatments
  • Clinical Nutrition and Gastroenterology

Universitätsklinikum Knappschaftskrankenhaus Bochum
2019-2025

Ruhr University Bochum
2019-2025

University Hospitals of the Ruhr-University of Bochum
2020-2025

Otto-von-Guericke University Magdeburg
2017-2024

Australasian Gastro Intestinal Research Foundation
2024

National Health and Medical Research Council
2024

University of Duisburg-Essen
2010-2022

LWL-Universitätsklinikum Bochum
2022

Fondazione IRCCS Ca' Granda Ospedale Maggiore Policlinico
2022

University Hospital Magdeburg
2017-2021

Inflammasome activation plays a central role in the development of drug-induced and obesity-associated liver disease. However, sources mechanisms inflammasome-mediated damage remain poorly understood. Our aim was to investigate effect NLRP3 inflammasome on using novel mouse models. We generated global myeloid cell-specific conditional mutant Nlrp3 knock-in mice expressing D301N mutation (ortholog D303N human ), resulting hyperactive NLRP3. To study presence significance NLRP3-initiated...

10.1002/hep.26592 article EN Hepatology 2013-06-28

Nonalcoholic fatty liver disease (NAFLD) is a serious health problem. Although NAFLD represents form of lipotoxicity, its pathogenesis remains poorly understood. The aim this study was to examine the cellular mechanisms involved in free acid (FFA)-mediated hepatic lipotoxicity. FFA treatment cells resulted Bax translocation lysosomes and lysosomal destabilization with release cathepsin B (ctsb), cysteine protease, into cytosol. This process also partially dependent on ctsb. Lysosomal nuclear...

10.1002/hep.20283 article EN Hepatology 2004-07-01

Abstract Non‐alcoholic fatty liver disease (NAFLD) is the most common in developed countries, and accumulating evidence suggests it as hepatic manifestation of metabolic syndrome (MS). Although published prevalence hepatocellular carcinoma (HCC) low NAFLD/NASH patients, these data have been derived from areas endemic for viral hepatitis. We recruited 162 adults with HCC between February 2007 March 2008, investigated underlying etiologies determined MS related features within each group....

10.1002/ijc.25797 article EN International Journal of Cancer 2010-12-02

Hepatocyte apoptosis by death receptors, hepatic inflammation, and fibrosis are prominent features of liver diseases. However, the link between these processes remains unclear. Our aim was to ascertain whether engulfment apoptotic bodies Kupffer cells promotes inflammation fibrosis. Isolated murine efficiently engulfed generated from UV–treated mouse hepatocytes. Engulfment bodies, but not latex beads, stimulated cell generation ligands, including Fas ligand, tumor necrosis factor α (TNF–α)....

10.1053/jhep.2003.50472 article EN Hepatology 2003-10-23

Abstract Non‐alcoholic fatty liver disease ( NAFLD ) represents the most common in Western countries and often progresses to non‐alcoholic steatohepatitis NASH leading ultimately fibrosis cancer. The occurrence of hepatocyte cell death—so far characterized as apoptosis—represents a fundamental step from benign steatosis toward progressive steatohepatitis. In contrast, function RIP 3‐dependent “necroptosis” ‐induced is currently unknown. We show that 3 upregulated human dietary mouse model...

10.15252/emmm.201403856 article EN cc-by EMBO Molecular Medicine 2014-06-24

The prevalence of nonalcoholic steatohepatitis (NASH) associated hepatocellular carcinoma (HCC) is increasing. However, strategies for detection early-stage HCC in patients with NASH have limitations. We assessed the ability GALAD score, which determines risk based on patient sex; age; and serum levels α-fetoprotein (AFP), AFP isoform L3 (AFP-L3), des-gamma-carboxy prothrombin (DCP), to detect NASH.We performed a case-control study 125 (20% within Milan Criteria) 231 without (NASH controls)...

10.1016/j.cgh.2019.11.012 article EN cc-by-nc-nd Clinical Gastroenterology and Hepatology 2019-11-08

Abstract Nonalcoholic fatty liver disease (NAFLD) is the most common in industrialized countries and may proceed to steatohepatitis (NASH). Apoptosis free acid (FFA)-induced lipotoxicity are important features of NASH pathogenesis. We have shown a hepatoprotective effect adiponectin steatotic livers hepatitis C virus (HCV) patients recent data links bile (BA) metabolism pathogenesis NAFLD. The aim this study was identify potential interactions between BA FFA Liver biopsies serum samples from...

10.1002/hep.26225 article EN Hepatology 2013-01-09

Based on positive results from small single center studies, granulocyte-colony stimulating factor (G-CSF) is being widely used for the treatment of patients with acute-on-chronic liver failure (ACLF). Herein, we aimed to evaluate safety and efficacy G-CSF in ACLF.In this multicenter, prospective, controlled, open-label phase II study, 176 ACLF (EASL-CLIF criteria) were randomized receive (5 μg/kg daily first 5 days every third day thereafter until 26) plus standard medical therapy (SMT) (n =...

10.1016/j.jhep.2021.07.033 article EN cc-by-nc-nd Journal of Hepatology 2021-08-05

Behavioral conditioned immunosuppression has been described in rodents as the most impressive demonstration of brain-to-immune system interaction. To analyze whether behavioral is possible humans, healthy subjects this double-blind, placebo-controlled study were four sessions over 3 consecutive days, receiving immunosuppressive drug cyclosporin A an unconditioned stimulus paired with a distinctively flavored drink (conditioned stimulus) each 12 h. In next week, re-exposure to (drink), but...

10.1096/fj.02-0389com article EN The FASEB Journal 2002-12-01

Liver injury is characterized by hepatocyte apoptosis and collagen-producing activated hepatic stellate cells (HSC). Hepatocyte promotes liver fibrosis, whereas HSC limits fibrosis. Pharmacological inhibition of cell may potentially attenuate fibrosis blocking or promote permitting accumulation HSCs. To ascertain the net effect inhibiting on injury, inflammation, fibrogenesis, we examined a pancaspase IDN-6556 these parameters in bile duct ligated (BDL) mouse. was assessed terminal...

10.1124/jpet.103.060129 article EN Journal of Pharmacology and Experimental Therapeutics 2003-11-14

Summary. Acute hepatitis B progresses to liver failure with the need of transplantation in about 1% cases. We treated patients severe acute or fulminant lamivudine an attempt prevent virus (HBV) reinfection after potential transplantation. Since September 2000, 17 HBV infection were 100 150 mg daily once we had evidence for a course as indicated by INR >2.0. These compared historic control from our unit and external patients. Fourteen (82.4%) survived full recovery without All these 14...

10.1111/j.1365-2893.2005.00695.x article EN Journal of Viral Hepatitis 2006-02-20

Although a lysosomal, cathepsin B–dependent (Ctsb-dependent) pathway of apoptosis has been described, the contribution this to tissue damage remains unclear. Our aim was ascertain if Ctsb inactivation attenuates liver injury, inflammation, and fibrogenesis after bile duct ligation (BDL). In 3-day BDL mice, hepatocyte apoptosis, mitochondrial cytochrome c release, serum alanine aminotransferase (ALT) values were reduced in Ctsb–/– versus Ctsb+/+ animals. Likewise, R-3032 (a inhibitor) also...

10.1172/jci17740 article EN Journal of Clinical Investigation 2003-07-15
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