Mohammed Jarrar (11 results)

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Condition: New. Non alcoholic fatty liver disease is the hepaticmanifestation of metabolic syndrome that mayprogress from simple steatosis to nonalcoholicsteatohepatitis, cirrhosis and hepatocellularcarcinoma. Expansion of omental adipose isaccompanied by alteration in pro.

Taschenbuch. Condition: Neu. Adipokines and Pathogenesis of Non Alcoholic Fatty Liver Disease | Pathogenesis of Non Alcoholic Fatty Liver Disease and Circulatory Levels of Adipocytokines | Mohammed Jarrar | Taschenbuch | Kartoniert / Broschiert | Englisch | 2013 | VDM Verlag Dr. Müller | EAN 9783639091656 | Verantwortliche Person für die EU: OmniScriptum GmbH & Co. KG, Bahnhofstr. 28, 66111 Saarbrücken, info[at]akademikerverlag[dot]de | Anbieter: preigu.…

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Taschenbuch. Condition: Neu. nach der Bestellung gedruckt Neuware - Printed after ordering - Non alcoholic fatty liver disease is the hepatic manifestation of metabolic syndrome that may progress from simple steatosis to nonalcoholic steatohepatitis, cirrhosis and hepatocellular carcinoma. Expansion of omental adipose is accompanied by alteration in profiles of adipocytokines that contribute to NAFLD through enhanced steatogenesis in the liver and its inflammation. Gene transcription studies demonstrated a prominent adipose-specific deregulation of the inflammation and immune system related genes in NASH. Serum levels of soluble adipokines and cytokines can reliably predict NASH in the cohort of morbidly obese patients. Histologic fibrosis in patients with NASH could be predicted by TNF- level. There is also strong connection between the HCV genotype 3, steatosis and increases in IL-8 serum levels. HCV genotype specific differences in soluble cytokine concentrations may help to elucidate pathogenesis of HCV hepatitis and potential triggers for HCV-related steatosis. These results should be of interest to the researchers of the clinical and fundamental aspects of human metabolism, obesity, diabetes, and hepatitis C.; Non alcoholic fatty liver disease is the hepaticmanifestation of metabolic syndrome that mayprogress from simple steatosis to nonalcoholicsteatohepatitis, cirrhosis and hepatocellularcarcinoma. Expansion of omental adipose isaccompanied by alteration in profiles ofadipocytokines that contribute to NAFLD throughenhanced steatogenesis in the liver and itsinflammation. Gene transcription studiesdemonstrated a prominent adipose-specificderegulation of the inflammation and immune systemrelated genes in NASH. Serum levelsof soluble adipokines and cytokines can reliablypredict NASH in the cohort of morbidly obesepatients. Histologic fibrosis in patients with NASHcould be predicted by TNF-a level. There is alsostrong connection between the HCV genotype 3steatosis and increases in IL-8 serum levels. HCVgenotype specific differences in soluble cytokineconcentrations may help to elucidate pathogenesis ofHCV hepatitis and potential triggers for HCV-relatedsteatosis. These results should be of interest tothe researchers of the clinical and fundamentalaspects of human metabolism, obesity, diabetes, andhepatitis C.…