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Molecular Pathogenesis of Liver Steatosis Induced by Hepatitis C Virus

References 1. Chang ML, Yeh HC, Tsou YK, Wang CJ, Cheng HY, Sung CM, et al. HCV core-induced nonobese hepatic steatosis is associated with hypoadiponectinemia and is ameliorated by adiponectin administration. Obesity (Silver Spring) 2012; doi: 10.1038/ oby.2012.45. 2. Sato S, Fukasawa M, Yamakawa Y, Natsume T, Suzuki T, Shoji I, et al. Proteomic profiling of lipid droplet proteins in hepatoma cell lines expressing hepatitis C virus core protein. J Biochem 2006;139:921-930. 3. Congiu M, Ryan MC, Desmond PV. No

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Pathological Alterations in Hepatocytes of Dairy Cows With a Tendency to Emaciation and Fattening

. Li, M., Song, J., Mirkov, S., Xiao, S. Y., Hart, J., Liu, W., 2011: Comparing morphometric, biochemical and visual measurements of macrovesicular steatosis of liver. Hum. Pathol., 42, 356-360. 18. Mak, K. M., Kwong, A. J., Chu, E., Hoo, N. M., 2012: Hepatic steatosis, fibrosis and cancer in elderly cadavers. Anat. Rec., 295, 40-50. 19. Makovicky, P., Dudova, M., Tumova, E., Rajmon, R., Vodkova, Z., 2011: Experimental study of non-alcoholic fatty liver disease (NAFLD) on a model of starving chickens: is generalization of steatosis

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Influence of Non-Oxidised and Oxidised Rapeseed Oil Consumption on Liver Metabolism Pathways and Non-Alcoholic Steatohepatitis Development in Rabbits

References 1. Bandsma R.H., Wiegman C.H., Herling A.W., Burger H.J., ter Harmsel A., Meijer A.J., Romjin J.A., Reijngoud D.J., Kuipers F.: Acute inhibition of glucose- 6-phoshpate translocator acitvity leads to increase de novo lipogenesis and development of hepatic steatosis without VLDL production in rats. Diabetes 2001, 50, 2591-2597. 2. Champe P.C., Harvey R.A.: Biochemistry, Philadelphia, USA, 1994. 3. Choe E., Min D.B.: Chemistry of deep-fat frying oils. J Food Sci 2007, 72 77

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Influence of α-lipoic acid on morphology of organs of rabbits fed a high fat diet with the addition of oxidised rapeseed oil

References 1. Berliner J.A., Heinecke W.J.: The role of oxidized lipoproteins in atherogenesis. Free Radic Biol Med 1996, 20, 707–727. 2. Brukow K.G.: Oxidized lipids: The two faces of vascular inflammation. Curr Atheroscler Rep 2006, 8, 223–231. 3. Bukol-Krawczyk K.: Nonalcoholic steatosis of the liver – to treat or not to treat? Forum Metabol Disord 2010, 1, 66–72. 4. Choe E., Min D.B.: Chemistry of deep-fat frying oils. J Food Sci 2007, 72, 77–86. 5. Cohn J.: Oxidized fat in the diet, postprandial lipaemia and cardiovascular

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Non-invasive quantification of liver fibrosis regression following successful treatment of chronic hepatitis C with direct acting antivirals

Abstract

Introduction. The past years have revolutionized the treatment of hepatitis C virus (HCV) infection, with high rates of sustained virologic response (SVR). Furthermore, liver fibrosis has recently been redefined as a dynamic, reversible process. Methods. We performed a prospective cohort study to assess the role of laboratory evaluations and non-invasive measurement of liver stiffness in establishing the right time for starting treatment and in assessing the regression of liver fibrosis in Romanian patients treated with direct acting antivirals (DAA) for genotype 1b chronic hepatitis C. Results. We present the results for 102 patients, with a mean age of 58.5 years, and a rate of SVR of 100%. Our study has ruled out older age (p=0.628), IL28B non-CC genotype (p=0.693), baseline viral load above the cutoff of 600,000 IU/mL (p=0.353), and the presence of diabetes mellitus (p=0.272) or baseline steatosis (p=0.706) as factors potentially influencing the regression of liver fibrosis following DAA treatment of HCV infection with the 3D regimen. The quantitative regression of liver stiffness was inversely correlated with the duration of HCV infection (p=0.017), suggesting that timely treatment might associate better outcomes in terms of liver fibrosis. Conclusion. Our study’s results point towards the need to start DAA treatment earlier in patients with HCV infection.

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Thirty years in hemostasis research in Cluj Napoca

References 1. Brudaşcă I, Cucuianu M. Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for metabolic syndrome, hepatic steatosis and steatohepatitis. Rom J Intern Med. 2007;45(2):149-57. 2. Cucuianu M, Brudaşcă I. Coagulation factor XIII, impaired fibrinolysis and cardiovascular disease. Rev Romana Med Lab. 2011;19(2):119-27. 3. Brudaşcă I, Cucuianu M. Anticoagulant mechanisms are modulated by vascular endothelial cells. Rev Romana Med Lab. 2010;18(3):7-14. 4

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Abnormal lipid metabolism in metabolic syndrome: an epigenetic perspective

epigenome and later health consequences. Food Science and Human Wellness. 2013;2(1):1-11. DOI: 10.1016/j.fshw.2013.03.002. 4. Ginsberg HN, Stalenhoef AFH. The metabolic syndrome: targeting dyslipidaemia to reduce coronary risk. J Cardiovasc Risk. 2003; 10(2):121-8. DOI: 10.1177/174182670301000207 DOI: 10.1097/00043798-200304000-00007. 5. Brudaşcă I, Cucuianu M. Pathogenic role of abnormal fatty acids and adipokines in the portal flow. Relevance for the metabolic syndrome, hepatic steatosis and steatohepatitis. Rom J Int Med. 2007

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Editorial. The Role of Autophagy in Hepatitis C Virus Infection

al. Hepatitis C virus protein and iron overload induce hepatic steatosis through the unfolded protein response in mice. Liver Int 2010;30:683-692. 33 Ferraris P, Blanchard E, Roingeard P. Ultrastructural and biochemical analyses of hepatitis C virus-associated host cell membranes. J Gen Virol 2010;91:2230-2237. 34 Merquiol E, Uzi D, Mueller T, Goldenberg D, Nahmias Y, Xavier RJ, et al. HCV causes chronic endoplasmic reticulum stress leading to adaptation and interference with the unfolded protein response. PLoS One 2011;6:e24660

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