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non-alcoholic fatty liver disease/protease
Nuoroda įrašoma į mainų sritį
Puslapis 1 nuo 743 rezultatus
Transport of proteases across neonatal intestine and development of liver disease in infants with alpha-1 antitrypsin deficiency.
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The transport of macromolecules from the intestinal lumen into the systemic circulation is considerably greater in neonatal than in adult animals. Transport of both immunoglobin and non-immunoglobulin proteins is enhanced. It is postulated that luminal enzymes are also transported into the systemic
Protease inhibitors in liver disease.
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Measurements of the principal protease inhibitors were carried out in patients with two types of chronic liver disease: alcoholic cirrhosis and primary biliary cirrhosis. Measurement of the two major protease inhibitors operative in the haemostatic mechanism--that is, antithrombin III and alpha
Limited effectiveness and safety profile of protease inhibitor-based triple therapy against chronic hepatitis C in a real-world cohort with a high proportion of advanced liver disease.
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OBJECTIVE
Triple therapy with pegylated-interferon-α, ribavirin, and a protease inhibitor (PI), boceprevir or telaprevir, is the standard of care for the treatment of chronic hepatitis C genotype 1 in several countries. Pivotal studies showed reasonable results for safety and efficacy. However, it
[Serine protease inhibitors prevent alcoholic liver injury].
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The hepatotoxic effects of alcohol have been described in detail, but factors responsible for its hepatotoxicity have only partially characterized. It now appears that Kupffer cell derived TNF-alpha participates in several aspects of alcoholic liver injury. On the other hand, protease inhibitors
Serum protease inhibitors in opisthorchiasis, hepatoma, cholangiocarcinoma, and other liver diseases.
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Serum alpha 1-antitrypsin, alpha 1-antichymotrypsin and alpha 2-macroglobulin increased significantly in patients suffering from liver diseases: hepatoma, amoebic liver abscess, hepatitis, hepatic cirrhosis, cholangiocarcinoma, carcinoma of the head of pancreas including liver fluke infection
Mutation analysis of the cystic fibrosis transmembrane conductance regulator (CFTR) gene, the cationic trypsinogen (PRSS1) gene, and the serine protease inhibitor, Kazal type 1 (SPINK1) gene in patients with alcoholic chronic pancreatitis.
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Susceptibility to alcoholic chronic pancreatitis (ACP) could be genetically determined. Mutations in cationic trypsinogen (PRSS1), cystic fibrosis transmembrane conductance regulator (CFTR), and serine protease inhibitor, Kazal type 1 (SPINK1) genes have been variably associated with both the
Ubiquitin-specific protease 4 is an endogenous negative regulator of metabolic dysfunctions in nonalcoholic fatty liver disease.
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Nonalcoholic fatty liver disease (NAFLD), characterized by hepatic steatosis, insulin resistance and inflammation, poses a high risk of cardiometabolic disorders. Ubiquitin specific protease 4 (USP4), a deubiquitinating enzyme, is pivotally involved in regulating multiple inflammatory pathways;
Improvement in liver steatosis after the switch from a ritonavir-boosted protease inhibitor to raltegravir in HIV-infected patients with non-alcoholic fatty liver disease.
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Background: The ritonavir-boosted protease inhibitor (PI/r) use has been associated with several metabolic abnormalities, and the non-alcoholic fatty liver disease (NAFLD) is becoming a very frequent comorbidity among HIV-infected patients. Methods: We performed an observational,
Alcoholic Extract of Lotus Leaves Improves Lipid Profile in Rats with HIV Protease Inhibitor-induced Dyslipidaemia.
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OBJECTIVE
To examine the effect of the alcoholic extract of lotus leaves (AELL) on antiretroviral treatment-induced dyslipidaemia in a rat model.
METHODS
Lotus leaves were extracted by 95% ethanol. Seventy male Sprague-Dawley rats were given lopinavir/ritonavir for six weeks. At week 0 and 6, sera
The prevalence of cationic trypsinogen (PRSS1) and serine protease inhibitor, Kazal type 1 (SPINK1) gene mutations in Polish patients with alcoholic and idiopathic chronic pancreatitis.
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BACKGROUND
The main cause of chronic pancreatitis (CP) is excessive alcohol consumption. On the other hand, only 5-10% of heavy drinkers develop chronic pancreatitis. We have only limited information regarding the pathogenic mechanism by which alcohol leads to the disease. Mutations of the PRSS1 and
Natural protease inhibitors to fibrinolysis in liver diseases.
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The newly discovered alpha 2-antiplasmin and some inhibitors of fibrinolysis were measured in 40 patients with liver diseases. alpha 2-antiplasmin was low in liver cirrhosis, but unchanged in cholestasis when compared with controls.
SUMO-specific protease 3 is a key regulator for hepatic lipid metabolism in non-alcoholic fatty liver disease.
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Non-alcoholic fatty liver disease (NAFLD) is characterized by excessive lipid accumulation in hepatocytes. The role of SENP3 in lipid metabolism, particularly NAFLD, is unclear. Our results showed that hepatic SENP3 was up-regulated in NAFLD patients and an animal model in vivo and after loading
Human immunodeficiency virus protease inhibitors modulate Ca2+ homeostasis and potentiate alcoholic stress and injury in mice and primary mouse and human hepatocytes.
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A portion of human immunodeficiency virus (HIV)-infected patients undergoing protease inhibitor (PI) therapy concomitantly consume or abuse alcohol leading to hepatic injury. The underling mechanisms are not known. We hypothesize that HIV PIs aggravate alcohol-induced liver injury through an
Is it appropriate to study blood ghrelin and obestatin in non-alcoholic fatty liver disease (NAFLD) without using protease inhibitors?
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To what extent is it right to measure serum vaspin, obestatin, and apelin-36 levels without a protease inhibitor in nonalcoholic fatty liver disease?
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