alcoholism/protease

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Ethanol enhances carbachol-induced protease activation and accelerates Ca2+ waves in isolated rat pancreatic acini.

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Alcohol abuse is a leading cause of pancreatitis, accounting for 30% of acute cases and 70-90% of chronic cases, yet the mechanisms leading to alcohol-associated pancreatic injury are unclear. An early and critical feature of pancreatitis is the aberrant signaling of Ca(2+) within the pancreatic

Mutations in serine protease inhibitor Kazal type 1 are strongly associated with chronic pancreatitis.

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BACKGROUND Although chronic pancreatitis is associated with risk factors such as alcoholism, hyperparathyroidism, and hypertriglyceridaemia, little is known of the actual aetiology of the disease. It is thought that inappropriate activation of trypsinogen causes pancreatitis, and indeed in cases of

Soluble α-Klotho in Liver Cirrhosis and Alcoholism.

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Alpha Klotho is a transmembrane protein that serves as co-receptor for FGF23. Ectodomain of membrane bound α Klotho may be shed by membrane bound proteases (activated, among other factors, by tumor necrosis factor (TNF)-α) generating the soluble form of the protein (sKl) that functions

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

Genetic approaches to alcohol addiction: gene expression studies and recent candidates from Drosophila.

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Ethanol intake causes gene expression changes resulting in cellular and molecular adaptations that could be associated with a predisposition to alcohol dependence. Recently, several research groups have used high-throughput gene expression profiling to search for alcohol-responsive genes in

Anti-intoxication and protective effects of a recombinant serine protease inhibitor from Lentinula edodes against acute alcohol-induced liver injury in mice.

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Serine protease inhibitors (serpins) are involved in inflammation, coagulation, fibrinolysis, tumor suppression, molecular chaperone, chromatin densification, and hormone transport. However, their anti-intoxication activity has not been determined. Here, we heterologously expressed the serpin gene

FDA-approved thiol-reacting drugs that potentially bind into the SARS-CoV-2 main protease, essential for viral replication.

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Emergent novel SARS-CoV-2 is responsible for the current pandemic outbreak of severe acute respiratory syndrome with high mortality among the symptomatic population worldwide. Given the absence of a current vaccine or specific antiviral treatment, it is urgent to search for FDA-approved drugs that

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

Interaction between marginal zinc deficiency and chronic alcoholism: pancreatic structure and function in rats in vitro.

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The present study was done to determine interaction of ethanol and marginal zinc nutriture on morphology and function of rat pancreas. Sprague-Dawley rats were maintained on Wayne Rodent-Blox ad libitum; marginal zinc-deficient diet plus ethanol ad libitum and pair fed with animals fed marginal

Assessment in vitro and in vivo of muscle degradation in chronic skeletal muscle myopathy of alcoholism.

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1. Muscle protein breakdown in vivo has been studied by measurements of urinary 3-methyl-histidine/creatinine ratios. No differences were found between control subjects and chronic alcoholics either with or without proximal muscle wasting or cirrhosis. 2. Calculation of muscle turnover rates, with

HIV infection and the pancreas: risk factors and potential management guidelines.

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One thousand and eighty-one evaluable HIV-infected patients were assessed for pancreatic abnormalities in a prospective case-control study including the whole follow-up period of each patient (minimum 12 months). The 435 patients (40.2%), who experienced at least one episode of confirmed pancreatic

[Antiretroviral therapy for HIV-infected patients with schizophrenia. Coordinated multidisciplinary management (7 cases)].

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OBJECTIVE Schizophrenia might appear to be an obstacle to the initiation of and especially compliance with antiretroviral therapy for HIV-infected patients. The aims of this study were to describe the clinical, immunologic and virologic course after initiation of antiretroviral therapy in 7 HIV

STATIN-ASSOCIATED INTOLERANCE AND ITS PREVENTION.

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The review analyzes the literature data, which covers the intolerance of statins associated with myopathy. The article gives a definition of statin intolerance, analyzed data from a randomized, controlled trials, where are indicated frequency of statin-associated myopathy, its symptoms in

Functional polymorphism of the MMP-1 promoter (-1607 1G/2G) in potentially malignant and malignant head and neck lesions in an Indian population.

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Matrix metalloproteinases (MMP) are a family of zinc-dependent proteases that degrade the entire component of the extracellular matrix. Our study explores the association of the MMP1 gene promoter (-1607 1G/2G) polymorphisms in oral submucous fibrosis (OSMF) and head and neck squamous cell carcinoma

Pancreatic acinar cell function and morphology in rats fed zinc-deficient and marginal zinc-deficient diets.

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The prevalence of marginal zinc nutriture in several populations of people in this country and the lack of reports on the effect of marginal zinc nutriture in experimental animals prompted us to look at pancreatic acinar cell function and morphology in rats fed a zinc-deficient diet ad libitum: 4

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