Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, serum Zn(2+) content was determined by a new enzymatic method. The method depends on the reactivation of apocarbonic anhydrase proportional to the Zn(2+) content of the sample. Carbonic anhydrase was purified from bovine erythrocytes by affinity chromatography. The Zn(2+) in its structure was removed by dialysis against pyridine 2,6-dicarboxylic acid, resulting in a pure apoenzyme with a yield of 100%. The activity of the enzyme was determined by its esterase effect on 4-nitrophenyl acetate. Zn(2+) levels were determined in the serum samples obtained from 100 healthy subjects, 10 patients with cirrhosis, 12 diabetic patients and 15 patients with chronic renal failure by this enzymatic method and by atomic absorption for comparison. There was a good correlation between the two methods in all patients and controls and intraassay CV% was 2.4 and 4.2 for enzymatic and atomic absorption methods, respectively and interassay CV% as 3.9 and 6.1 respectively.
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PMID:An enzymatic method for zinc determination in serum. 834 75

Diuretic therapy is a drug therapy that increases urine volume, but not glomerular filtration rate (GFR). The diuretics act predominantly on tubular sites; the drugs that increase GRF are the aminophyllines, the positive inotropy or vasoactive substances that increase afferent arteriolar flux or intraglomerular pressure. We can divide the diuretics into six categories: 1) carbonic anhydrase inhibitors: acetazolamide, dichlorphenamide, methazolamide; 2) osmotic diuretics: glycerol, mannitol, urea; 3) loop diuretics: furosemide, bumetanide, ethacrynic acid, piretanide, torsemide; 4) thiazide and thiazide-like diuretics: chlorothiazide, trichlormethiazide, indapamide, chlorthalidone, metolazone; 5) potassium-sparers: a) kidney epithelial sodium channel inhibitors: amiloride and triamterene; b) aldosterone receptor antagonists: spironolactone, canrenoate potassium, eplerenone; 6) ADH antagonists: lithium salts, demeclocycline and ethanol. Diuretic therapy is useful in treating acute and chronic renal insufficiency, congestive heart failure, cirrhosis, overhydration and hypertension. Diuretic therapy increases urine volume, ion loss (except Na+, K+), and modifies diffusion (dilute urine) and convection mechanisms (reduced tubular absorption). Therefore, diuretics are very useful non-dangerous drugs.
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PMID:[Diuretic therapy in heart failure]. 1663 1

Heart failure, hypertension, cirrhosis and nephritic syndrome are among conditions that alter volume and composition of body fluids and are modulated by diuretics. Natural products are important source of diuretics and have been considered remarkable alternative with greater effectiveness and fewer side effects. However, many of these plants used in traditional medicine must be scientifically assessed about their efficacy and toxicity. Despite the large number of published articles claiming that plants or plant-derived components may act as diuretic agents, few studies have addressed the mechanism of action of medicinal plants. Thus, the aim of this review was to provide an overview of the current knowledge about the major cellular and molecular mechanisms of diuretic plants and/or their main compounds. Many well-established mechanisms (water channels, renal carriers, nitric oxide-cGMP and prostaglandin-cAMP pathways, renin-angiotensin and kinin-kallikrein systems, carbonic anhydrase, and osmotic effects), along with other newly identified targets, are connected to the diuretic activity of many natural products. However, the central path responsible for the activity of these agents remains unclear. Further studies may help clarifying the central role of each of these pathways in the pleiotropic response of these agents.
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PMID:Cellular and Molecular Mechanisms of Diuretic Plants: An Overview. 2775 2

Almost all the patients with hepatocellular carcinoma (HCC) at advanced stage experience pathological changes of chronic liver cirrhosis, which generally leads to moderate ascites. Recognition of novel biomarkers in malignant ascites could be favorable for establishing a diagnosis for the HCC patients with ascites, and even predicting prognosis, such as risk of distant metastasis. To distinguish the proteomic profiles of malignant ascites in HCC patients from those with nonmalignant liver cirrhosis, an iTRAQ pipeline was built up to analyze the differentially distributed proteins in the malignant ascites from HCC patients (n=10) and benign ascites from hepatic decompensation (HD) controls (n=9). In total, 112 differentially distributed proteins were identified, of which 69 proteins were upregulated and 43 proteins were downregulated (ratio <0.667 or >1.3, respectively) in the malignant ascites. Moreover, 19 upregulated proteins (including keratin 1 protein and rheumatoid factor RF-IP20, ratio>1.5) and 8 downregulated proteins (including carbonic anhydrase 1, ratio<0.667) were identified from malignant ascites samples. Functional categories analyses indicated that membrane proteins, ion regulation, and amino acid metabolism are implicated in the formation of HCC malignant ascites. Pathways mapping revealed that glycolysis/gluconeogenesis and complement/coagulation cascades are the mostly affected cell life activities in HCC malignant ascites, suggesting the key factors in these pathways such as Enolase-1 and fibrinogen are potential ascitic fluid based biomarkers for diagnosis and prognosis for HCC.
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PMID:Identification of Candidate Biomarkers in Malignant Ascites from Patients with Hepatocellular Carcinoma by iTRAQ-Based Quantitative Proteomic Analysis. 3034 3