Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Using the alkaline phosphatase test, the authors studied the capillaries of 41 fields in clinically healthy people aged 22-64 years and animals (dogs, cats, rats) and also in individuals aged 45 to 64 years with mild atherosclerosis in the area of the median cerebral artery trunk. It has been established that unlike "normal" people, atherosclerotic patients of the respective age show an increase in the volume of deposited blood in the presence of a reduction of the working surface and the average indices of the activity of alkaline phosphatase leading to a considerable diminution (21.5-23.5%) in the intensity of metabolic processes.
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PMID:[Histochemical characteristics of the vascular-capillary bed of the brain during aging and in arteriosclerosis]. 647 21

Bilaterally vasectomized langur monkeys were compared with age matched sham operated controls for biochemical constituents of the blood following 1.5, 2.0 and 2.5 years of surgery. No appreciable changes were observed in blood glucose and blood urea and serum total protein, total lipid, phospholipid, total cholesterol, sialic acid, electrolytes (chloride, phosphorus, magnesium, sodium, potassium, copper and zinc) and enzymes (LDH, alkaline phosphatase SGOT and SGPT) suggesting that long-term vasectomy does not cause adverse effects on general body metabolism including atherosclerosis.
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PMID:Effect of vasectomy on biochemical constituents of the blood in langur monkey--a 2 1/2 years follow up. 653 74

To study the effect of hemodialysis on serum lipids and lipoproteins, five patients with normal renal function who had undergone hemodialysis for schizophrenic symptoms for 10 weeks in a crossover study were investigated. Active or sham (no dialysate flow through the filter) dialysis was instituted randomly. Serum lipids were isolated by ultracentrifugation and precipitation before and after each period. High density lipoprotein (HDL) cholesterol levels were constantly low and correlated negatively with serum alkaline phosphatase concentrations (p less than 0.05). Serum and very low density lipoprotein (VLDL) triglycerides and VLDL cholesterol increased during active, and to a lesser extent during sham, dialysis. Dialysis of this intensity does not affect HDL. The low levels may be secondary to subclinical cholestasis from neuroleptic drug treatment. Some individuals may develop hypertriglyceridemia of unknown pathogenesis during hemodialysis. Both these lipoprotein abnormalities are risk factors for the development of atherosclerosis.
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PMID:Serum lipids and lipoproteins in schizophrenic patients with normal renal function treated with hemodialysis. 657 52

Parallel stereo- and cytospectrophotometric examinations of human myocardial capillaries, 20-60 min after biological death were carried out. The activity of alkaline phosphatase, adenosine triphosphatase, lactate dehydrogenase and NAD-diaphorase in the capillary wall in relation to the sex and age in cardiovascular pathology, renal diseases and leukemias were studied. The permeability and level of energy supply of transendothelial transport were found to depend on the kind of the main pathological process and type of death. According to the parameters under study, the functional state of the capillary network of the myocardium in atherosclerosis with or without its combination with hypertension and also in secondary renal hypertension is described.
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PMID:[Stereological characteristics and enzymatic activity of myocardial capillaries in different variants of pathology and death (data from immediate autopsies)]. 686 Jan 68

A chondroitin sulfate-dermatan sulfate proteoglycan was isolated from bovine aorta intima by extraction of the tissue with 4 M guanidine hydrochloride. The proteoglycan was purified by CsCl isopycnic centrifugation followed by gel filtration and ion exchange chromatography. A monoclonal antibody C8F4 was developed to this core protein. The characteristics and specificity of the antibody were studied by an enzyme-linked immunosorbent assay (ELISA) using an alkaline phosphatase conjugated antibody (goat anti-mouse IgG). The antibody binding to the core protein was found specific and optimal at pH 7.0. The antibody recognizes either intact chondroitin sulfate-dermatan sulfate proteoglycan monomer, chondroitinase ABC digested monomer or chemically deglycosylated proteoglycan. Free chondroitin sulfates, keratan sulfate and hyaluronic acid did not compete for the antigenic sites in ELISA. Limited hydrolysis of the core protein by trypsin resulted in three peptides and only the peptide with a molecular weight M(r) = 40,000 was found capable of binding to hyaluronic acid. The antibody C8F4 recognized this hyaluronic acid binding peptide but did not recognize the other two peptides suggesting that the epitope(s) for this antibody is in the hyaluronic acid-binding region of the core protein. The antibody recognized the core proteins from bovine nasal cartilage proteoglycan and human aorta proteoglycan but did not recognize bovine aorta link protein, bovine serum albumin, human serum albumin, human transferrin, collagen Type I and fibronectin. The antibody was found useful to localize proteoglycans in atherosclerotic lesions in human aorta by immunohistochemical techniques.
Atherosclerosis 1993 Jan 25
PMID:A monoclonal antibody that recognizes hyaluronic acid binding region of aorta proteoglycans. 768 Dec 90

Risk factors for primary cerebral hemorrhage remain uncertain. The population-based Stroke Registry of Dijon provides data on the risk factors. Among residents of Dijon (France), 130 cases of primary cerebral hemorrhage hospitalized from 1985 to 1992 were matched with 130 controls by age and sex. The following data were collected: history of hypertension, alcohol consumption, tobacco consumption, history of coagulation disorder, diabetes mellitus, dyslipidemia, and infectious disease in the 7 days before admission. The following parameters were measured on admission: blood pressure, blood glucose, cholesterol, triglycerides, hematocrit, fibrinogen, prothrombin levels, platelet counts, prothrombin time, bilirubin, transaminases, gamma-glutamyltransferase, and alkaline phosphatase. Electrocardiogram and Doppler ultrasound examination of cervical arteries were performed. Statistical analysis was performed by means of relative risk ratio for paired samples when dealing with proportions, and Student's t test for quantitative variables. A stepwise discriminant analysis was carried out to establish the relative weight of the different risk factors and their discriminant values. Among the qualitative data, the significant factors were history of hypertension, alcohol consumption, cardiac arrhythmia, atherosclerosis of carotid arteries and a previous infectious disease in the 7 days before admission. Among the quantitative data, the significant factors were early hypertension, high blood glucose levels, high hematocrit, and low cholesterol levels, in the acute stage of the stroke. After multifactorial analysis, only two factors were significant: hypertension and low cholesterol levels. Our population-based case-control study showed that hypertension and low cholesterol levels are the two discriminant risk factors for both lobar and basal ganglia primary cerebral hemorrhage. Therefore, treatment of hypercholesterolemia may increase risk of cerebral hemorrhage.
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PMID:Risk factors for primary cerebral hemorrhage: a population-based study--the Stroke Registry of Dijon. 789 3

A total of 123 patients with primary hypercholesterolemia were randomized on a 2:1 ratio to receive either fluvastatin at 20 mg once daily at night (n = 82) or gemfibrozil at 600 mg twice daily (n = 41) in a double-blind, double-dummy comparison of the effects on plasma lipid parameters and tolerability over 8 weeks. All patients had either low-density lipoprotein cholesterol (LDL-C) concentrations > or = 160 mg/dL (4.1 mmol/L) in association with definite coronary artery disease (CAD) or > or = 2 risk factors, or LDL-C > or = 190 mg/dL (4.9 mmol/L) with no CAD and < 2 risk factors. All had triglyceride (TG) levels < or = 350 mg/dL (4.0 mmol/L). After 8 weeks of treatment, fluvastatin produced significant reductions from baseline of 17.4% (p < 0.001) in LDL-C, 13.2% (p < 0.001) in total cholesterol (TC), 13.8% (p < 0.001) in very low-density lipoprotein cholesterol (VLDL-C), and 6.4% (NS) in TG. High-density lipoprotein cholesterol (HDL-C) was increased by 5.6% (p < 0.001), and the ratio of LDL-C:HDL-C (Friedewald) was decreased by 21.2% (p < 0.001). Gemfibrozil reduced LDL-C by 15.8%, TC by 13.4%, VLDL-C by 32.2%, LDL-C:HDL-C by 24.8%, and TG by 34.2%, and increased HDL-C by 13.9% (all changes were statistically significant, p < 0.001) compared with baseline. Gemfibrozil produced significantly greater changes in VLDL-C (p < 0.01), HDL-C (p < 0.001), and TG (p < 0.001), but not in LDL-C: HDL-C, compared with fluvastatin. Both drugs significantly reduced apolipoprotein (apo) B and lipoparticles (Lp) E:B, and increased apo A-I but had divergent effects on LpA-I (increased with fluvastatin and reduced with gemfibrozil; p < 0.05). At the end of the study, 43.8% of fluvastatin patients and 45% of gemfibrozil patients achieved a reduction of > 20% in LDL-C levels. Normalization of LDL-C levels was achieved (according to European Atherosclerosis Society guidelines) by 13.4% of fluvastatin- and 14.6% of gemfibrozil-treated patients. Both drugs were well tolerated; adverse events occurred in 36.6% of fluvastatin recipients compared with 58.5% of patients taking gemfibrozil. No clinically notable elevations of aspartate or alanine aminotransferases, alkaline phosphatase, or creatine phosphokinase occurred. No patient developed new or worsening lens opacities associated with a reduction in optically corrected visual acuity. The most commonly reported adverse events were headache and gastrointestinal upset. There were no serious drug-related adverse events.
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PMID:Comparison of lipid-lowering effects of low-dose fluvastatin and conventional-dose gemfibrozil in patients with primary hypercholesterolemia. 801 67

Previous studies in our laboratory demonstrated messenger RNA for bone morphogenetic protein-2a in human calcified plaque, suggesting that arterial calcification is a regulated process, similar to osteogenesis. To further test this hypothesis, we have isolated and cloned a subpopulation of cells from bovine aortic media that show osteoblastic potential. These novel cells are primarily distinguished from smooth muscle cells by expression of a surface marker preliminarily identified as a modified form of the ganglioside sialyl-lactosylceramide (GM3). Osteoblastic potential was indicated by high levels of alkaline phosphatase and collagen I, expression of osteopontin and osteonectin (SPARC), and production of bone-specific osteocalcin and hydroxyapatite. Cultures of these cells were stimulated to form increased numbers of calcium-mineral-producing nodules by the oxysterol 25-hydroxycholesterol as well as by transforming growth factor-beta 1, both known to be present in atherosclerotic lesions. The stimulation of calcifying vascular cells in the artery wall by these two factors suggests a possible mechanism for the colocalization of calcification with atherosclerosis in vivo.
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PMID:TGF-beta 1 and 25-hydroxycholesterol stimulate osteoblast-like vascular cells to calcify. 818 41

Patients with primary hyperparathyroidism have increased bone turnover, but it is less well documented how brief periods of excess parathyroid hormone (PTH) (endogenous or exogenous) affect bone metabolism. In the present double blind study, we examined the effect of either ethylenediaminetetraacetatic acid (EDTA) or placebo on serum levels of PTH and biochemical markers of bone turnover in 15 women and 39 men (aged 41 to 81 years) suffering intermittent claudication due to atherosclerosis. Disodium EDTA was administered as 20 repeated infusions of 3 grams during a period of 5-9 weeks. Serum calcium and serum phosphate decreased following treatment (p < 0.001) and remained unchanged in the placebo group. However, the differences between the groups were insignificant (ANOVA p = 0.13 and p < 0.10, respectively). PTH increased 2 1/2 fold following EDTA treatment (p < 0.001, ANOVA). The change in serum PTH was inversely correlated with the change in serum calcium (r = -0.53, p < 0.01). In the EDTA group, urinary hydroxyproline/creatinine and calcium/creatinine increased after treatment (ANOVA p < 0.001 and p < 0.05, respectively). Serum bone alkaline phosphatase decreased significantly in the EDTA group immediately after treatment (p < 0.001, ANOVA) and returned to baseline level at three months while only an insignificant decrease in serum osteocalcin was seen following treatment. We conclude that EDTA treatment increases endogenous PTH secretion considerably and leads to increased bone resorption. However, no changes in osteoblastic markers indicating increased activation of bone remodeling could be demonstrated. Our findings support that chelation therapy with EDTA is accompanied by bone loss.
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PMID:Effects of intravenous EDTA treatment on serum parathyroid hormone (1-84) and biochemical markers of bone turnover. 829 6

Disorders in lipoprotein metabolism (dyslipidemia) can result in premature atherosclerosis or pancreatitis. Dyslipidemias can be classified as hypercholesterolemia, hypertriglyceridemia, combined hyperlipidemia, and low levels of high density lipoprotein (HDL) cholesterol. All of the dyslipidemias can be primary or secondary. Both elevated levels of low density lipoprotein cholesterol and decreased levels of HDL cholesterol predispose to premature atherosclerosis. Triglyceride levels greater than 1,000 mg/dL increase the risk for pancreatitis. In the appraisal of the dyslipidemias, measurement of serum cholesterol, triglycerides, HDL-cholesterol and obtaining the LDL cholesterol by Friedewald equation is usually sufficient in the majority of patients. However, in some cases, such as the diagnosis of the Type III dyslipidemia and when triglycerides are > or = 400 mg/dL, ultracentrifugation is required to determine the VLDL or LDL cholesterol. Lipoprotein electrophoresis can be useful in the diagnosis of Type III dyslipidemia (broad beta band) and also to detect chylomicrons. In young subjects with coronary artery disease with a normal LDL cholesterol an apolipoprotein B-100 level may be a useful test. In children and young adults with severe hypertriglyceridemia, measurement of lipoprotein lipase activity or assaying apolipoprotein C-II levels can be useful in elucidating the cause. Also, laboratory tests are useful in excluding a secondary cause of dyslipidemia (urinalysis, plasma creatinine, TSH, glucose, protein electrophoresis, alkaline phosphatase and transaminases). Thus, laboratory investigations play an important role in the management of dyslipidemia.
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PMID:A practical approach to the laboratory diagnosis of dyslipidemia. 870 23


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