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)

It has been suggested that hypertrophic cardiomyopathy (HCM) may be associated with hyperparathyroidism. We evaluated parathyroid function in 15 patients with HCM and 14 patients with primary dilated cardiomyopathy (DCM), measuring different parameters of calcium metabolism (total serum calcium, ionized calcium, PTH, vitamin D metabolites, alkaline phosphatase, osteocalcin). As a group PTH levels were normal in HCM (intact PTH 3.9 +/- 1.6 pmol/l, midmolecular PTH 59 +/- 13 pmol/l and carboxyterminal PTH 0.6 +/- 0.4 ng/ml), but in 3 patients carboxyterminal PTH levels were persistently higher than normal, while all other parameters of calcium metabolism were normal. We conclude that parathyroid function is normal in patients with HCM, although some of them may have an abnormal secretion and/or metabolism of carboxyterminal PTH fragments, or a circulating substance the interferes with this PTH assay. Parathyroid function in DCM patients was normal, except in a patient who had hyperparathyroidism secondary to vitamin D deficiency.
Rev Esp Cardiol
PMID:[Parathyroid function in hypertrophic myocardiopathy]. 175 23

The relation between coronary patency after infusion of recombinant tissue-type plasminogen activator (rt-PA) and clinical and laboratory findings was assessed in patients with acute myocardial infarction. This study focused primarily on information available early in the hospitalization phase. Data were available for 243 patients who received the full dose of rt-PA and who had assessable coronary angiograms 90 min after the start of the intravenous infusion. The infarct-related vessel was scored by an independent assessment committee as being patent in 65% of patients. The left anterior descending coronary artery was involved in 53% of patients, and proximal localization of the infarct-related vessel occurred in 65%. In the majority of patients (85%), the infusion was started within 4 h of the acute event. Neither the angiographic location of the infarct-related vessel nor electrocardiographic evidence of infarct severity or location appeared to have a bearing on thrombolysis with rt-PA. Multivariate logistic regression analysis identified three independent predictors of coronary patency: hematocrit 43 to 47%, blood plasminogen level greater than or equal to 90% of normal and serum alkaline phosphatase greater than or equal to 82% of the local upper normal limit. In addition, the use of intravenous nitrates suggests a positive association with patency.
J Am Coll Cardiol 1988 Apr
PMID:Coronary patency after intravenous infusion of recombinant tissue-type plasminogen activator in acute myocardial infarction. 312 50

The clinical characteristics of 107 patients younger than 60 years with mitral anular calcium (MAC) were compared with those of 107 age- and sex-matched control subjects. The patients with MAC included 55 men and 52 women, mean age 51 years. The control group included 55 men and 52 women, mean age 51 years. Patients with MAC had a higher prevalence of cardiomegaly on chest x-ray (p less than 0.0001), left atrial and left ventricular enlargement by echocardiography (p less than 0.0001), precordial murmurs (p less than 0.0001), diabetes mellitus (p less than 0.0001), systemic hypertension (p less than 0.025) and total conduction defects on surface electrocardiograms (p less than 0.0001) compared with the age- and sex-matched control subjects. The mean serum phosphorus and product of serum calcium and phosphorus were higher in patients with MAC (p less than 0.0025) than in the control subjects. The prevalence of coronary heart disease, aortic stenosis and hypertrophic cardiomyopathy and the mean serum cholesterol, triglyceride, total protein, albumin, creatinine, alkaline phosphatase and calcium levels were not significantly different between patients with MAC and the control subjects.
Am J Cardiol 1984 Dec 01
PMID:Clinical characteristics of patients younger than 60 years with mitral anular calcium: comparison with age- and sex-matched control subjects. 650 99

The aim of this study was to examine the individual contribution of specific heat stress proteins in primary rat cardiocytes to any protection observed following lethal heat stress or simulated lethal ischaemia. cDNAs for the inducible heat stress protein 70, for heat stress proteins 90 or 60, or a control plasmid were contransfected with a detectable marker, alkaline phosphatase, into cardiocytes. Survival assays were performed after the lethal stress. Transfection of the inducible heat stress protein 70 was found to increase survival following a lethal heat stress by 2.45-fold (P < 0.01) and against lethal ischaemia by 2.71-fold (P < 0.01). Transfection of heat stress protein 90 improved survival against heat by 2.55-fold (P < 0.05) but failed to have any effect on survival against lethal ischaemia. Transfection of heat stress protein 60 offered no protection against either stress.
J Mol Cell Cardiol 1996 Dec
PMID:Differential protection of primary rat cardiocytes by transfection of specific heat stress proteins. 900 51

The beta 1 integrin adhesion receptors mediate the binding of cells to extracellular matrices, facilitating their growth, migration, and capacity to deposit matrix proteins: important factors in arterial restenosis and atherosclerosis. The expression of integrins in human coronary artery is, however, unexplored. The aim of the current study was, therefore, to define the expression of beta 1 integrins by cultured human coronary artery vascular smooth muscle cells (hCAVSMC) and in normal human coronary artery; confirming whether or not this differs from the repertoire found in other species and human vessels. The expression of beta 1 integrins by hCAVSMC was assessed by immuno-precipitation and the alkaline phosphatase anti-alkaline phosphatase (APAAP) immunochemical technique. In addition, mRNA expression was defined by reverse transcription polymerase chain reaction (RT-PCR). Normal adult human coronary arteries (n = 4) were also stained by the APAAP method. In vitro hCAVSMC express alpha 2 beta 1 (a collagen and occasional laminin receptor) and alpha 5 beta 1 (a fibronectin receptor) with lesser expression of alpha 3 beta 1 (a multifunctional receptor). They do, however, possess mRNA for several other integrins. Cells within the media of human coronary artery wall express alpha 3 beta 1 and alpha 5 beta 1 but not alpha 2 beta 1: instead the alternative collagen/laminin receptor, alpha 1 beta 1, is expressed in vivo. This pattern of expression differs subtly from that described in rats through it closely parallels that found in other human arteries.
Basic Res Cardiol 1998 Aug
PMID:The expression of beta 1 integrins in human coronary artery. 978 72

Crystalline nicotinic acid (immediate-release niacin) is effective therapy for lipoprotein regulation and cardiovascular risk reduction. However, inconvenient regimens and unpleasant side effects decrease compliance. Sustained-release formulations designed to circumvent these difficulties increase hepatotoxicity. Niaspan, a new US Food and Drug Administration (FDA)-approved, once-daily, extended-release form, has been found effective and safe in short-term trials. The long-term efficacy and safety of Niaspan lipid monotherapy was studied in 517 patients (aged 21-75 years) for < or =96 weeks in dosages < or =3,000 mg/day. Primary efficacy endpoints were low-density lipoprotein (LDL) cholesterol and apolipoprotein B (apo B) changes from baseline; secondary efficacy endpoints were changes in total cholesterol, triglycerides, high-density lipoprotein (HDL) cholesterol, lipoprotein(a), and total cholesterol/HDL-cholesterol ratio; safety data included adverse events and laboratory values over the 2-year study period. LDL-cholesterol levels decreased significantly: 18% at week 48 and 20% at week 96; apo B reduction was similar (16% decrease at week 48 and 19% at week 96). Large elevations in HDL cholesterol (26%, week 48; 28%, week 96) allowed only modest decreases in total cholesterol (12% and 13%, respectively), whereas total cholesterol/HDL-cholesterol ratio decreased by almost one third. Triglyceride and lipoprotein(a) levels were decreased by 27% and 30%, respectively (week 48), and by 28% and 40%, respectively (week 96). All changes from baseline were significant (p <0.001). Niaspan was generally well tolerated, although flushing was common (75%); however, there was a progressive decrease in flushing with time from 3.3 episodes in the first month to < or = 1 episode by week 48. Aspirin was used by one third of patients before Niaspan dosing to minimize flushing episodes. Although serious adverse events occurred in about 10% of patients, none were considered probably or definitely related to Niaspan. Adverse events in general varied widely, but their true relation to the study drug is difficult to ascertain without a placebo (control) group. No deaths occurred. There were statistically significant changes in hepatic transaminases, alkaline phosphatase, direct bilirubin, phosphorus, glucose, amylase, and uric acid. However, these changes were mostly small and are not likely to be biologically or clinically significant (the decrease in phosphorus is a new finding in niacin therapy). No myopathy was observed. Thus, this long-term study confirms the earlier short-term findings that Niaspan is safe and effective as monotherapy in plasma lipoprotein regulation.
Am J Cardiol 1998 Dec 17
PMID:Efficacy and safety of an extended-release niacin (Niaspan): a long-term study. 991 66

To find the clinical variables associated with atorvastatin's effects on bone metabolism markers, 35 patients with heterozygous familial hypercholesterolemia were treated with atorvastatin for 24 weeks, and the levels of bone formation markers (bone-specific alkaline phosphatase and osteocalcin) and resorption marker (urine collagen type-1 cross-linked N-telopeptide) were determined. Pretreatment vitamin D levels showed significant and positive associations with changes in 2 bone formation markers. The serial changes in 3 markers were favorable-increased bone formation markers and unchanged bone resorption marker-but the changes occurred only in patients with pretreatment vitamin D levels >50 pg/ml.
Am J Cardiol 2003 Nov 01
PMID:Effect of pretreatment vitamin D levels on in vivo effects of atorvastatin on bone metabolism in patients with heterozygous familial hypercholesterolemia. 1458 68

Liver disease following the use of hypolipidemic drugs has been reported as a cellular damage (increases in AST or ALT enzymes) without cholestatic alterations (bilirubin and or alkaline phosphatase increases). Six mechanisms were proposed for hepatotoxicity: 1. High energy reactions on P450 cytochrome impairing calcium homeostasis with rupture of intracellular fibrils and hepatocyte lysis. 2. Impairment of transporter proteins related to the bile acids flux (mechanism proposed for fibrate liver toxicity). 3. Immune reactions due to the formation of metabolites linked to enzymes following liver metabolism of hypolipidemic drugs. 4. Hepatotoxicity by T cells with additional inflammation mediated by neutrophils. 5. Apoptosis mediated by TNF and Fas (immune mediated). 6. Oxidative stress due to damage of intracellular organelles. In addition, advanced age, alcohol in excess, high doses of hypolipidemic drugs, interaction with other drugs, and previous active liver disease might increase liver toxicity.
Arq Bras Cardiol 2005 Oct
PMID:[Mechanisms of hepatotoxicity]. 1640 Mar 94

Human bone-marrow-derived mesenchymal stem cells (MSC) are responsible the remodeling of human tissue. However, damaged aortic valves are lack the ability to regenerate which is an active cell-mediated process. Diseased aortic valve remodeling has similarities even to bone formation. In this study, the prerequisites for cultured MSCs to undergo osteoblastic differentiation on aortic valves were explored. An ex vivo model using a human aortic valve microenvironment was developed. The expression of type I procollagen, alkaline phosphatase activity, osteocalcin secretion and osteocalcin immunostaining were studied to evaluate the induction of osteogenesis of the MSCs on noncalcified and calcified human aortic valves. Aortic valves were exposed to freeze-thaw injury to devitalize valves in order to separately study the role of valve matrix vs. endothelial cells in the explants. Thus, valves were assigned to 1 of 4 treatment groups: noncalcified uninjured valves, calcified uninjured valves, noncalcified injured and calcified injured. Finally, valves were decalcified to separately explore the effect of a calcified matrix on the osteogenesis. In this co-culture system, the noncalcified uninjured valves inhibited osteogenesis of MSCs, whereas the calcified valves promoted differentiation towards osteoblastic lineage. Devitalization of the valve matrix inflicted a significant increase in the osteogenesis of co-cultured MSCs. Calcified matrix in the valves seemed to have a role in the spontaneous osteogenesis of the MSCs. This spontaneous matrix induced differentiation of MSCs into osteoblast lineage could not be inhibited by pravastatin, indomethacin or tetracycline. In conclusion, these results suggest that interactions between MSCs and aortic valve matrix components and cells modulate MSC phenotype in this environment. Further studies are required to characterize this interesting phenomenon in greater detail.
J Mol Cell Cardiol 2006 Oct
PMID:Calcification and cellularity in human aortic heart valve tissue determine the differentiation of bone-marrow-derived cells. 1693 7

Primary (AL) amyloidosis is the most common form of systemic amyloidosis seen in current clinical practice. The symptoms of the disease are usually vague, special features are seen in fewer than one fifth of patients, and the combination of organs and systems involved provides a clue for the diagnosis. We describe a patient in whom asymptomatic hepatomegaly, cardiomegaly, hyperlipidaemia and elevated serum alkaline phosphatase level were found during routine examination; the final diagnosis was primary systemic AL amyloidosis with severe cardiomyopathy, resulting in a fatal outcome within eight months from the diagnosis.
Hellenic J Cardiol
PMID:Unusual initial presentation of primary systemic (AL) amyloidosis with severe cardiomyopathy and fatal outcome. 1724 12


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