Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.1.3.1 (alkaline phosphatase)
47,916 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Spontaneous renal artery embolism is not rare, but a correct diagnosis and appropriate treatment are often delayed. Clinical features and follow-up of 17 cases are reported. Cardiac disease or arrhythmias pre-existed in 16 patients. Initial symptoms included flank pain (seven cases), abdominal or chest pain alone (seven), and nausea and vomiting (eight). Fever (greater than or equal to 37.5 degree C) occurred in 10 cases and flank tenderness in only eight. Laboratory findings included leukocytosis, proteinuria, hematuria, and elevated levels of lactic dehydrogenase, serum glutamic-oxalacetic transaminase, serum glutamic-pyruvic transaminase, and alkaline phosphatase. Serum creatinine level exceeded 1.3 mg/dl in 88% and 4.0 mg/dl in 65%; four patients required dialysis. The diagnosis, made by scintiscan, arteriography, or both was often delayed. Renal embolization was bilateral in seven patients and unilateral in 10, with serum creatinine level above 4.0 mg/dl in five of the latter. Emboli to other organs caused early death; cardiovascular disease led to later death. With anticoagulants, renal function returned in patients surviving more than 1 month, even those with bilateral emboli. Thus, renal embolism is recognizable if the disease is considered, and a favorable outcome is common with long-term anticoagulants.
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PMID:Renal artery embolism: clinical features and long-term follow-up of 17 cases. 69 26

To investigate the effect of moderate alcohol consumption on blood constituents related to cardiovascular disease, 12 male volunteers consumed (instead of their usual alcoholic drinks) four different standardized amounts of red wine in addition to their habitual diet. Each dose was given to the subjects during a period of 5 weeks in a randomized order, all subjects receiving the four doses. They consisted of 0, 2, and 4 glasses/d, providing 0, 23, and 46 g alcohol/d as well as in "binge drinking" (14 glasses in the weekend, comparable to an average of 2 glasses/d). The results showed a clear dose-related response to the drinking for several blood constituents. Most marked was a decrease in the tissue-type plasminogen activator activity and to a lesser degree an increase in plasminogen levels. Collagen-induced platelet aggregation was reduced, affecting all parameters measured. Levels of HDL3-cholesterol, gammaglutamyltransferase, and urate showed a small but significant increase. No change was noted in the levels of alkaline phosphatase, alanine-aminotransferase, aspartate-aminotransferase, bile acids, folate, fibrinogen, the ADP-induced platelet aggregation, platelet secretion, or in hematologic values. The results are only partially in accordance with the presumed protective action of moderate drinking on the cardiovascular system and show a stronger response to the consumption of alcohol in coagulation and fibrinolysis factors than in blood lipids.
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PMID:Effects of moderate alcohol consumption on platelet aggregation, fibrinolysis, and blood lipids. 288 51

Heritability analyses were performed with clinical chemistry data collected on 360 twin pairs of white, middle-aged male veterans during the second examination of the NHLBI Twin Study, a multicenter study of cardiovascular disease risk factors. Significant genetic variability was present for albumin, alkaline phosphatase, blood urea nitrogen, 1-hr postload glucose, phosphorus, total protein, and uric acid. Calcium and aspartate aminotransferase had significantly different means by zygosity, which precluded further analysis. Total bilirubin and lactate dehydrogenase did not show evidence for genetic variation at this examination. Comparisons are made to results from similar twin studies and the first examination of the NHLBI Twin Study. Heritability estimates for phosphorus and blood urea nitrogen exhibited marked stability across studies, while heritability estimates for total bilirubin, total protein, and uric acid decreased in older study populations. The heritability of 1-hr postload blood glucose decreased from 0.88 at the first NHLBI examination to 0.52 at the second one. Interpretation of these results requires consideration of possible selection biases, methodologic and demographic issues, and the view that for some clinical chemistries, biological aging along with prolonged environmental exposures may alter the amount of phenotypic variation explained by the additive effect of genes alone.
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PMID:Heritability of clinical chemistries in an older twin cohort: the NHLBI Twin Study. 356 74

1. The welfare of male and female male-line turkeys fed ad libitum or food-restricted was determined at 4, 8, 12, 16, 20, 24, 28, 36(38) and 46(48) weeks of age using behavioural and physiological indices of well-being. Traditional turkeys fed ad libitum were kept as a control treatment. Restricted male and female male-line turkeys were fed to 0-5 during rearing and subsequently to 0-8 of sex-specific ad libitum-fed body weight. In another treatment, male-line males were fed ad libitum to 18 weeks and 0.8 of ad libitum thereafter. 2. Traditional turkeys and restricted male-line turkeys were more active than ad libitum-fed birds of both sexes. Restricted turkeys showed a high incidence of wall pecking. In the breeding period, about 0.4 of the observations of male-line males were of strutting behaviour whereas traditional male turkeys showed no strutting behaviour at the end of the breeding period. 3. The heterophil lymphocyte ratio (HLR) and the proportion of basophils were not increased in food-restricted turkeys. The HLR was relatively low in traditional birds, compared with male-line turkeys during the rearing period. 4. Plasma corticosterone concentrations were increased by food restriction during the rearing period. Corticosterone concentrations were relatively high in traditional turkeys at 4 and 8 weeks of age only. 5. Plasma lactate dehydrogenase (LIDH) activity was higher from 12 to 24 weeks of age in ad libitum-fed male-line turkeys and was consistent with mortality from cardiovascular disease in this group of turkeys. The pattern of activity of aspartate transaminase was similar, and alkaline phosphatase was inversely related to that of LDH. 6. It was concluded that turkeys may be better able to adjust physiologically to the demands of food restriction than broiler breeders and that there were few deleterious consequences of restricting male turkeys after 18 weeks of age. Male-line turkeys were less active than traditional turkeys.
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PMID:Welfare of food restricted male and female turkeys. 1040 31

Liver transplant recipients have an increased risk for cardiovascular disease because of a high incidence of obesity, arterial hypertension, diabetes mellitus, and hyperlipidemia. Hyperhomocysteinemia has been found to be an important risk factor for cardiovascular disease in large studies. Fasting serum levels of homocysteine were measured in 105 liver transplant recipients, and hyperhomocysteinemia was defined as a fasting serum homocysteine level greater than 13 micromol/L. Patients with versus without hyperhomocysteinemia were compared. The possible association of hyperhomocysteinemia with age, sex, cause of liver disease, time elapsed since liver transplantation, immunosuppressive therapy, folic acid level, liver function test results, renal function, and other cardiovascular risk factors was investigated. Patients with serum homocysteine levels greater than 15 micromol/L were treated with folic acid, 10 mg/d, and serum homocysteine levels were measured again 1 to 3 months later in 10 patients. Hyperhomocysteinemia was detected in 28 patients (27%). In univariate analysis, it was associated with hepatitis C virus infection, treatment with mycophenolate mofetil, and greater serum levels of alkaline phosphatase, gamma-glutamyl transpeptidase, urea, and creatinine. In multivariate analysis, only greater serum levels of creatinine (P =.006) were associated with hyperhomocysteinemia. Treatment with folic acid resulted in a decrease in fasting serum homocysteine levels in 9 of the 10 patients tested (P =.01). Hyperhomocystinemia, associated with renal dysfunction, is a frequent finding in liver transplant recipients. Treatment with folic acid may reduce fasting homocysteine levels.
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PMID:Hyperhomocysteinemia in liver transplant recipients: prevalence and multivariate analysis of predisposing factors. 1098 61

Leptin, the product of the ob gene, regulates food intake, energy expenditure, and other physiological functions of the peripheral tissues. Leptin receptors have been identified in the hypothalamus and in extrahypothalamic tissues. Increased circulating leptin levels have been correlated with cardiovascular disease, obesity, aging, infection with bacterial lipopolysaccharide, and high-fat diets. All these conditions have also been correlated with increased vascular calcification, a hallmark of atherosclerotic and age-related vascular disease. In addition, the differentiation of marrow osteoprogenitor cells is regulated by leptin. Thus, we hypothesized that leptin may regulate the calcification of vascular cells. In this report, we tested the effects of leptin on a previously characterized subpopulation of vascular cells that undergo osteoblastic differentiation and calcification in vitro. When treated with leptin, these calcifying vascular cells had a significant 5- to 10-fold increase in alkaline phosphatase activity, a marker of osteogenic differentiation of osteoblastic cells. Prolonged treatment with leptin enhanced the calcification of these cells, further supporting the pro-osteogenic differentiation effects of leptin. Furthermore, the presence of the leptin receptor on calcifying vascular cells was demonstrated using reverse transcriptase polymerase chain reaction, immunocytochemistry, and Western blot analysis. We also identified the presence of leptin receptor in the mouse artery wall, localized to subpopulations of medial and adventitial cells, and the expression of leptin by artery wall cells and atherosclerotic lesions in mice. Taken together, these results suggest that leptin regulates the osteoblastic differentiation and calcification of vascular cells and that the artery wall may be an important peripheral tissue target of leptin action.
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PMID:Leptin enhances the calcification of vascular cells: artery wall as a target of leptin. 1134 6

Primary hyperparathyroidism (pHPT) is associated with an increased fracture risk, and decreased bone density thus has been considered an indication for surgery. However, many pHPT patients have a multifactorial risk profile for osteoporosis and bone fractures. The aim of the present study was to evaluate variables associated with fracture risk within the group of pHPT patients. A series of 203 consecutive patients operated for pHPT were investigated with bone mineral content and biochemical and clinical risk factors for bone fracture. Seventeen patients (8%) had a history of at least one bone fracture up to 5 years before pHPT surgery. Twenty-six patients (13%) had a history of at least one fracture during the 10-year period prior to surgery. In the univariate analyses corticosteroid treatment, serum levels of alkaline phosphatase, 25-hydroxyvitamin D3, type I collagen telopeptide, and bone mineral content were found to be associated with a history of bone fractures up to 10 years before surgery. Additionally, age and menopausal status were of importance for fractures during the 10-year-period, whereas a history of cardiovascular disease was important for fractures during the 5-year-period prior to surgery. Multivariate analyses showed that serum level of PTH was independently associated with bone fractures during the 5-year period prior to pHPT surgery and further that serum level of 25-hydroxyvitamin D3 was associated with fractures up to 10 years before surgery. In conclusion, serum levels of 25-hydroxyvitamin D3 and PTH were independently associated with a history of bone fractures in pHPT. These variables should be considered when evaluating patients for parathyroid surgery.
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PMID:Multifactorial risk profile for bone fractures in primary hyperparathyroidism. 1229 14

Accumulating evidence has suggested the protective role of HDL in cardiovascular disease processes. Calcification is a common feature of atherosclerotic lesions and contributes to cardiovascular complications due to the loss of aortic resilience and function. Recent studies have suggested that vascular calcification shares several features with skeletal bone formation at the cellular and molecular levels. These include the presence of osteoblast-like calcifying vascular cells in the artery wall that undergo osteoblastic differentiation and calcification in vitro. We hypothesized that HDL may also protect against vascular calcification by regulating the osteogenic activity of these calcifying vascular cells. When treated with HDL, alkaline phosphatase activity, a marker of osteogenic differentiation of osteoblastic cells, was significantly reduced in those cells. Prolonged treatment with HDL also inhibited calcification of these cells, further supporting the antiosteogenic differentiation property of HDL when applied to vascular cells. Furthermore, HDL inhibited the osteogenic activity that was induced by inflammatory cytokines interleukin (IL)-1beta and IL-6 as well as by minimally oxidized LDL. HDL also partially inhibited the IL-6-induced activation of signal transducer and activator of transcription 3 in calcifying vascular cells, suggesting that HDL may inhibit cytokine-induced signal transduction pathways. The inhibitory effects of HDL were mimicked by lipids extracted from HDL but not by HDL-associated apolipoproteins or reconstituted HDL. Furthermore, oxidation of HDL rendered it pro-osteogenic. Taken together, these results suggest that HDL regulates the osteoblastic differentiation and calcification of vascular cells and that vascular calcification may be another target of HDL action in the artery wall.
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PMID:High-density lipoprotein regulates calcification of vascular cells. 1236 84

Ectopic calcification is commonly associated with cardiovascular disease, injury, aging, and biomaterial implantation. We hypothesized that the normal mechanical environment of smooth muscle cells (SMCs) inhibits a phenotypic switch to a pattern of gene expression more typical for bone and inducive for calcification. This hypothesis was tested using a 3-D engineered smooth muscle tissue model subjected to cyclic mechanical strain. This simplified model maintained a 3-D tissue architecture while eliminating systemic effects as can be seen with in vivo models. All engineered tissues were found to express bone-associated genes (osteopontin, matrix gla protein, alkaline phosphatase, and the transcription factor CBFA-1). Strikingly, however, expression of these genes was down-regulated in tissues exposed to cyclic strain at all time points ranging from 5 to 150 days. Furthermore, long-term strain played a protective role in regard to calcification, as unstrained tissues exhibited increased calcium deposition with respect to strained tissues. The results of this study suggest that without an appropriate mechanical environment, SMCs in 3-D culture undergo a phenotypic conversion to an osteoblast-like pattern of gene expression. This finding has significant implications for the mechanisms underlying a variety of cardiovascular diseases and indicates the broad utility of engineered tissue models in basic biology studies.
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PMID:Cyclic strain inhibits switching of smooth muscle cells to an osteoblast-like phenotype. 1251 16

Infectious disease, commonly caused by bacterial pathogens, is now the world's leading cause of premature death and third overall cause behind cardiovascular disease and cancer. Urinary Tract Infection (UTI), caused by E. coli bacteria, is a very common bacterial infection, a majority in women (85%) and may result in severe kidney failure if not detected quickly. Among hundreds of strains the bacteria, E. coli 0157:H7, is emerging as the most aggressive one because of its capability to produce a toxin causing hemolytic uremic syndrome (HUS) resulting in death, especially in children. In the present study, a project has been undertaken for developing a rapid method for UTI detection in very low bacteria concentration, applying current knowledge of nano-technology. Experiments have been designed for the development of biosensors using nano-fabricated structures coated with elements such as gold that have affinity for biomolecules. A biosensor is a device in which a biological sensing element is either intimately connected to or integrated within a transducer. The basic principle for the detection procedure of the infection is partly based on the enzyme-linked immunosorbent assay system. Anti-E. coli antibody-bound Gold Nanowire Arrays (GNWA) prepared on anodized porous alumina template is used for the primary step followed by binding of the bacteria containing specimen. An alkaline phosphatase-conjugated second antibody is then added to the system and the resultant binding determined by both electrochemical and optical measurements. Various kinds of GNWA templates were used in order to determine the one with the best affinity for antibody binding. In addition, an efficient method for enhanced antibody binding has been developed with the covalent immobilization of an organic linker Dithiobissuccinimidylundecanoate (DSU) on the GNWA surface. Studies have also been conducted to optimize the antibody-binding conditions to the linker-attached GNWA surfaces for their ability to detect bacteria in clinical concentrations.
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PMID:Nano-biosensor development for bacterial detection during human kidney infection: use of glycoconjugate-specific antibody-bound gold NanoWire arrays (GNWA). 1575 Jul 90


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