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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

High plasma homocysteine (tHcy) is a risk factor for cardiovascular disease and stroke and Alzheimer's disease (AD). An inverse relationship has been reported between tHcy and plasma B12 and folate levels. Seventy-nine AD patients and 156 controls from three Arab villages in northern Israel participated. Plasma tHcy, B12 and folate levels were determined. Data were analyzed using univariate statistical tests and logistical regression with confounders. tHcy was significantly higher in AD patients (20.6+/-8.7 micromol/l) than in controls (16.4+/-6.5 micromol/l) (p=0.03) after correction for year of birth, gender and smoking status. Plasma B12 (322.9+/-136.0/350.5+/-175.3 pmol/l) and plasma folate (4.5+/-3.8/4.9+/-2.6 nmol/l) levels did not differ significantly between AD patients and controls. Subjects in the highest tHcy tertile or in the lowest B12 and folate tertiles did not have greater risk to develop AD. In this population residing in Arab villages in northern Israel, tHcy levels were significantly higher among AD patients than in controls. Plasma B12 and folate levels were lower among cases but were not significant. There was not a significant association between plasma tHcy, B12 and folate levels in controls or AD patients. High levels of tHcy may suggest the need for folate and vitamin B12 supplementation in this population.
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PMID:Plasma homocysteine, vitamin B12 and folate in Alzheimer's patients and healthy Arabs in Israel. 1554

Over the last 30 years, cardiovascular diseases (CVDs), including stroke and myocardial infarction, have increased in developing countries. Serum lipids and diet of the Fulani, a rural Nigerian population, were previously studied. Despite their consumption of a diet rich in saturated fat, the overall blood lipid profiles of Fulani men and women are generally favourable. However, Fulani males in the same study had mean serum levels of homocysteine, an emerging risk factor for CVD, that exceeded the upper limit of the homocysteine reference range. The authors were interested in knowing if these findings in the Fulani nomads were representative of the biochemical parameters of CVD risk in other ethnic groups in the same region of Nigeria. To address this question, the nutrient content of diets of 55 men, aged 20-75 years, and 77 women, aged 20-70 years, who were inhabitants of a large urban centre in northern Nigeria, was assessed, and their serum levels of total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides, and homocysteine were determined. These data were compared with those of the same rural Fulani population studied previously. Urban subjects consumed more calories than rural subjects (men: 2061 vs 1691 kcal; women: 1833 vs 1505 kcal) and had a significantly higher mean body mass index (BMI) and percentage of body fat than rural subjects. Both urban males and females had carbohydrate intakes that were greater than those of Fulani pastoralists (men: 56% vs 33% total calories; women: 51% vs 38% total calories), but had a significantly lower dietary intake of total fat and saturated fat (men: 36% vs 51% of total calories; women: 40% vs 51% of total calories). With the exception of HDL-cholesterol levels, which were significantly lower in the rural population, the blood lipid profiles of rural subjects were more favourable compared to those of urban subjects. Both urban and rural males had homocysteine levels above the upper limit of the reference range for healthy adults (urban males--12.7 micromol/L; rural males-15.2 micromol/L). The dietary intakes of folate and vitamin B12 were lower for rural Fulani subjects, and this was reflected in their significantly lower serum concentrations of these two vitamins. Results of this study suggest that, although the lipid profiles of urban and rural men and women in northern Nigeria indicate a relatively low risk for CVD, their elevated serum homocysteine levels are a cause for concern. The high homocysteine levels among rural men and women could be explained in part at least by their marginal status with respect to folate and vitamin B12.
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PMID:Risk factors for cardiovascular disease and diet of urban and rural dwellers in northern Nigeria. 1566 69

Our previous study showed that overuse of the nonparetic hand and wrist of the nonparetic side following stroke result in significantly more abnormal on the nonparetic side than on the hemiparetic side in terms of electrophysiologic indices of median nerve function. The purpose of this study was to evaluate the effects of the orally administered mecobalamin, an analogue of vitamin B12, for carpal tunnel syndrome (CTS) in the nonparetic side in patients following stroke. In a randomized open label and prospective study of stroke patients, 67 received of 1500 mug mecobalamin daily for 2 years, and the remaining 68 (untreated group) did not. At baseline, sensory nerve conduction velocity, motor nerve conduction velocity, sensory nerve action potentials (SNAP) at the wrist, palm-to-wrist distal sensory latency, palm-to-wrist SNAP, motor nerve conduction velocity compound motor action potentials, and distal motor latency of median nerve were significantly more abnormal on the nonparetic side than on the hemiparetic side or in controls. Before the treatment 21 patients (31%) of untreated and 20 patients (30%) of treated group met electrophysiologic criteria for CTS. Sensory impairment of the nonparetic side had lessened in the treated group. After 2 years, all electrophysiologic indices of nonparetic side were significantly improved in the treated group compared with those in the untreated group. The improvement from baseline of electrophysiologic parameters in sensory nerve in the treated group was greater than the improvement measured in motor nerve. There were no side effects. Oral mecobalamin treatment is a safe and potentially beneficial therapy for CTS in stroke patients.
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PMID:Amelioration by mecobalamin of subclinical carpal tunnel syndrome involving unaffected limbs in stroke patients. 1579 15

Arteriosclerosis and its complications, such as heart attack and stroke, are the major causes of death in developed countries. It was believed that age, hyperlipidemia, hypertension, diabetes and smoking are common risk factors for cardiovascular disease. In addition, overwhelming clinical and epidemiological studies have identified homocysteine (Hcy) as a significant and independent risk factor for cardiovascular disease. In healthy individuals, plasma Hcy is between 5 and 10 micromol/L. One cause of severe hypehomocys- teinemia (HHcy) is the deficiency of cystathionine beta-synthase (CBS), which converts Hcy to cystathionine. CBS homozygous deficiency results in severe HHcy with Hcy levels up to 100 to 500 micromol/L. Patients with severe HHcy usually present with neurological abnormalities, premature arteriosclerosis. It has been reported that lowering plasma Hcy improved endothelial dysfunction and reduced incidence of major adverse events after percutaneous coronary intervention. The mechanisms by which Hcy induces atherosclerosis are largely unknown. Several biological mechanisms have been proposed to explain cardiovascular pathological changes associated with HHcy. These include: (1) endothelial cell damage and impaired endothelial function; (2) dysregulation of cholesterol and triglyceride biosynthesis; (3) stimulation of vascular smooth muscle cell proliferation; (4) thrombosis activation and (5) activation of monocytes. Four major biochemical mechanisms have been proposed to explain the vascular pathology of Hcy. These include: (1) autooxidation through the production of reactive oxygen species; (2) hypomethylation by forming SAH, a potent inhibitor of biological transmethylations; (3) nitrosylation by binding to nitric oxide or (4) protein homocysteinylation by incorporating into protein. In summary, our studies, as well as data from other laboratories support the concept that Hcy is causally linked to atherosclerosis, and is not merely associated with the disease. Although folic acid, vitamin B12 and B6 can lower plasma Hcy levels, the long-term effects on cardiovascular disease risk are still unknown and judgments about therapeutic benefits await the findings of ongoing clinical trials.
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PMID:Hyperhomocysteinemia and atherosclerosis. 1583 93

The present review focuses on the B-vitamins, i.e. folate, vitamin B12, vitamin B6 and riboflavin, that are involved in homocysteine metabolism. Homocysteine is a S-containing amino acid and its plasma concentrations can be raised by various constitutive, genetic and lifestyle factors, by inadequate nutrient status and as a result of systemic disease and various drugs. Hyperhomocysteinaemia is a modest independent predictor of CVD and stroke, but causality and the precise pathophysiological mechanism(s) of homocysteine action remain unproven. The predominant nutritional cause of raised plasma homocysteine in most healthy populations is folate insufficiency. Vitamin B12 and, to a lesser extent, vitamin B6 are also effective at lowering plasma homocysteine, especially after homocysteine lowering by folic acid in those individuals presenting with raised plasma homocysteine. However, riboflavin supplementation appears to be effective at lowering plasma homocysteine only in those individuals homozygous for the T allele of the C677T polymorphism of the methylenetetrahydrofolate reductase (MTHFR) gene. This gene codes for the MTHFR enzyme that produces methyltetrahydrofolate, which, in turn, is a substrate for the remethylation of homocysteine by the vitamin B12-dependent enzyme methionine synthase. Individuals with the MTHFR 677TT genotype are genetically predisposed to elevated plasma homocysteine, and in most populations have a markedly higher risk of CVD.
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PMID:B-vitamins, homocysteine metabolism and CVD. 1583 Nov 32

Helicobacter pylori (H. pylori) is the commonest bacterial pathogen found worldwide and more than half the world population aged 40 years and above is colonized with it. The infection rate is >95 % in some African countries. In 1994, the International Agency for Research on cancer classified H. pylori as a class I carcinogen in humans. It causes chronic active gastritis, duodenal and gastric ulcer and gastric malignancy, and is thought to be associated with coronary artery disease, cerebral stroke, vitamin B12 and iron-deficiency anaemia, etc. Therefore, non-invasive test-and-treatment strategies are widely recommended in primary care settings. Conventionally, H. pylori infection can be diagnosed by invasive techniques using an upper gastrointestinal endoscope for obtaining multiple biopsies from different sites of the stomach for RUT, culture, histological examination, polymerase chain reaction (PCR), etc. and by non-invasive tests such as Urea breath test (UBT), stool antigen test and blood serology. At present, 13/14C-UBT is considered the test of choice for confirmation of H. pylori infection. The UBT is based on the principle, that isotopically labelled urea ingested by an H. pylori--infected patient is rapidly hydrolysed by the microbial urease. The released 13/14CO2 is absorbed across the mucous layer to the gastric mucosa and hence, excreted via the systemic circulation in the breath which is collected and measured. The non-hydrolysed urea is excreted completely in the urine within 3-4 days. 13C-UBT being non-radioactive, 13C-UBT can be used in pregnant women and children, and a user's license is not required. There is still no standard protocol accepted and followed internationally for this test. Although the methods are almost similar, various laboratories/clinics use variable tracer doses, test meals, timings and methods for breath collection, and different cut-off values, which make formal validation studies necessary. This review describes the present status of the UBT and its application in the detection of H. pylori infection.
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PMID:Urea breath test for Helicobacter pylori detection: present status. 1591 72

Moderate hyperhomocysteinaemia is established as an independent risk factor for atherosclerosis, thrombosis, stroke and dementia. Hyperhomocysteinaemia is mostly caused by the deficiency of B-vitamins folate and vitamin B12, which are essential cofactors in the remethylation of homocysteine to methionine. Interestingly, moderate hyperhomocysteinaemia is also often observed in chronic diseases, in which also elevated immune activation markers such as neopterin or sTNFR-II are found. In order to simulate immune activation in vitro, human peripheral blood mononuclear cells (PBMC) were stimulated with mitogens. Stimulation significantly increased homocysteine production in comparison with unstimulated PBMC; in parallel also neopterin formation was induced. Homocysteine formation was due to cell proliferation, proliferating T lymphocytes, and also the myelomonocytic cell line U-937 produced homocysteine. Treatment with the anti-inflammatory drug aspirin dose-dependently inhibited homocysteine production and also neopterin formation in human PBMC. Treatment with salicylic acid showed similar effects as aspirin; FACS analysis showed that both compounds inhibited cell proliferation by arresting cells in the G0/G1-phase. In U-937, both compounds also slightly induced apoptosis at 5 mm. Proliferation-induced homocysteine formation and in parallel also monocyte activation can be suppressed effectively by aspirin and salicylic acid in vitro, suggesting that also in vivo aspirin may downregulate not only inflammation but also formation of homocysteine.
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PMID:Aspirin downregulates homocysteine formation in stimulated human peripheral blood mononuclear cells. 1610 22

Plasma total homocysteine (tHcy) concentrations are associated with deficits in cognitive performance in persons free from dementia. The extent to which age modifies these associations is in need of further investigation in large, community-based, prospective studies combining the following elements: 1) multiple cognitive tests; 2) statistical adjustment for the role of the vitamin cofactors folate, vitamin B6, and vitamin B12; and 3) adjustment for the presence of risk factors for cardiovascular disease and stroke. Using data collected between 1991 and 2002, the authors investigated the associations between tHcy and multiple measures of cognitive performance in 2,096 dementia- and stroke-free participants of the Framingham Offspring Study, who were stratified into three age groups (40-49 years, 50-59 years, 60-82 years), after findings of statistically significant tHcy-by-age interactions for multiple cognitive measures. Regardless of statistical adjustment for age, sex, gender, the vitamin cofactors, and cardiovascular risk factors, statistically significant inverse associations between tHcy and multiple cognitive domains were observed for individuals aged 60 or more years; no such associations were observed for participants aged less than 60 years. Early preventive interventions may be important, because the inverse association between tHcy and cognitive performance is observed beyond middle age.
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PMID:Homocysteine and cognitive performance in the Framingham offspring study: age is important. 1610 67

Type 2 diabetes mellitus and higher total plasma homocysteine concentrations are each associated with an increased incidence of cardiovascular disease and with diminished cognitive performance. Relations between homocysteine concentrations and cardiovascular disease incidence are stronger in the presence of type 2 diabetes mellitus. Therefore, we hypothesized that relations between homocysteine concentrations and cognitive performance would be stronger in the presence of type 2 diabetes. We related homocysteine concentrations and cognitive performance on the Mini-Mental State Examination in 817 dementia- and stroke-free participants of the Maine-Syracuse Study, 90 of whom were classified with type 2 diabetes mellitus. Regardless of statistical adjustment for age, sex, gender, vitamin co-factors (folate, vitamin B6, vitamin B12), cardiovascular disease risk factors, and duration and type of treatment for type 2 diabetes mellitus, statistically significant inverse associations between homocysteine concentrations and cognitive performance were observed for diabetic individuals. The weaker inverse associations between homocysteine concentrations and cognitive performance obtained for non-diabetic individuals were not robust to statistical adjustment for some covariates. Interactions between homocysteine concentrations and type 2 diabetes mellitus are observed such that associations between homocysteine and cognitive performance are stronger in the presence of diabetes.
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PMID:Homocysteine, type 2 diabetes mellitus, and cognitive performance: The Maine-Syracuse Study. 1619 5

Children with homocystinuria have markedly elevated plasma homocysteine concentrations and increased risks of stroke and coronary heart disease (CHD). Supplementation with folic acid, vitamin B6, and vitamin B12 lower homocysteine levels and such therapy is remarkably effective in delaying the occurrence of vascular events in affected individuals. The relevance, if any, of moderately elevated homocysteine levels to cardiovascular disease in the general population is uncertain. The results of retrospective studies of homocysteine and risk of cardiovascular disease (where blood is collected after the onset of disease) indicate that CHD or stroke patients invariably have higher homocysteine levels than age-matched controls. In contrast, the results of prospective studies (where blood is collected before onset of disease) show much weaker associations of homocysteine with cardiovascular disease. This article examines the background, epidemiological evidence relating homocysteine with vascular disease, and effects of vitamin supplements on homocysteine concentrations. Large-scale clinical trials of folic acid-based vitamin supplements are currently in progress to test whether lowering blood homocysteine levels can reduce the risks of CHD and stroke.
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PMID:Homocysteine and coronary heart disease. 1622 29


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