Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Elevated plasma homocysteine has been found to be a risk factor for Alzheimer's disease as well as cerebral vascular disease, suggesting that some risk factors can accelerate or increase the severity of several CNS disease processes. We screened plasma total homocysteine levels of 193 schizophrenic patients vs. 762 controls for plasma homocysteine levels. The effect of schizophrenia was marked (p<0.0001) and mean homocysteine level was 16.3+/-12 (S.D.) microM in schizophrenic patients vs. 10.6+/-3.6 (S.D.) microM in healthy controls. The increase was almost entirely in young male schizophrenic patients. It seemed important to determine if this finding is already present in newly admitted schizophrenic patients. Serum homocysteine levels were studied in 184 consecutively admitted schizophrenic patients and 305 control subjects. Homocysteine levels were markedly increased in this population of newly admitted schizophrenic patients, especially in young males. However, no difference was found for CSF homocysteine levels between schizophrenia patients and controls. We also examined homocysteine levels in 41 euthymic outpatients with bipolar disorder. Functional deterioration in patients was rated as 'present' or 'absent' by consensus of two treating clinicians. Young male bipolar patients were found to have higher homocysteine levels than controls. Among the male subjects, bipolar patients showing deterioration had homocysteine levels which were significantly higher than other patients. We attempted to develop a model of homocysteine neurotoxicity in mice. Mice were fed homocysteine in water at a dose of 200 mg/kg per mouse per day. Independent samples of animals were studied at 2 to 6 months with behavioral tests including apomorphine-induced stereotypy and spatial learning and memory in the Morris Water Maze. Homocysteine levels were elevated up to 800% at months 5 and 6 by this procedure. No homocysteine-induced defects were found in any behavioral test until month 5 when mild but statistically significant abnormalities in the Morris Water Maze were detected.
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PMID:High homocysteine serum levels in young male schizophrenia and bipolar patients and in an animal model. 1611 16

The study included 31 patients with constrictive and stenotic angiopathy (CSAP) that had developed due subarachnoidal hemorrhage. All the patients were operated on within the first 4 days after the moment of blood bleeding. Since the onset of CSAP, Groups 1 (n = 14) 2 (n = 17) received normovolemic and hypervolemic infusion therapy, respectively. In both groups, cerebral circulatory changes were found to depend primarily on cardiac productive parameters. The nature of infusion therapy had no impact on the results of treatment (according to the Glasgow scale). Hypervolemia used in such patients has no advantages over normovolemic water load when hyperdynamic circulation is created when inotropic agents are used.
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PMID:[Effect of infusion therapy on central hemodynamics and the outcome of treatment in patients with subarachnoidal hemorrhages]. 1620 89

The relation between drinking water and cardiovascular disease has been evaluated in a number of studies. Certain of these show strong relationships whereas others do not. This review analyses the methodological aspects on epidemiological studies in terms of dose-range, confounding factors and multiple exposures. It is concluded that there is good evidence for a relation between drinking water quality and cardio-vascular disease, that several methodological criteria for such studies need to be considered, that there is little evidence for magnesium as the single causative agent, and that the relevant exposure should be considered as a mixture of minerals.
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PMID:Magnesium in drinking water and cardio-vascular disease--an epidemiological dilemma. 1627 8

Endothelial dysfunction caused by increases in vascular oxidant stress that decrease bioavailable nitric oxide (NO) plays a critical role in the vascular pathobiology of hyperhomocysteinemia. Boosting cellular glutathione levels or increasing the activity of cellular glutathione peroxidase can compensate for homocysteine's effects on endothelial function. Aged garlic extract (AGE) contains water- and oil-soluble sulfur compounds that modify the intracellular thiol and redox state, minimize intracellular oxidant stress, and stimulate NO generation in endothelial cells and animals. We performed a placebo-controlled, blinded, crossover trial to examine whether AGE reduces macro- and microvascular endothelial dysfunction during acute hyperhomocysteinemia induced by an oral methionine challenge in healthy subjects. Acute hyperhomocysteinemia leads to a significant decrease in flow-mediated vasodilation of the brachial artery as determined by vascular ultrasound, indicative of macrovascular endothelial dysfunction. In addition, acute hyperhomocysteinemia leads to a decrease in acetylcholine-stimulated skin perfusion as measured by laser-Doppler flowmetry. This indicates microvascular endothelial dysfunction, which is presumably a result of impairment of the endothelium-derived hyperpolarizing factor pathway. Pretreatment with AGE for 6 wk significantly diminished the adverse effects of acute hyperhomocysteinemia in both vascular territories. We conclude that AGE may at least partly prevent a decrease in bioavailable NO and endothelium-derived hyperpolarizing factor during acute hyperhomocysteinemia. This pilot study warrants further investigations on the effects of AGE on endothelial dysfunction in patients with other cardiovascular risk factors or established vascular disease and on the clinical outcome of patients with cardiovascular disease.
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PMID:Aged garlic extract improves homocysteine-induced endothelial dysfunction in macro- and microcirculation. 1648 56

The uremic syndrome is the result of the retention of solutes, which under normal conditions are excreted by the healthy kidneys into the urine. The most practical classification of uremic toxins is based on their physicochemical characteristics that influence their dialytic removal, in (a) small water soluble compounds, (b) the larger "middle molecules," and (c) the protein bound compounds. Most small water soluble compounds are not very toxic and the toxic ones often show a kinetic behavior that is different from that of urea. The incidence of vascular disease and the morbidity and mortality related to it are extremely high in the population of uremic patients. A large proportion of uremic patients suffer from inflammation. Most often, the uremic solutes that play a role in inflammation and cardio-vascular complications are middle molecules and/or protein bound. Protein bound toxins inhibit several biochemical functions. High concentrations of cytokines with an immune activating potential are present in the plasma of uremic patients.
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PMID:[Uraemic toxins and cardiovascular diseases]. 1662 9

In July 1988, 20 tonnes of aluminium sulphate was discharged by the South West Water Authority into the drinking water supplied to a large region of North Cornwall. Up to 20,000 people were exposed to concentrations of aluminium which were 500-3000 times the acceptable limit under European Union legislation (0.200 mg/l). Although this incident is currently the topic of a government inquiry, nothing is known about its longer-term repercussions on human health. The first neuropathological examination of a person who was exposed and died of an unspecified neurological condition was carried out. A rare form of sporadic early-onset beta amyloid angiopathy in cerebral cortical and leptomeningeal vessels, and in leptomeningeal vessels over the cerebellum was identified. In addition, high concentrations of aluminium were found coincident with the severely affected regions of the cortex. Although the presence of aluminium is highly unlikely to be adventitious, determining its role in the observed neuropathology is impossible. A clearer understanding of aluminium's role in this rare form of Alzheimer's related disease should be provided by future research on other people from the exposed population as well as similar neuropathologies in people within or outside this group.
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PMID:Severe cerebral congophilic angiopathy coincident with increased brain aluminium in a resident of Camelford, Cornwall, UK. 1662 36

To determine the relationship of arsenic, copper, cadmium, manganese, lead, zinc and selenium to Blackfoot disease (BFD, a peripheral vascular disorder endemic to areas of Taiwan, which has been linked to arsenic in drinking water) the authors measured the amount of these substances in urine from BFD patients, using atomic absorption spectrometry. Results indicate significantly higher amounts of urinary arsenic, copper, cadmium, manganese, and lead for BFD patients than for normal controls, also significantly lower urinary zinc and selenium.
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PMID:Determination of urinary trace elements (arsenic, copper, cadmium, manganese, lead, zinc, selenium) in patients with Blackfoot disease. 1678 78

Chronic arsenic exposure is associated with nervous system damage, vascular disease, hepatic and renal damage as well as different types of cancer. Alterations of nitric oxide (NO) in the periphery have been detected after arsenic exposure, and we explored here NO production in the brain. Female Wistar rats were exposed to arsenite in drinking water (4-5 mg/kg/day) from gestation, lactation and until 4 months of age. NOS activity, NO metabolites content, reactive oxygen species production (ROS) and lipid peroxidation (LPx) were determined in vitro in the striatum, and NO production was estimated in vivo measuring citrulline by microdialysis. Exposed animals showed a significantly lower response to NMDA receptor stimulation, reduction of NOS activity and decreased levels of nitrites and nitrates in striatum. These markers of NO function were accompanied by significantly higher levels of LPx and ROS production. These results provide evidence of NO dysfunction in the rat brain associated with arsenic exposure.
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PMID:Decreased nitric oxide production in the rat brain after chronic arsenic exposure. 1687 39

CAWS, a water-soluble extracellular polysaccharide fraction obtained from the culture supernatant of Candida albicans, is one of the fungal pathogen-associated molecular patterns (PAMPs). It has been reported to show potent activity inducing arteritis and coronaritis in mice. Especially, CAWS-induced arteritis has a 100% incidence and severe mortality in the DBA/2 mouse strain. This artificial vasculitis was reported to provide a good murine model of Kawasaki disease and other inflammatory vascular disease. However, severe mortality was observed only in DBA/2 mice, which is a CAWS-sensitive strain. In this study, to clarify the mechanisms of CAWS-induced arteritis and mortality, we investigated microscopic histopathological changes in cardiovascular tissues in DBA/2 mice. Severe inflammatory infiltration was observed from the external elastic lamina in the aorta and proximal coronary arteries within 1 week after CAWS administration. Severe stenosis of the aorta and coronary arteries was observed more than 3 weeks after CAWS administration. Fibrinoid necrosis was observed in these vessel walls. All CAWS-treated mice died between the fifth and twelfth week after administration. Severe inflammatory change with aortic valve transformation suggested that CAWS-treated mice died of valvular endocarditis or cardiac dysfunction. Based on the simple induction method and complete incidence, these data suggest that CAWS-induced arteritis is a good model of not only Kawasaki disease but also other cardiovascular diseases such as valvular endocarditis.
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PMID:[Histopathological examination and analysis of mortality in DBA/2 mouse vasculitis induced with CAWS, a water-soluble extracellular polysaccharide fraction obtained from Candida albicans]. 1688 Jul 22

The authors report a case report of rare disease interesting the digestive tract and often associated to the other gastrointestinal pathologies and/or pulmonary diseases and can be also associated to not gastrointestinal conditions such as collagen-vascular disease, transplantation, AIDS, use of corticosteroid and chemotherapy; other causes can be iatrogenic such as traumatic gastrointestinal endoscopy (a mucoses biopsy, a polipectomy) or the assumption of lattulosio; in 15-20% of cases the pneumatosis cystoides intestinalis is considered primitive. In the our case the Pneumatosis coli was associated to administration of acarbose; in international literature only four papers in the English language were reported. Our patient showed a strongly aspecific symptomatology and easily attributable in first line or to the pathology of base (diabetic patient) or to the assumption of the acarbose; from about 7-8 months she showed unexplained episodes of crampy abdominal pain, diarrhea with 3-4 defecations/die with semiliquid and normochromic stools, tenesmus and a not better specified loss of weight. The diagnosis was been performed by colonoscopy and confirmed by abdominal CT scan with water enema and histologically; we have used the traditional radiology only to exclude the involvement of other gastroenteric districts. The patient was been treated with O2-therapy associated to antibiotics treatment; the suspension of the causal factor, the acarbose, has been of not secondary importance; the complete resolution of disease was obtained after 15 days of therapy.
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PMID:Pneumatosis coli induced by acarbose administration for diabetes mellitus. Case report and literature review. 1697 79


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