cystathionine/infarto

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Plasma cystathionine and risk of acute myocardial infarction among patients with coronary heart disease: Results from two independent cohorts.

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BACKGROUND Cystathionine is a thio-ether and a metabolite formed from homocysteine during transsulfuration. Elevated plasma cystathionine levels are reported in patients with cardiovascular disease; however prospective relationships with acute myocardial infarction (AMI) are unknown. We investigated

"Zipped Synthesis" by Cross-Metathesis Provides a Cystathionine β-Synthase Inhibitor that Attenuates Cellular H2S Levels and Reduces Neuronal Infarction in a Rat Ischemic Stroke Model.

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The gaseous neuromodulator H2S is associated with neuronal cell death pursuant to cerebral ischemia. As cystathionine β-synthase (CBS) is the primary mediator of H2S biogenesis in the brain, it has emerged as a potential target for the treatment of stroke. Herein, a "zipped" approach by alkene

[A case of young adult presenting with cerebral infarction caused by homocystinuria].

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Homocystinuria is a congenital metabolic disorder, and has been known as life-threatening risk factor of vascular disease including ischemic stroke. We report a case of cerebral infarction due to homocystinuria. The patient was a 21-year-old woman exhibiting left hemiparesis and a previous history

Fasting plasma homocysteine levels are increased in young patients with acute myocardial infarction from Western India.

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BACKGROUND Fasting hyperhomocysteinemia is positively associated with atherothrombosis and acute myocardial infarction in several prospective and retrospective studies. In India folic acid deficiency is not uncommon, and subclinical folic acid deficiency is known to cause hyperhomocysteinemia

Stroke in young patients with hyperhomocysteinemia due to cystathionine beta-synthase deficiency.

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BACKGROUND Although hyperhomocyst(e)inemia (Hyper-Hcy) may predispose to atherosclerosis and venous thrombosis, the mechanisms of stroke associated with Hyper-Hcy are not defined. METHODS Clinical and biochemical phenotypes and genetic features of three unrelated patients with premature stroke and

Polymorphisms in MTHFR, MS and CBS genes and premature acute myocardial infarction in a Pakistani population.

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High prevalence of premature coronary heart disease in Pakistanis compared to other populations points towards the genetic predisposition of this population to develop this disease. Since no investigations have been carried out in Pakistan to study the relationship of polymorphisms in genes involved

Determinants of early-onset cardiovascular disease: a case-control study of young myocardial infarction patients.

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BACKGROUND The present case-control investigation was undertaken with the aim of thoroughly assessing the risk profile of young coronary patients and to correlate it with their endothelium-dependent vasodilation and with the presence of atherosclerotic lesions. METHODS Forty-eight subjects (age < 41

Total Flavones of Rhododendron simsii Planch Flower Protect against Cerebral Ischemia-Reperfusion Injury via the Mechanism of Cystathionine-γ-Lyase-Produced H2S.

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Total flavones of Rhododendron simsii Planch flower (TFR) have a significant protective effect against cerebral ischemia-reperfusion injury. However, its mechanism is unclear. This study investigated the protection of TFR against cerebral ischemia-reperfusion injury via cystathionine-γ-lyase- (CSE-)

Selective homocysteine lowering gene transfer improves infarct healing, attenuates remodelling, and enhances diastolic function after myocardial infarction in mice.

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OBJECTIVE Homocysteine levels predict heart failure incidence in prospective epidemiological studies and correlate with severity of heart failure in cross-sectional surveys. The objective of this study was to evaluate whether a selective homocysteine lowering intervention beneficially affects

Elevated plasma cystathionine is associated with increased risk of mortality among patients with suspected or established coronary heart disease.

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Elevated circulating cystathionine levels are related to atherosclerotic cardiovascular disease, a leading cause of death globally.We investigated whether plasma cystathionine was associated with mortality in patients with suspected or established coronary

Fatal haemorrhagic infarct in an infant with homocystinuria.

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Thrombotic and thromboembolic complications are the main causes of morbidity and mortality in patients with homocystinuria. However, it is unusual for thrombosis and infarction to be the presenting feature leading to investigation for homocystinuria and cerebrovascular lesions in the first year of

Folic acid mitigated cardiac dysfunction by normalizing the levels of tissue inhibitor of metalloproteinase and homocysteine-metabolizing enzymes postmyocardial infarction in mice.

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Myocardial infarction (MI) results in significant metabolic derangement, causing accumulation of metabolic by product, such as homocysteine (Hcy). Hcy is a nonprotein amino acid generated during nucleic acid methylation and demethylation of methionine. Folic acid (FA) decreases Hcy levels by

[A hyperhomocysteinemia study in a population with a familial factor for acute myocardial infarct and sudden cardiac death at a young age].

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The alterations of the metabolism of methionine determining an accumulation of homocysteine in blood (hyperhomocysteinemia) recognize a multifactorial etiology, hereditary as well as acquired. To date several case-control studies have documented that the condition of hyperhomocysteinemia can be

Folate dependence of hyperhomocysteinemia and vascular dysfunction in cystathionine beta-synthase-deficient mice.

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Hyperhomocysteinemia is a risk factor for stroke, myocardial infarction, and venous thrombosis. Moderate hyperhomocysteinemia is associated with impaired endothelial function, but the mechanisms responsible for endothelial dysfunction in hyperhomocysteinemia are poorly understood. We have used

MicroRNA-186 promotes macrophage lipid accumulation and secretion of pro-inflammatory cytokines by targeting cystathionine γ-lyase in THP-1 macrophages.

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Several studies suggest that cardiomyocyte-enriched miR-186 is involved in cardiac injury and myocardial infarction, and also plays an important role in atherosclerotic diseases, but the underlying mechanism is unknown. Cystathionine-γ-lyase (CSE) is the predominant enzyme to produce H2S in the

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