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lipoxygenase/infarci

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Altered lipoxygenase metabolites and leukocyte involvement in an acute occlusion-reperfusion model of canine myocardial infarction.

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We compared amounts of lipoxygenase products with the extent of leukocyte infiltration in the ischemic myocardium with an occlusion-reperfusion model of open-chest dog. Changes in peripheral leukocyte count and leukocyte function estimated by neutrophil aggregation induced by calcium ionophore

Common Polymorphisms in the 5-Lipoxygenase Pathway and Risk of Incident Myocardial Infarction: A Danish Case-Cohort Study.

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BACKGROUND The 5-lipoxygenase pathway (5-LOX) has been implicated in the development of cardiovascular disease and studies have suggested that genetic polymorphisms related to key enzymes in this pathway may confer risk of myocardial infarction (MI). This study investigated the association of
OBJECTIVE Haplotypes based on polymorphisms in the gene encoding 5-lipoxygenase-activating protein have been linked with susceptibility to myocardial infarction in Iceland and the United Kingdom. We sought to replicate these association findings in a large case-control sample from
Leukotrienes are implicated in the pathogenesis of coronary artery disease. Recently two haplotypes (HapA and HapB) in the gene encoding ALOX5AP (arachidonate 5-lipoxygenase-activating protein), the main regulator of 5-lipoxygenase, have been associated with a doubling of the risk of myocardial

Validation of the association between the gene encoding 5-lipoxygenase-activating protein and myocardial infarction in a Japanese population.

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BACKGROUND Recently, the 5-lipoxygenase activating protein gene (ALOX5AP) was reported to confer a risk of myocardial infarction (MI) and stroke, independent of conventional risk factors. The purpose of the present study was to validate those findings in a Japanese population. RESULTS The study
We studied the effects of a thromboxane A2 synthetase inhibitor (RS-5186), a thromboxane A2 antagonist (ONO-3708), a 5-lipoxygenase inhibitor (AA-861) and a peptidoleukotriene antagonist (ONO-1078) on infarct size, polymorphonuclear leukocyte infiltration, gross myocardial hemorrhage and arrhythmias
OBJECTIVE Recent findings have implicated specific gene polymorphisms of arachidonate 5-lipoxygenase-activating protein (ALOX5AP), and 2 at-risk haplotypes (HapA, HapB) in myocardial infarction and stroke. To date, no prospective data are available. METHODS We evaluated 10 specific Icelandic ALOX5AP

A functional Sp1/Egr1-tandem repeat polymorphism in the 5-lipoxygenase gene is not associated with myocardial infarction.

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Arachidonate 5-lipoxygenase is an enzyme encoded by the ALOX5 gene, and plays an important role in the synthesis of leukotrienes. These are inflammatory mediators, and have been involved in atherosclerosis and other pathological processes that require proinflammatory activities. Human and animal
Patients with coronary artery disease remain at increased risk of recurrent life-threatening cardiovascular events even after adequate guideline-based treatment of conventional risk factors, including blood lipid levels. Inflammation is a critical pathway in the pathogenesis of atherosclerosis and
Stroke is one of the most frequent causes of death and disability worldwide causing a major clinical and socioeconomic impact. Although the pathophysiology of brain ischemia and reperfusion is complex, the inflammatory process plays an important role in pathogenesis, contributing to the expansion of
OBJECTIVE The purpose of this study was to assess the effect of the dual cyclooxygenase-lipoxygenase blocking agent BW755C on the extent of myocardial infarction in the pig and to identify the mechanisms of any cardioprotective action of this drug. BACKGROUND Activated neutrophils contribute to

Arachidonate 5-lipoxygenase (5-LO) promoter genotype and risk of myocardial infarction: a case-control study.

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BACKGROUND Leukotrienes are inflammatory mediators derived from arachidonic acid via the 5-lipoxygenase pathway. Both experimental and clinical studies implicate the 5-lipoxygenase pathway in the pathophysiology of atherosclerosis. In a previous study, a microsatellite polymorphism in the

Nutrigenetic association of the 5-lipoxygenase gene with myocardial infarction.

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BACKGROUND 5-Lipoxygenase (5-LO) catalyzes the rate-limiting step of the biosynthesis of proinflammatory leukotrienes from arachidonic acid (AA) and has been associated with atherosclerosis in animal models and humans. We previously reported that variants of a 5-LO promoter repeat polymorphism were

5-Lipoxygenase facilitates healing after myocardial infarction.

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Early healing after myocardial infarction (MI) is characterized by a strong inflammatory reaction. Most leukotrienes are pro-inflammatory and are therefore potential mediators of healing and remodeling after myocardial ischemia. The enzyme 5-lipoxygenase (5-LOX) has a key role in the transformation
Background: The 5-lipoxygenase pathway has been linked to atherothrombotic disease, and a functional tandem repeat polymorphism in the arachidonate lipoxygenase-5 (ALOX-5) gene has been associated with the risk of myocardial infarction (MI). Interestingly, 2 studies have reported an interaction
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