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phosphatidyl choline/infarction

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6 結果

[Mechanism of action of sodium oxybutyrate in experimental myocardial infarction].

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Effect of sodium hydroxybutyrate on lipid metabolism was studied in experimental infarction of rabbit myocardium. Administration of 80 mg of sodium hydroxybutyrate per kg of body mass caused a decrease of free fatty acids content in the infarction zone, in surrounding zones and in blood. Treatment

Low dietary intake of linoleic acid predisposes to myocardial infarction.

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Thirty-two men who had recently had a myocardial infarction were matched individually for age with controls who had no evidence of heart disease. The patients had a significantly lower proportion of linoleic acid and a higher proportion of palmitic acid in their plasma triglyceride fatty acids.

UPLC-HRMS-Based Plasma Metabolomic Profiling of Novel Biomarkers by Treatment with KDZI in Cerebral Ischemia Reperfusion Rats.

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Kudiezi injection (KDZI), also known as Diemailing injection, is a traditional Chinese medicine injection of the composite plant Ixeris sonchifolia Hance (also known as Kudiezi), and has been widely used to treat coronary heart disease, angina pectoris, and cerebral infarction, but its

Cerebrospinal fluid corticotropin-releasing hormone and ACTH, and peripherally circulating choline-containing phospholipid in senile dementia.

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Cerebrospinal fluid (CSF) levels of corticotropin-releasing hormone (CRH) and ACTH, plasma levels of ACTH and cortisol, and serum levels of phospholipid and its fractions were determined in samples taken simultaneously from patients with senile dementia of the Alzheimer type (SDAT), multi-infarct
Background: Currently, no drug has been approved for the management of postischemic neuronal damage. Existing studies show that calcium channel blockers have neuroprotective properties, while citicoline is involved in maintaining neuronal

Comprehensive targeted and non-targeted lipidomics analyses in failing and non-failing heart.

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Myocardial infarction (MI) and subsequent progressive heart failure pathology is the major cause of death worldwide; however, the mechanism of this pathology remains unclear. The present work aimed at testing the hypothesis whether the inflammatory response is superimposed with the formation of
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