guanine/infarction

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Isoflurane preconditions myocardium against infarction via activation of inhibitory guanine nucleotide binding proteins.

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BACKGROUND Isoflurane-induced myocardial protection during ischemia is mediated by adenosine triphosphate-regulated potassium (KATP) channels; however, the intracellular signal transduction cascade responsible for this process has been incompletely evaluated. The authors tested the hypothesis that

DNA and RNA oxidative damage are associated to mortality in patients with cerebral infarction.

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Secondary injury due to oxidation may occur during ischemic stroke, possibly leading to oxidative damage to deoxyribonucleic acid (DNA) and ribonucleic acid (RNA). Higher blood concentrations of 8-hydroxy-2'-deoxyguanosine (8-OHdG) (through the oxidation of guanosine from DNA) have

D2 dopamine receptors in the human brain: heterogeneity based on differences in guanine nucleotide effect on agonist binding, and their presence on corticostriatal nerve terminals.

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In human brain, regulation of agonist binding to the D2 dopamine receptors by guanine nucleotides is different between several regions. In membranes of the anterior pituitary lobe, agonist binding is fully sensitive to GTP or Gpp(NH)p, whereas it is resistant in membranes of globus pallidus. Both

Higher frequency of rs4977574 (the G Allele) on chromosome 9p21.3 in patients with myocardial infarction as revealed by PCR-RFLP analysis.

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Single Nucleotide Polymorphisms (SNPs) can genetically predispose individuals for certain diseases and therefore are of clinical significance. Myocardial infarction (MI) was investigated in large genetic association studies revealing novel SNPs associated with MI. rs4977574 is a non-protein coding

Mesenteric infarction due to combined protein C deficiency and prothrombin 20210 defects.

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The prothrombin gene mutation, 20210A, a guanine to adenine substitution at nucleotide position 20210, has recently been described as an additional risk factor for venous thromboembolic disease. We describe the case of a patient with combined heterozygous prothrombin 20210A mutation and type 1

Genetic profiling of fatty acid desaturase polymorphisms identifies patients who may benefit from high-dose omega-3 fatty acids in cardiac remodeling after acute myocardial infarction-Post-hoc analysis from the OMEGA-REMODEL randomized controlled trial.

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The double-blind OMEGA-REMODEL placebo-controlled randomized trial of high-dose omega-3 fatty acids (O-3FA) post-acute myocardial infarction (AMI) reported improved cardiac remodeling and attenuation of non-infarct myocardial fibrosis. Fatty acid desaturase 2 (FADS2) gene cluster

Investigation of effects of Lacidipine, Ramipril and Valsartan on DNA damage and oxidative stress occurred in acute and chronic periods following isoproterenol-induced myocardial infarct in rats.

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In this study, effects of Lacidipine (LAC), Ramipril (RAM) and Valsartan (VAL) on DNA damage and oxidative stress occurred in acute and chronic periods after isoproterenol (ISO)-induced myocardial infarct (MI) were investigated in rats. LAC, RAM and VAL had been administered by oral gavage at 3, 3

Genetic variation of the androgen receptor and risk of myocardial infarction and ischemic stroke in women.

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OBJECTIVE Androgen receptors (AR) are expressed in endothelial cells and vascular smooth-muscle cells. Some studies suggest an association between AR gene variation and risk of cardiovascular disease (CVD) in men; however, the relationship has not been examined in women. METHODS Six haplotype

Elevated expression of C3G protein in the peri-infarct myocardium of rats.

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BACKGROUND The integrin β1 subunit and its downstream molecules such as integrin-linked kinase (ILK) and focal adhesion kinase (FAK) are indispensable to the inhibition of postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure. As a component of the integrin pathway, C3G (Crk

Endothelial nitric oxide synthase gene polymorphism and acute myocardial infarction.

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Recently a point mutation of guanine to thymine at nucleotide position 1917 in the endothelial nitric oxide synthase (eNOS) gene has been reported to be associated with coronary artery spasm. In addition, a significant association of the 4a/b polymorphism in intron 4 of the eNOS gene with coronary

Plasminogen activator inhibitor-1 4G/5G gene polymorphism in patients with myocardial or cerebrovascular infarction in Tianjin, China.

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OBJECTIVE To investigate the association between the plasminogen activator inhibitor-1 (PAI-1) 4G/5G gene polymorphism and the occurrence of myocardial and cerebrovascular infarctions in individuals from Tianjin, China. METHODS The PAI-1 genotype was determined using allele-specific polymerase chain

A Preliminary Study of the Association between Apolipoprotein E Promoter Methylation and Atherosclerotic Cerebral Infarction.

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To investigate association of Apolipoprotein E (ApoE) gene promoter methylation with atherosclerotic cerebral infarction (ACI) in the Han Chinese population.Twenty-six ACI patients (the case group) and 26 healthy (the control group) were recruited randomly

Prediction of myocardial infarction, stroke and cardiovascular mortality with urinary biomarkers of oxidative stress: Results from a large cohort study.

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BACKGROUND Oxidative stress contributes to endothelial dysfunction and is involved in the pathogenesis of cardiovascular diseases (CVD). However, large population-based cohort studies are sparse and biomarkers of oxidative stress have not been evaluated for CVD risk prediction so far. METHODS The

Single nucleotide polymorphisms in multiple novel thrombospondin genes may be associated with familial premature myocardial infarction.

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BACKGROUND Recent advances in high-throughput genomics technology have expanded our ability to catalogue allelic variants in large sets of candidate genes related to premature coronary artery disease. RESULTS A total of 398 families were identified in 15 participating medical centers; they fulfilled

Paroxetine-mediated GRK2 inhibition reverses cardiac dysfunction and remodeling after myocardial infarction.

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Heart failure (HF) is a disease of epidemic proportion and is associated with exceedingly high health care costs. G protein (heterotrimeric guanine nucleotide-binding protein)-coupled receptor (GPCR) kinase 2 (GRK2), which is up-regulated in the failing human heart, appears to play a critical role

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