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glutamic acid/infarzierung
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Seite 1 von 53 Ergebnisse
Identification of a glutamic acid repeat polymorphism of ALMS1 as a novel genetic risk marker for early-onset myocardial infarction by genome-wide linkage analysis.
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BACKGROUND
Myocardial infarction (MI) is a leading cause of death worldwide. Given that a family history is an independent risk factor for coronary artery disease, genetic variants are thought to contribute directly to the development of this condition. The identification of susceptibility genes for
Differences in the distribution of glutamic acid-oxalacetic acid transaminase- and aldolase-activity among serum protein fractions in patients with acute myocardial infarct and hepatocellular damage.
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[Acute abdominal pain due to splenic infarction in a patient with heterozygous sickle cell disease exposed to high altitude].
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Hemoglobinopathy S, Depranocytosis or Sickle Cell Disease is the most common hemoglobinopathy in the world. In its heterozygous form (Sickle Cell Trait), it affects 8% of the black population in the U.S. and 25% of the black population in Africa, and is found less frequently in the Mediterranean
[Studying the neuroprotective effect of the novel glutamic acid derivative neiroglutam on focal cerebral ischemia in rats].
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We have studied the neuroprotective effect of the novel glutamic acid derivative neiroglutam on reversible focal cerebral ischemia in rats. The neuroprotective drug action was assessed by the ability to reduce the severity of neurological deficit (1, 2, 3, 5 and 7 days), forelimb fine-motor
Effects of aging and dementia on the levels of thiobarbituric-acid-reactive products stimulated by L-glutamic acid in human autopsy and biopsy brain tissue.
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Basal and stimulated (by L-glutamic acid, GA) levels of thiobarbituric-acid-reactive products were estimated in the brain tissue (hippocampus, cortex and cerebellum) from autopsy samples of people with Alzheimer disease (AD), multi-infarct dementia (MID) and from nondemented control patients. The
Poly-arginine peptides reduce infarct volume in a permanent middle cerebral artery rat stroke model.
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We recently reported that poly-arginine peptides have neuroprotective properties both in vitro and in vivo. In cultured cortical neurons exposed to glutamic acid excitotoxicity, we demonstrated that neuroprotective potency increases with polymer length plateauing at R15 to R18 (R = arginine
Homolateral cerebrocortical changes in neuropeptide and receptor expression after minimal cortical infarction.
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A cortical infarct of 2 mm diameter was obtained in the parietal cortex after a craniotomy, disruption of the dura mater and topical application of 3 M KCl. It has been shown previously that the presence of a small cortical infarct induces an increase in immediate early gene messenger RNA expression
Permanent increase of immunocytochemical reactivity for gamma-aminobutyric acid (GABA), glutamic acid decarboxylase, mitochondrial enzymes, and glial fibrillary acidic protein in rat cerebral cortex damaged by early postnatal hypoxia-ischemia.
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A former study indicated that hypoxic-ischemic encephalopathy in rat sustained during early postnatal life may result in permanent epileptic activity in the baseline electroencephalogram. We, therefore, investigated whether the presumed higher firing frequency and metabolic activity of neurons in
[Spleen infarction and S hemoglobinopathies S in the high altitude lands].
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The hemoglobin S is a consequence of the substitution of valine for glutamic acid at position 6 of beta globin chain. The problem arises when some individuals with Hb S is moved to the mountains and exposed to hypoxia. The decrease in oxygen saturation distorts the red blood cell with HbS-shaped
[Clinical and experimental study on treatment of acute cerebral infarction by zhongfeng no. II oral liquid].
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OBJECTIVE
To explore the effect and mechanism of Zhongfeng No. II Oral Liquid (ZF II) in treating acute cerebral infarction (CI).
METHODS
Randomly controlled clinical study was conducted in 160 patients with CI, they were treated with ZF II plus western medicine (treated group) and western medicine
[tRNA and aminoacyl-tRNA synthetases from the liver of rabbits in experimental myocardial infarction].
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An acceptor activity of tRNA for glycine, glutamic acid, leucine, serine and phenylalanine was decreased in rabbit liver tissue within 6, 12 and 24 hrs after myocardial infarction; the activity was reduced within 72 hrs. Heating of tRNA under conditions of transition of biologically inactive
Poly-arginine R18 and R18D (D-enantiomer) peptides reduce infarct volume and improves behavioural outcomes following perinatal hypoxic-ischaemic encephalopathy in the P7 rat.
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We examined the neuroprotective efficacy of the poly-arginine peptide R18 and its D-enantiomer R18D in a perinatal hypoxic-ischaemic (HI) model in P7 Sprague-Dawley rats. R18 and R18D peptides were administered intraperitoneally at doses of 30, 100, 300 or 1000 nmol/kg immediately after HI (8%
Aldehyde dehydrogenase 2 gene is a risk factor for myocardial infarction in Japanese men.
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In epidemiological studies, moderate alcohol consumption has been consistently associated with a reduced risk of myocardial infarction (MI). About half of Japanese show an extremely high sensitivity to alcohol (ethanol), which is due to a missense mutation from glutamic acid (Glu) to lysine (Lys) at
Association between a genetic variant related to glutamic acid metabolism and coronary heart disease in individuals with type 2 diabetes.
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OBJECTIVE
Diabetes is associated with an elevated risk of coronary heart disease (CHD). Previous studies have suggested that the genetic factors predisposing to excess cardiovascular risk may be different in diabetic and nondiabetic individuals.
OBJECTIVE
To identify genetic determinants of CHD that
[Ghrelin protects against hippocampal injury after global cerebral ischemia/reperfusion and regulate glutamic acid/γ-aminobutyric acid sensitive neuron discharge]
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To observe the protective effect of ghrelin on hippocampal injury induced by global cerebral ischemia/reperfusion (I/R) and explore its effect mechanisms.
The male Sprague-Dawley (SD) rats were randomly divided into four groups,namely sham group, I/R group,normal saline (NS)+I/R group and
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