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OBJECTIVE
To explore risk factors for stroke independent of hypertension and the relationship between riboflavin kinase (RFK) and stroke.
METHODS
Gene expression profiling in the brains of spontaneously hypertensive rats (SHR) and stroke-prone spontaneously hypertensive rats (SHRSP) was
BACKGROUND
There is experimental evidence that riboflavin (vitamin B2) supplementation reduces oxidative damage and cerebral oedema following acute stroke.
OBJECTIVE
To measure riboflavin levels in acute stroke before and after supplementation with this vitamin.
METHODS
Ninety-six acute ischaemic
Between 1986 and 1991, 29,584 persons took part in a randomized nutritional intervention trial in Linxian, China, an area whose residents had chronically low intakes of several nutrients and high rates of esophageal and gastric cardia cancer as well as stroke. Using a one-half replicate of a 2(4)
OBJECTIVE
Blood/brain-glutamate grabbing is an emerging concept in the treatment of acute ischemic stroke, where essentially the deleterious effects of glutamate after ischemia are ameliorated by coaxing glutamate to enter the bloodstream and thus reducing its concentration in the brain. Aiming to
BACKGROUND
Meta-analyses predict that a 25% lowering of plasma homocysteine would reduce the risk of coronary heart disease by 11% to 16% and stroke by 19% to 24%. Individuals homozygous for the methylenetetrahydrofolate reductase (MTHFR) 677C-->T polymorphism have reduced MTHFR enzyme activity
Abnormal riboflavin status in the absence of a dietary deficiency was detected in 31 consecutive outpatients with Parkinson's disease (PD), while the classical determinants of homocysteine levels (B6, folic acid, and B12) were usually within normal limits. In contrast, only 3 of 10 consecutive
Stroke patients often experience a walking dysfunction caused by decreased mobility, weakened muscular strength, abnormal posture control, and cognitive dysfunction. Anxiety/depression is the most important and prevalent neuropsychiatric complication of stroke survivors. Brain injury and the
The spontaneously hypertensive stroke-prone rat (SHRSP) is a recognized animal model for the study of severe hypertension and stroke, being characterized by presenting an elevated tissue levels of free radicals. Therefore, this study has the main goal to identify the effect of B vitamins, closely
BACKGROUND
Stroke is a leading cause of death. Current therapeutic strategies have been unsuccessful. Several studies have reported benefits on reducing stroke risk and improving the poststroke associated functional declines in patients who ate foods rich in fruits and vegetables. Their potential
NADPH-dependent methemoglobin reductase, first detected in erythrocytes sixty years ago, has subsequently been purified and characterized as a methylene blue reductase and a flavin reductase. The reductase plays no role in methemoglobin reduction under normal conditions, but its activity serves as
BACKGROUND
Although a number of risk factors for fatal stroke are well established in Western populations, this is less true for Asian countries, many of which have stroke mortality rates that are historically high. In a prospective study in Shanghai, China, we determined whether the same factors
To perform a pharmacoeconomic analysis of the most frequently prescribed neuroprotective medicines for treating patients with mild ischemic stroke in the acute and early rehabilitation periods in the Russian Federation.Three medical technologies were Human riboflavin kinase (HsRFK) catalyzes vitamin B2 (riboflavin) phosphorylation to flavin mononucleotide (FMN), obligatory step in flavin cofactor synthesis. HsRFK expression is related to protection from oxidative stress, amyloid-β toxicity, and some malignant cancers progression. Its
We report a patient with MELAS treated for 24 months with idebenone and riboflavin, during which no stroke-like episodes occurred. Moreover neurological symptoms clearly improved, and a recovery of brain MRI and EEG abnormalities was observed. We conclude that the combined treatment with idebenone
Oxidized irwN has been proposed as a mediator of the free radical-induced damage that occurs during cerebral ischemia. Dihydroriboflavin, a compound produced from riboflavin (B2) by NADPH-dependent flavin reductase, rapidly reduces oxidized iron. Since treatment with riboflavin offers protection