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isocitrate dehydrogenase/schlaganfall

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12 Ergebnisse

Identification of proteins in hyperglycemia and stroke animal models.

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BACKGROUND Stroke is a major cause of disability and death in adults. Diabetes mellitus is a metabolic disorder that strongly increases the risk of severe vascular diseases. This study compared changes in proteins of the cerebral cortex during ischemic brain injury between nondiabetic and diabetic
Humans with underlying cardiovascular disease, including stroke, are more susceptible to ambient particulate matter (PM)-induced morbidity and mortality. We hypothesized that stroke-prone spontaneously hypertensive rats (SHRSP) would be more susceptible than healthy Wistar Kyoto (WKY) rats to

Role of liraglutide in brain repair promotion through Sirt1-mediated mitochondrial improvement in stroke.

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Brain repair, especially axonal sprouting, is critical to restore motor function in disabled stroke patients. Liraglutide (LG) is a new kind of long-acting analogue of glucagon-like peptide-1 (GLP-1) and has potential protective effects in stroke. The mitochondria participate in brain repair after
Resveratrol has a neuroprotective effect against cerebral ischemia. The objective of this study was to identify proteins that are differentially expressed in the cerebral cortex of vehicle- and resveratrol-treated animals during ischemic injury. Focal cerebral ischemia was induced as middle cerebral

Alterations in mitochondrial DNA and enzyme activities in hypertrophied myocardium of stroke-prone SHRS.

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To clarify the pathophysiological alteration of mitochondria in SHRSP hypertrophied heart, mitochondria-related enzyme changes were examined and compared to those in WKY. Furthermore, the structure alteration in mitochondrial DNA (mtDNA) was examined by restriction fragment length polymorphisms

Mitochondrial abnormalities in hypertrophied myocardium of stroke-prone spontaneously hypertensive rats.

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1. To clarify the pathogenesis of cardiac disorders in SHRSP which showed severe cardiac hypertrophy and myocardial degeneration in the hypertensive stage, restriction fragment length polymorphisms (RFLP) of mitochondrial DNA (mtDNA), and morphological and functional changes of mitochondria were

Diffuse low-grade glioma mimicking ischaemic infarct: a case report.

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Diffuse Low-Grade Gliomas (LGGs) include World Health Organization (WHO) grade II diffuse astrocytoma, oligodendroglioma and oligoastrocytoma. Since the neurological symptoms of LGGs are often subtle and deceptive, LGGs are easily overlooked at their early stage. Here, we report a case of a
Objective: Isocitrate dehydrogenase (IDH)-wildtype glioblastomas are the most malignant glial tumours. Median survival is only 14-16 months after diagnosis, with patients aged ≥ 65 years reportedly showing worse outcome. This study aimed
Central post-stroke pain (CPSP) is one of the complications of cerebral ischemia and neuropathic pain syndrome. At present, there are few studies of pain in regions such as the spinal cord or sciatic nerve in cerebral ischemic animal models. To identify proteomic changes in the spinal cord and
BACKGROUND Myocardial infarction (MI) is an acute and fatal condition that threatens human health. Dl-3-n-butylphthalide (NBP) has been used for the treatment of acute ischemic stroke. Mitochondria may play a protective role in MI injury. However, there are few reports on the cardioprotective effect
World Health Organization (WHO) grade II low-grade gliomas (LGGs) in adults are rare, and patients' mean overall survival (OS) is relatively long. Epidemiological data on factors influencing tumor genesis and progression are scarce, and prospective data on surgical management are

Tricarboxylic acid cycle enzyme activities in a mouse model of methylmalonic aciduria.

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Methylmalonic acidemia (MMA) is a propionate pathway disorder caused by dysfunction of the mitochondrial enzyme methylmalonyl-CoA mutase (MMUT). MMUT catalyzes the conversion of methylmalonyl-CoA to succinyl-CoA, an anaplerotic reaction which feeds into the tricarboxylic acid (TCA) cycle. As part of
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