succinic dehydrogenase/mŕtvica

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Acetylsalicylic acid increases tolerance against hypoxic and chemical hypoxia.

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OBJECTIVE Treatment with acetylsalicylic acid (ASA) is established for secondary stroke prevention. Recent studies showed neuroprotection of ASA against glutamatergic excitants. The goal of this study was to investigate the time course of neuroprotection of ASA against indirect excitotoxicity by

3-Nitropropionic acid preconditioning ameliorates delayed neurological deterioration and infarction after transient focal cerebral ischemia in gerbils.

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The effect of 3-nitropropionic acid (3-NP), a selective inhibitor of succinic dehydrogenase, preconditioning on postischemic neurological deterioration and infarction was examined in gerbils after transient ischemia. The animals were pretreated with 1-80mg/kg of 3-NP 1 day before ischemia induced by

[MELAS without ragged-red fibers: a case report].

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A female patient who had clinical characteristics of MELAS but with no apparent muscle symptoms was reported. She was in good health until 12 years and 5 months of age when she began to have afebrile generalized tonic-clonic convulsions. Thereafter, she had repeated stroke-like episodes, including

Mitochondrial encephalomyopathy showing prominent microvacuolation and necrosis of intestinal smooth muscle cells: a case diagnosed by rectal biopsy.

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A 40-year-old woman who developed intestinal dysmobility was found, at rectal biopsy, to have marked microvacuolation of mucosal muscle layer cells, which corresponded to increased accumulation of abnormal mitochondria. Skeletal muscle biopsy specimens showed ragged-red fibers, vessels strongly

Brain damage related to hemorrhagic transformation following cerebral ischemia and the role of K ATP channels.

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BACKGROUND Hemorrhagic transformation (HT) is a major factor limiting the use of thrombolytic treatment for stroke. Animal model can help us to understand HT. This study is to establish a HT model in rats to compare HT with uncomplicated cerebral infarction in neurobehavioral deficit, brain edema,

Mitochondrial dysfunction in myofibrillar myopathy.

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'Myofibrillar myopathy' defines a myopathic condition with focal myofibrillar destruction and accumulation of degraded myofibrillar elements. Despite the fact that a number of mutations in different genes as well as cytotoxic agents lead to the disease, abnormal accumulation of desmin is a typical,

Protective effects of oleanolic acid on cerebral ischemic damage in vivo and H(2)O(2)-induced injury in vitro.

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BACKGROUND Oleanolic acid (OA), a triterpenoid compound, exists in many plants. It has numerous bioactivities and has been used to treat hepatitis in China. However, few studies have reported its effect on the central nervous system, especially in ischemic stroke. OBJECTIVE To explore the protective

Neurological mitochondrial cytopathies.

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The mitochondrial cytopathies are genetically and phenotypically heterogeneous group of disorders caused by structural and functional abnormalities in mitochondria. To the best of our knowledge, there are very few studies published from India till date. Selected and confirmed fourteen cases of

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