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succinate dehydrogenase/accident vasculaire cérébral
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Strongly succinate dehydrogenase-reactive blood vessels in muscles from patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.
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Intramuscular blood vessels were examined with succinate dehydrogenase stain in skeletal muscle biopsy specimens from 6 patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Almost all arteries had large granular deposits with high succinate
Diazoxide increases liver and kidney HSP25 and HSP70 after shock and stroke.
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BACKGROUND
The compound, diazoxide (DZ), is known to induce preconditioning through its effect as a mitochondrial K(ATP) channel opener and succinate dehydrogenase inhibitor. Our team tested the hypothesis that pharmacological induction of ischemic preconditioning with DZ can offer cytoprotection
Diazoxide, as a postconditioning and delayed preconditioning trigger, increases HSP25 and HSP70 in the central nervous system following combined cerebral stroke and hemorrhagic shock.
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Combined hemorrhagic shock (Shock) and unilateral common carotid artery occlusion (Stroke) results in a decrease of oxygen availability to peripheral tissues and organs and the central nervous system (CNS). A variety of biochemical processes ensue, including organ failure, cellular apoptosis, and
Autopsied case with MERRF/MELAS overlap syndrome accompanied by stroke-like episodes localized to the precentral gyrus.
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We present an autopsied case with A8344G-mutated myoclonus epilepsy with ragged red fibers (MERRF)/mitochondrial encephalomyopathy with lactic acidosis and stroke-like episodes (MELAS) overlap syndrome accompanied by stroke-like episodes localized to the precentral gyrus. A 16-year-old Japanese
[Strongly succinate dehydrogenase-reactive blood vessels (SSV) in various neuromuscular diseases].
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The strongly succinate dehydrogenase-reactive blood vessels (SSV) are shown to have increased numbers of enlarged mitochondria in smooth muscle cells of the vessel wall on electron microscopy. They are seen in biopsied skeletal muscles from patients with mitochondrial myopathy, encephalopathy,
Vascular involvement in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes.
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A 26-year-old man with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) was admitted to our hospital for further cardiovascular examination. A muscle biopsy demonstrated strongly succinate dehydrogenase-reactive blood vessels. Pulse wave contour analysis
Heteroplasmic mitochondrial DNA mutation in a patient with mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes.
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A 16-year-old female presented with clinical, morphologic and molecular features of mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes (MELAS). Her early development was normal. Starting from the age of 14 years, she experienced recurrent episodes of headaches, with
Mitochondrial DNA 10158T>C mutation in a patient with mitochondrial encephalomyopathy with lactic acidosis, and stroke-like episodes syndrome: A case-report and literature review (CARE-complaint)
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Rationale: Mitochondrial encephalomyopathy with lactic acidosis and stroke- like episodes (MELAS) syndrome is caused by mitochondrial respiratory chain dysfunction and oxidative phosphorylation disorder. It is a rare clinical metabolic
Single muscle fiber analysis of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
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We examined muscle sections from 3 patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), using single-fiber polymerase chain reaction, histochemistry, and in situ hybridization. Most type 1 ragged-red fibers showed positive cytochrome c oxidase
Increased mitochondrial DNA in blood vessels and ragged-red fibers in mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS).
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Using in situ hybridization, we studied muscle biopsy specimens from 4 patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS). Three of the 4 patients with MELAS had a mutation at position 3243 of mitochondrial DNA (mtDNA) in the transfer RNALeu(UUR)
Malignant paraganglioma presenting with hemorrhagic stroke in a child.
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Sympathetic paragangliomas are rare catecholamine-secreting tumors of extra-adrenal origin, and their diagnosis in children is even more infrequent. They usually manifest as hypertension, palpitations, headache, sweating, and pallor. Malignant paragangliomas are identified by the presence of
Ischemic stroke and rhabdomyolysis in a 15-year-old girl with paraganglioma due to an SDHB exon 6 (Q214X) mutation.
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BACKGROUND
We report a 15-year-old girl with a recent diagnosis of type 2 diabetes mellitus who presented in malignant hypertensive crisis (BP 210/120 mm Hg). Abdominal CT showed an 8.2 x 4.7 x 7.0 cm mass in the region of the organ of Zuckerkandl. MIBG scan showed a single paraganglioma without
When should MELAS (Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes) be the diagnosis?
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Mitochondrial myopathy, Encephalopathy, Lactic Acidosis, and Stroke-like episodes (MELAS) is a rare mitochondrial disorder. Diagnostic criteria for MELAS include typical manifestations of the disease: stroke-like episodes, encephalopathy, evidence of mitochondrial dysfunction (laboratorial or
Fenofibrate attenuates cardiac and renal alterations in young salt-loaded spontaneously hypertensive stroke-prone rats through mitochondrial protection.
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OBJECTIVE
The simultaneous presence of cardiac and renal diseases is a pathological condition that leads to increased morbidity and mortality. Several lines of evidence have suggested that lipid dysmetabolism and mitochondrial dysfunction are pathways involved in the pathological processes affecting
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
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