cytochrome c/headache

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[A case of MELAS (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke-like episodes) with progressive cytochrome c oxidase deficiency].

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We report a 9 year-old boy with MELAS. High dosed oral thiamine administration and high fat diet induced remarkable neurological and biochemical improvement. His mother had episodic headaches and hemiplegia, probably MELAS. He complained muscle weakness and repeated episodes of vomiting started from

MELAS syndrome: peripheral neuropathy and cytochrome C-oxidase deficiency: a case report and review of the literature.

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A 4-year-old boy presented with developmental delay, aggressive behavior, and incoordination. His EEG showed a diffuse encephalopathy. At age 10 he developed convulsions and severe migraine-like headaches. Muscle wasting, arreflexia, and lactic acidemia following exercise were noted.

Treatment of mitochondrial encephalomyopathy with a combination of cytochrome C and vitamins B1 and B2.

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The therapeutic efficacy of a regimen consisting of intravenous injection of Cardiocrome, containing cytochrome c, flavin mononucleotide and thiamine diphosphate for mitochondrial encephalomyopathy (MEM) was examined. This combined therapy was applied to nine patients with MEM, including four with

PHYLOGENY OF ANGIOSTRONGYLUS CANTONENSIS IN THAILAND BASED ON CYTOCHROME C OXIDASE SUBUNIT I GENE SEQUENCE.

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Angiostrongylus cantonensis is an emerging infectious agent causing eosinophilic meningitis or meningoencephalitis in humans with clinical manifestation of severe headache. Molecular genetic studies on classification and phylogeny of A. cantonensis in Thailand are limited. This study surveyed A.

[MELAS (mitochondrial encephalopathy, lactic acidosis and stroke-like episodes): report of a case].

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The case of 12 years-old boy with seizures, headache, severe vomit and focal neurological signs is reported. These episodes had several recurrences and regression with little neurologic deficits. In the investigation it was found: lactic acidosis; stroke like episodes and calcification in the basal

MERRF/MELAS overlap syndrome due to the m.3291T>C mutation.

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We report the case of a 19-year-old Chinese female harboring the m.3291T>C mutation in the MT-TL1 gene encoding the mitochondrial transfer RNA for leucine. She presented with a complex phenotype characterized by progressive cerebellar ataxia, frequent myoclonus seizures, recurrent stroke-like

Catastrophic presentation of mitochondrial disease due to a mutation in the tRNA(His) gene.

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The authors describe a patient who presented with headache, seizures, and severe cerebral edema in whom they identified a novel mutation in the mitochondrial (mt-) tRNA(His) gene. This G12147A transition is heteroplasmic, predicted to disrupt a highly conserved base pair, and segregates with the

A novel m.11406T>A mutation in mitochondrial ND4 gene causes MELAS Syndrome

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Pathogenic point mutations of mitochondrial DNA (mtDNA) are associated with a large number of heterogeneous diseases involving multiple systems with which patients may present with a wide range of clinical phenotypes. In this study, we describe a novel heteroplasmic missense mutation, m.11406T>A,

New Variant of MELAS Syndrome With Executive Dysfunction, Heteroplasmic Point Mutation in the MT-ND4 Gene (m.12015T>C; p.Leu419Pro) and Comorbid Polyglandular Autoimmune Syndrome Type 2.

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Background: Mitochondrial diseases are caused by dysfunctions in mitochondrial metabolic pathways. MELAS syndrome is one of the most frequent mitochondrial disorders; it is characterized by encephalopathy, myopathy, lactic acidosis, and stroke-like episodes. Typically, it is associated with a

Tanacetum polycephalum (L.) Schultz-Bip. induces mitochondrial-mediated apoptosis and inhibits migration and invasion in MCF7 cells.

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Tanacetum polycephalum (L.) Schultz-Bip (Mokhaleseh) has been traditionally used in the treatment of headaches, migraines, hyperlipidemia and diabetes. The present study aimed to evaluate its anticancer properties and possible mechanism of action using MCF7 as an in vitro model. T. polycephalum

Molecular analysis of Dirofilaria repens removed from a subcutaneous nodule in a Japanese woman after a tour to Europe.

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A premature female Dirofilaria species, subsequently identified as Dirofilaria repens by its morphological features and mitochondrial 12S ribosomal RNA (12S rRNA) gene sequence, was removed from a subcutaneous nodule of the right temporal region of the head in a Japanese woman 2 years after she

Mitochondrial dysfunction in migraine.

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Migraine is the most frequent type of headache in children. In the 1980s, scientists first hypothesized a connection between migraine and mitochondrial (mt) disorders. More recent studies have suggested that at least some subtypes of migraine may be related to a mt defect. Different types of

Mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) syndrome: an autopsy report.

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Autopsy reports of patients with mitochondrial encephalopathy with lactic acidosis and strokelike episode (MELAS) are rare. This report documents the clinical and autopsy findings of a 47-year-old woman with MELAS syndrome. The diagnosis was corroborated by documenting a mitochondrial DNA mutation

Valproic acid-induced hepatotoxicity in Alpers syndrome is associated with mitochondrial permeability transition pore opening-dependent apoptotic sensitivity in an induced pluripotent stem cell model.

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Valproic acid (VPA) is widely used to treat epilepsy, migraine, chronic headache, bipolar disorder, and as adjuvant chemotherapy, but potentially causes idiosyncratic liver injury. Alpers-Huttenlocher syndrome (AHS), a neurometabolic disorder caused by mutations in mitochondrial DNA polymerase gamma

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