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Dynamic derangement in amino acid profile during and after a stroke-like episode in adult-onset mitochondrial disease: a case report.

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Maternally inherited diabetes and deafness, and mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes are examples of mitochondrial diseases that are relatively common in the adult population. Mitochondrial myopathy, encephalopathy, lactic acidosis, and

The effect of citrulline and arginine supplementation on lactic acidemia in MELAS syndrome.

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Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is a mitochondrial disorder in which nitric oxide (NO) deficiency may play a role in the pathogenesis of several complications including stroke-like episodes and lactic acidosis. Supplementing the NO

Assessment of Nitric Oxide Production in Mitochondrial Encephalomyopathy, Lactic Acidosis, and Stroke-Like Episodes Syndrome with the Use of a Stable Isotope Tracer Infusion Technique.

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Mitochondrial disorders result from dysfunctional mitochondria that are unable to generate sufficient energy to meet the needs of various organs. Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is one of the most frequent maternally inherited mitochondrial

The role of nitric oxide in the pathophysiology of thromboembolic stroke in the rat.

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Although nitric oxide (NO) has been shown to play an important role in the pathophysiology of cerebral ischemia, its contribution to the pathogenesis of experimentally induced thromboembolic stroke is unknown. In this study, we pharmacologically manipulated NO levels in the acute post-thrombotic

Discovery of a New Biomarker Pattern for Differential Diagnosis of Acute Ischemic Stroke Using Targeted Metabolomics.

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Stroke is one of the leading causes of disability all over the world. However, biomarkers for fast differential diagnosis of acute ischemic stroke (AIS) from vertigo or headache, remains lacking. Using a direct-infusion mass spectrometry method, it is possible to establish an efficient method for

Stroke-like episodes, peri-episodic seizures, and MELAS mutations.

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OBJECTIVE Stroke-like episodes (SLEs) are a hallmark of various mitochondrial disorders, in particular MELAS syndrome. SLEs manifest with vasogenic oedema (DWI and ADC hyperintensity) or partial cytotoxic oedema (DWI hyperintensity, ADC hypointensity) in the acute and subacute stage, and with

Oral L-citrulline supplementation attenuates blood pressure response to cold pressor test in young men.

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BACKGROUND Oral L-citrulline is efficiently converted to L-arginine, which has been shown to decrease brachial blood pressure (BP) at rest and during the cold pressor test (CPT). However, aortic BP may better reflect cardiovascular risk than brachial BP. The purpose of this study was to test the

Mitochondria: role of citrulline and arginine supplementation in MELAS syndrome.

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Mitochondria are found in all nucleated human cells and generate most of the cellular energy. Mitochondrial disorders result from dysfunctional mitochondria that are unable to generate sufficient ATP to meet the energy needs of various organs. Mitochondrial encephalomyopathy, lactic acidosis, and

Restoration of impaired nitric oxide production in MELAS syndrome with citrulline and arginine supplementation.

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Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is one of the most common mitochondrial disorders. Although the pathogenesis of stroke-like episodes remains unclear, it has been suggested that mitochondrial proliferation may result in endothelial

8-year retrospective analysis of intravenous arginine therapy for acute metabolic strokes in pediatric mitochondrial disease.

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Intravenous (IV) arginine has been reported to ameliorate acute metabolic stroke symptoms in adult patients with Mitochondrial Encephalopathy with Lactic Acidosis and Stroke-like Episodes (MELAS) syndrome, where its therapeutic benefit is postulated to result from arginine acting as a nitric oxide

Impaired nitric oxide production in children with MELAS syndrome and the effect of arginine and citrulline supplementation.

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Mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes (MELAS) syndrome is one of the most frequent maternally inherited mitochondrial disorders. The pathogenesis of this syndrome is not fully understood and believed to result from several interacting mechanisms including

Plasma nitric oxide (nitrate/nitrite) levels in acute stroke and their relationship with severity and outcome.

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Endothelium-derived nitric oxide is beneficial in experimental stroke. We assessed plasma NO levels in patients with acute stroke and their association with both severity and outcome. Plasma nitric oxide (NO), assessed as nitrate/nitrite (NOx), cyclic guanosine monophosphate (cGMP, second messenger

Arginine and citrulline for the treatment of MELAS syndrome.

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MELAS (mitochondrial encephalomyopathy, lactic acidosis, and stroke-like episodes) syndrome is a maternally inherited mitochondrial disease with a broad spectrum of manifestations. In addition to impaired energy production, nitric oxide (NO) deficiency occurs in MELAS syndrome and leads to impaired

Stroke in Children with Sickle Cell Disease.

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Children with sickle disease are at high risk for ischemic stroke and transient ischemic attacks, usually secondary to intracranial arteriopathy involving the terminal internal carotid and proximal middle cerebral and anterior cerebral arteries, which may be diagnosed using transcranial Doppler

Neuronal nitric oxide synthase activation and peroxynitrite formation in ischemic stroke linked to neural damage.

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Nitric oxide (NO) is a new intercellular messenger that occurs naturally in the brain without causing overt toxicity. Yet, NO has been implicated as a mediator of cell death in cell death. One explanation is that ischemia causes overproduction of NO, allowing it to react with superoxide to form the

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