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Puslapis 1 nuo 58 rezultatus
Controlled trial of ornithine alpha ketoglutarate (OAKG) in patients with stroke.
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A double blind controlled trial of ornithine alpha-ketoglutarate (OAKG) was carried out on 50 patients admitted to the Royal Free and Royal Northern Hospitals, London, suffering from a recent stroke. Significant improvement was found in patients treated with OAKG when examined on the fifth day of
Acute extrapyramidal syndrome in mild ornithine transcarbamylase deficiency: metabolic stroke involving the caudate and putamen without metabolic decompensation.
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A 6-year-old male with partial ornithine transcarbamylase (OTC) deficiency had acute and rapidly progressive symmetrical swelling of the head of the caudate nuclei and putamina. Clinical presentation was ataxia and dysarthria progressing to seizures and coma; these symptoms gradually resolved with
Successful early management of a female patient with a metabolic stroke due to ornithine transcarbamylase deficiency.
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BACKGROUND
Ornithine transcarbamylase deficiency (OTC-D) is a urea cycle disorder caused by dysfunction of ornithine transcarbamylase, which frequently leads to hyperammonemia. Hyperammonemia represents a medical emergency requiring prompt treatment to reduce plasma ammonia levels and prevent severe
Recurrent Stroke Like Episodes Secondary to Ornithine Transcarbamylase Deficiency.
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Oligodendrocyte Progenitor Cell Proliferation and Fate after White Matter Stroke in Juvenile and Adult Mice.
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The incidence of stroke in children is 2.4 per 100,000 person-years and results in long-term motor and cognitive disability. In ischemic stroke, white matter (WM) is frequently injured, but is relatively understudied compared to grey matter injury. Previous research suggests that the cellular
Neuroprotective role of ornithine decarboxylase activation in transient focal cerebral ischaemia: a study using ornithine decarboxylase-overexpressing transgenic rats.
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Nuclear magnetic resonance imaging (MRI) was used to study dynamics of maturation and the size of ischaemic stroke lesions in rats with greatly increased activity of ornithine decarboxylase (ODC). Syngenic rats, either with or without chronic pre-ischaemic treatment with an ODC inhibitor,
Brain neurons express ornithine decarboxylase-activating antizyme inhibitor 2 with accumulation in Alzheimer's disease.
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Polyamines are small cationic molecules that in adult brain are connected to neuronal signaling by regulating inward-rectifier K(+)-channels and different glutamate receptors. Antizyme inhibitors (AZINs) regulate the cellular uptake of polyamines and activate ornithine decarboxylase (ODC), the
Evidence for nuclear ornithine decarboxylase activity in different brain regions of the male rat.
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The subcellular distribution of ornithine decarboxylating activity in nucleus caudatus putamen, hippocampus, parietal cerebral cortex, cerebellum and hypothalamus of male rat brain has been investigated. The 7000 g supernatant (cytosolic fraction), the 7000 g sediment and the 700 g sediment (nuclear
Transgenic rats as models for studying the role of ornithine decarboxylase expression in permanent middle cerebral artery occlusion.
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OBJECTIVE
Cerebral ischemia causes activation of ornithine decarboxylase (ODC) gene and subsequent accumulation of putrescine, which might either directly or indirectly affect the outcome of cerebral infarct. We developed a transgenic rat overexpressing human ODC, which was used to explore the
Ornithine and Homocitrulline Impair Mitochondrial Function, Decrease Antioxidant Defenses and Induce Cell Death in Menadione-Stressed Rat Cortical Astrocytes: Potential Mechanisms of Neurological Dysfunction in HHH Syndrome.
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Hyperornithinemia-hyperammonemia-homocitrullinuria (HHH) syndrome is caused by deficiency of ornithine translocase leading to predominant tissue accumulation and high urinary excretion of ornithine (Orn), homocitrulline (Hcit) and ammonia. Although affected patients commonly present neurological
Ornithine transcarbamylase deficiency presenting with strokelike episodes.
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A girl with ornithine transcarbamylase deficiency had a history of recurrent strokelike episodes. The differential diagnosis of unexplained stroke should include primary urea cycle defects.
Protease-activated receptor 2 and bradykinin-mediated vasodilation in the cerebral arteries of stroke-prone rats.
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Protease-activated receptor 2 (PAR(2)) expression is up-regulated during vascular injury associated with edema. PAR(2) and bradykinin subtype 2 receptor (B(2)) expression and function were assessed in relation to hypertensive encephalopathy (HE) and cerebral hemorrhage (CH) in middle cerebral
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
Acute hemiparesis as the presenting sign in a heterozygote for ornithine transcarbamylase deficiency.
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Strokes in children occur in conjunction with cardiac disease, hematological disorders, trauma, intracranial infections and migraine. Recently several inborn errors of metabolism have been recognized as possible causes of stroke-like symptoms. We describe a female heterozygote of ornithine
Induction of ornithine decarboxylase mRNA in transient focal cerebral ischemia in the rat.
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We used in situ hybridization to localize the long-term changes in ornithine decarboxylase (ODC) expression after a 90 min occlusion of the middle cerebral artery (MCAO) in the rat. The ODC mRNA was induced in the ipsilateral dentate gyrus (DG) and throughout the ischemic cortex at 12 h and still at
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