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decarboxylase/oksentaminen
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Sivu 1 alkaen 58 tuloksia
Treatment of Parkinson's disease with levodopa combined with L-alpha-methyldopahydrazine, an inhibitor of extracerebral DOPA decarboxylase.
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Thirty patients with Parkinson's disease were treated for four weeks with levodopa combined with an inhibitor of extracerebral dopa decarboxylase, L-alpha-methyldopahydrazine (MK 486). The therapeutic results were compared with the effects of treatment of a group of 40 patients with levodopa alone.
Levodopa alone and in combination with a peripheral decarboxylase inhibitor benserazide (Madopar) in the treatment of Parkinson's disease: A controlled clinical trial.
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A combination of levodopa and the extracerebrally acting decarboxylase inhibitor benserazide (ratio 4:1) (Madopar), was compared with levodopa alone in a controlled double-blind clinical multicenter trial on 94 patients with Parkinson's disease. During 4 months of therapy levodopa + benserazide
Intestinal changes caused by DL-alpha-difluoromethylornithine (DFMO), an inhibitor of ornithine decarboxylase.
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Subacute (2 week) oral or intravenous administration of DL-alpha-difluoromethylornithine (DFMO), an irreversible inhibitor of ornithine decarboxylase (ODC), caused diarrhea and frequent emesis as early as 4 to 5 days in dogs (dose greater than or equal to 200 mg/kg/day). Diarrhea also occurred in
The effect of L-dopa with and without decarboxylase inhibitor on growth hormone secretion in children with short stature.
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The efficiency of L-dopa alone and L-dopa plus a dopa-decarboxylase inhibitor (carbidopa) in provoking growth hormome (GH) secretion was studied 40 children with short stature. By preventing the extracerebral metabolism, carbidopa increases the availability of L-dopa to the brain. The study was
L-dopa therapy combined with peripheral decarboxylase inhibitor (MK-486) in Parkinsonism.
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Eighteen patients with parkinsonism were treated with a combination of L-dopa and peripheral decarboxylase inhibitor, L-alphahydrazinomethyldopa (MK-486). Modification of L-dopa effect by MK-486 was also studied in parkinsonian patients as well as in cats. (1) Concentrations of dopa and dopamine in
Citrate treatment in a patient with pyruvate decarboxylase deficiency.
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A 5-year old boy with intermittent sopor, severe vomiting and ataxia since 2 1/2 years old was described. During attack period the patient showed elevation of blood pyruvate and alanine and also cerebrospinal-fluid pyruvate, whereas during the time free from attack only blood pyruvate was increased.
Malonyl coenzyme A decarboxylase deficiency. Clinical and biochemical findings in a second child with a more severe enzyme defect.
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A second child with a more severe deficiency of malonyl CoA decarboxylase is described. He is mildly mentally retarded and presented with vomiting, a seizure, hypoglycaemia and mild metabolic acidosis during a urinary tract infection. The urine contained increased amounts of malonic, methylmalonic,
Cloning and mutational analysis of human malonyl-coenzyme A decarboxylase.
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Malonyl coenzyme A (CoA) decarboxylase (E.C.4. 1.1.9) catalyzes the conversion of malonyl CoA to acetyl CoA. The metabolic role of malonyl CoA decarboxylase has not been fully defined, but deficiency of the enzyme has been associated with mild mental retardation, seizures, hypotonia, cardiomyopathy,
Malonyl coenzyme A decarboxylase deficiency.
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Two new cases of malonyl coenzyme A (CoA) decarboxylase deficiency are described. Hitherto, the worldwide experience of the disorder has been confined to reports on two affected Australian children. The new cases are Scots born and are the offspring of consanguinous parents of Scots/Irish origin.
Malonyl coenzyme A decarboxylase deficiency.
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A patient is described with a deficiency of the mitochondrial enzyme, malonyl CoA decarboxylase - an inborn error of metabolism not recognized previously. The enzyme defect was first suspected because of persistent excretion of malonic and methylmalonic acids in urine in a child with repeated
Treatment of parkinsonism with l-dopa and a decarboxylase inhibitor. An electrophysiological and clinical study.
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Twelve parkinsonian patients with an unsatisfactory therapeutic result on L-Dopa alone due to nausea, vomiting and involuntary movements were treated WITH L-Dopa and decarboxylase inhibitor. The daily dose reached 800mg L-Dopa and 200 mg decarboxylase inhibitor. Single doses of each of the
Rat malonyl-CoA decarboxylase; cloning, expression in E. coli and its biochemical characterization.
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Malonyl-CoA decarboxylase (E.C.4.1.1.9) catalyzes the conversion of malonyl-CoA to acetyl-CoA. Although the metabolic role of this enzyme has not been fully defined, it has been reported that its deficiency is associated with mild mental retardation, seizures, hypotonia, cadiomyopathy, developmental
Central and peripheral mechanisms contribute to the antiemetic actions of delta-9-tetrahydrocannabinol against 5-hydroxytryptophan-induced emesis.
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Delta-9-tetrahydrocannabinol (delta-9-THC) prevents cisplatin-induced emesis via cannabinoid CB(1) receptors. Whether central and/or peripheral cannabinoid CB(1) receptors account for the antiemetic action(s) of delta-9-THC remains to be investigated. The 5-hydroxytryptamine (5-HT=serotonin)
Comparison of dopa decarboxylase inhibitor (carbidopa) combined with levodopa and levodopa alone in Parkinson's disease.
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A double-blind study comparing the effects of carbidopa and levodopa combined in a single tablet with levodopa alone was undertaken in 50 patients with Parkinson's disease. After 6 months, there was a statistically significant improvement over baseline in total score, rigidity, and tremor only in
A case of pegylated interferon alpha-related diabetic ketoacidosis: can this complication be avoided?
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We report the case of a 42-year-old woman with chronic hepatitis C (genotype 1), who in June 2004 started therapy with pegylated interferon alpha (PEG-IFNalpha) plus ribavirin. Two months later, she discontinued treatment because of polydipsia, polyuria and vomiting leading to a marked dehydration.
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