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Sivu 1 alkaen 29 tuloksia
Are alanine, cysteine, glycine and valine amino acids the cause of non-immune hydrops fetalis?
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Our objective was to measure amniotic fluid amino acid concentrations in pregnant women diagnosed as having fetuses with non immune hydrops fetalis in the second trimester of pregnancy. Twenty-three pregnant women who had fetuses with non immune hydrops fetalis detected by ultrasonography (non
Metabolomic analysis of the plasma of patients with high-altitude pulmonary edema (HAPE) using 1H NMR.
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Upon rapid ascent to a high altitude, non-acclimatized individuals, although healthy, are highly prone to contracting high-altitude pulmonary edema (HAPE). Early diagnosis is difficult and there is no reliable biomarker available. We used proton ((1)H) NMR metabolomics to profile the altered
Revealing anti-inflammation mechanism of water-extract and oil of forsythiae fructus on carrageenan-Induced edema rats by serum metabolomics.
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Forsythiae Fructus is an important Chinese medicine which shows a significant effect against inflammation. This study aimed to investigate the preventive anti-inflammation mechanism of Forsythiae Fructus by serum metabolomics strategy and compare the difference of the metabolism pathways between
Role of ammonia in the pathogenesis of brain edema.
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The role of hyperammonemia in the pathogenesis of cerebral edema was investigated using mongrel dogs to develop a treatment for cerebral edema in acute hepatic failure. Intravenous infusion of ammonium acetate alone into dogs did not induce brain edema, although blood ammonia reached
An assessment of progression of brain edema with amino acid levels in cerebrospinal fluid and changes in electroencephalogram in an adult cat model of cold brain injury.
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We investigated the relationship between the changes of the electroencephalogram (EEG) and concentration of amino acids (AAs) in cerebrospinal fluid (CSF) using a model of cold brain injury. A cold injury was made over the motor area of anesthetized adult cats (n = 45). The AAs in CSF from cisterna
Metabolic findings on 3T 1H-MR spectroscopy in peritumoral brain edema.
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OBJECTIVE
Little is known about the metabolic properties of brain edema associated with tumors. This work was conducted on the basis of the assumption that, in the presence of intra-axial and extra-axial brain tumors, the white matter involved by the edema is a site of metabolic change that involves
L-ornithine-L-aspartate lowers plasma and cerebrospinal fluid ammonia and prevents brain edema in rats with acute liver failure.
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Brain edema sufficient to cause intracranial hypertension and brain herniation remains a major cause of mortality in acute liver failure (ALF). Studies in experimental animal models of ALF suggest a role for ammonia in the pathogenesis of both encephalopathy and brain edema in this condition. As
Intravenous nimodipine worsening prolonged attack of familial hemiplegic migraine.
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We present a Norwegian family with familial hemiplegic migraine (FHM) with possibly four affected in three generations. The family had a point mutation in the ATP1A2 gene that caused a change of the amino acid valine to methionine (V628 M). The symptoms were pure FHM with intra- and interindividual
The imprinted oedematous-small mutation on mouse chromosome 2 identifies new roles for Gnas and Gnasxl in development.
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The Gnas locus is highly complex and encodes several oppositely imprinted and alternatively spliced transcripts. Gnas itself encodes Gsalpha, which is involved in endocrine function and bone development, but the roles for the other transcripts have not been established. Here we describe a mouse
Apoptotic signaling pathways induced by acute administration of branched-chain amino acids in an animal model of maple syrup urine disease.
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Maple Syrup Urine Disease (MSUD) is an inborn error of metabolism caused by a deficiency of the branched-chain α-keto acid dehydrogenase complex activity. This blockage leads to accumulation of the branched-chain amino acids leucine, isoleucine and valine, as well as their corresponding α-keto acids
Quantification of branched-chain amino acids in blood spots and plasma by liquid chromatography tandem mass spectrometry for the diagnosis of maple syrup urine disease.
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Individuals with maple syrup urine disease (MSUD) have an inherited metabolic disorder resulting in a deficiency in the branched-chain keto-acid dehydrogenase complex. As a result, these individuals have elevated concentrations of the branched-chain amino acids valine, isoluecine, allo-isoleucine,
Posttraumatic dental implant placement in a patient with maple syrup urine disease.
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Maple syrup urine disease (MSUD) is an inborn error of metabolism resulting from a defect in the oxidation of the branched-chain amino acids leucine, isoleucine, and valine. Patients present in early infancy with brain edema; delay in diagnosis and treatment is common and associated with residual
Cerebral computed tomography in maple syrup urine disease.
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Maple syrup urine disease (MSUD) is an inherited metabolic disorder due to decreased decarboxylation of branched chain keto acids triggering an accumulation of leucine, isoleucine, and valine. We describe two infants with biochemically confirmed MSUD in whom computed tomography (CT) revealed
[Amino acid changes following intraperitoneal administration of Tityus zulianus scorpion venom in mice. Study with subcutaneous microdialysis and capillary electrophoresis].
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Scorpion human envenoming is a public health hazard in the southwest of Venezuela. Tityus zulianus is one of the scorpion species whose venom causes lung edema and cardiac failure in children. These occasionally deadly manifestations have been attributed to a massive sympathetic discharge. The
Late-onset ornithine transcarbamylase deficiency in male patients: prognostic factors and characteristics of plasma amino acid profile.
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BACKGROUND
The occurrence of male patients with ornithine transcarbamylase (OTC) deficiency during adolescence or in adulthood has now been recognized. The aim of this study was to determine the prognostic factors that affect the prognosis of life, to explore a basis for therapeutic
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