propionic acid/ضمور

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The effect of intravenous L-carnitine on propionic acid excretion in acute propionic acidaemia.

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A 6-week-old female infant presented in a severe metabolic crisis from propionic acidaemia. The condition was aggravated by pneumonia and heart insufficiency. In addition to the general supportive measures and caloric intake exclusively from glucose, intravenous L-carnitine treatment (2 g

Effect of propionic acid on fatty acid oxidation and ureagenesis.

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Propionic acid significantly inhibited 14CO2 production from [1-14C] palmitate at a concentration of 10 muM in control fibroblasts and 100 muM in methylmalonic fibroblasts. This inhibition was similar to that produced by 4-pentenoic acid. Methylmalonic acid also inhibited 14CO2 production from

[The effect of nutritional factors on the ruminal mucosa. 3. Condition of the mucosa after infusion of propionic acid, acetic acid and butyric acid].

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Three non-lactating cows (Deutsches Schwarzbuntes Rind) with large ruminal fistulas were fed coarsely structured food. Within a trial period of 21 weeks infusion periods lasting 3 weeks alternated with equally long control periods (K). During the 3 infusion periods, 8.4 mMol of propionic acid (P),

Characterization of the adipose tissue atrophy induced by peroxisome proliferators in mice.

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In the present study, we characterized the effects of peroxisome proliferators (PP) on adipose tissue in mice. Treatment with potent PP, such as perfluorooctanoic acid (PFOA), 2-methyl-2-(p(1,2,3,4-tetrahydroxy-naphthyl)-phenoxy)propionic acid, (4-chloro-6-(2,3-xylidino)2-pyrimidinylthio) acetic

Cell culture evidence for neuronal degeneration in amyotrophic lateral sclerosis being linked to glutamate AMPA/kainate receptors.

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Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder affecting motor neurons. Glutamate, a potent central-nervous-system toxin, has been proposed as one possible factor in this motoneuron disease. Serum from patients with ALS is known to be toxic when added to neurons in culture. We

Enduring changes in Purkinje cell electrophysiology following transient exposure to AMPA: correlates to dark cell degeneration.

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Purkinje cells (PCs) are selectively vulnerable to alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-mediated delayed toxicity that is manifested as dark cell degeneration (DCD) rather than necrosis. The purpose of the present study was to utilize electrophysiologic changes induced by

Continuous propionic acid fermentation by immobilized Propionibacterium acidipropionici in a novel packed-bed bioreactor.

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Continuous propionic acid fermentations of lactate by Propionibacterium acidipropionici were studied in spiral wound fibrous bed bioreactors. Cells were imobilized by natural attachment to fiber surfaces and entrapment in the void volume within the fibrous matrix. A high cell density of

Calcium-permeable alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors: a molecular determinant of selective vulnerability in amyotrophic lateral sclerosis.

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The cause of the selective degeneration of motor neurons in amyotrophic lateral sclerosis (ALS) remains unexplained. One potential pathogenetic mechanism is chronic toxicity due to disturbances of the glutamatergic neurotransmitter system, mediated via alpha-amino-3-hydroxy-5-methyl-4-isoxazole

Alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid-mediated excitotoxic axonal damage is attenuated in the absence of myelin proteolipid protein.

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In vivo and in vitro studies have shown that alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA)-receptor-mediated excitotoxicity causes cytoskeletal damage to axons. AMPA/kainate receptors are present on oligodendrocytes and myelin, but currently there is no evidence to suggest that

Isoflurane decreases AMPA-induced dark cell degeneration and edematous damage of Purkinje neurons in the rat cerebellar slices.

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This study was designed to investigate whether isoflurane, a commonly used volatile anesthetic with neuroprotective property, reduces alpha-amino-3-hydroxy-5-methyl-4-isoxazol propionic acid (AMPA)-induced neurotoxicity in a concentration- and time (when isoflurane was applied in relation to the

Inhibition of calpains, by treatment with leupeptin, improves motoneuron survival and muscle function in models of motoneuron degeneration.

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The effect of treatment with leupeptin, a calpain inhibitor, on motoneuron survival and muscle function was examined in in vitro and in vivo models of motoneuron degeneration. Exposure of primary rat motoneurons to alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid (AMPA) is an established in

Rasmussen's syndrome: intractable epilepsy and progressive neurological deterioration from a unilateral central nervous system.

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Rasmussen's syndrome (chronic encephalitis with epilepsy) is a rare neurological disorder of unknown cause characterized by severe epilepsy, hemiplegia, dementia, and inflammation of the brain, and progressive functional and structural destruction of a single cerebral hemisphere. While one mechanism

Long-term alterations in benzodiazepine, muscarinic and alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid (AMPA) receptor density following continuous cocaine administration.

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Animal models of clinical phenomena, such as stimulant-induced psychosis have focused primarily on persisting alterations that develop in brain after chronic stimulant administration. The present study utilized autoradiographic measures to examine changes in the density of benzodiazepine ([3H]

Efficacy of different triglycerides in total parenteral nutrition for preventing atrophy of the gut in traumatized rats.

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BACKGROUND The efficacy of different fat emulsions as components of a total parenteral nutrition (TPN) regimen on the integrity of the gut was assessed in traumatized rats. With the release of the short-chain fatty acids butyric or propionic acid during the hydrolysis of a structured triglyceride

Choline blocks AMPA-induced dark cell degeneration of Purkinje neurons: potential role of the alpha7 nicotinic receptor.

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The objective of the present study was to assess the contribution of sodium influx to development of dark cell degeneration (DCD) in Purkinje neurons (PNs) following AMPA (DL-amino-3-hydroxy-5-methyl-isoxazole-4-propionic acid) receptor activation. During the course of these experiments, we observed

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