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d mannitol/atrophy
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5 results
A case of adult-onset type II citrullinemia--deterioration of clinical course after infusion of hyperosmotic and high sugar solutions.
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BACKGROUND
Adult-onset type II citrullinemia (CTLN2) is an autosomal recessive disorder caused by mutations of SLC25A13 gene encoding citrin and is characterized by recurrent encephalopathy with hyperammonemia. Factors affecting disease progression remain unknown. We report a case with CTLN2, whose
Generation of chemiluminescence in experimental autoimmune uveitis.
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Using experimental model of uveitis, the inflammation-associated chemiluminescence was measured by luminol amplification method. The induction of uveitis in Lewis rats was carried out by immunizing bovine S-antigen in complete Freund's adjuvant on hind foot-pad. The chemiluminescence activity from
A zinc-containing mannitol-2-dehydrogenase from Leuconostoc pseudomesenteroides ATCC 12291: purification of the enzyme and cloning of the gene.
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Mannitol-2-dehydrogenase (EC 1.1.1.67) of Leuconostoc pseudomesenteroides ATCC 12291 catalyzing the NADH-dependent reduction of d-fructose to d-mannitol was purified to homogeneity. Native mannitol-2-dehydrogenase has a molecular mass of 155 kDa as determined by gel filtration chromatography. In
Expression of apoptosis-regulatory genes in renal proximal tubular epithelial cells exposed to high ambient glucose and in diabetic kidneys.
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BACKGROUND
Members of the bcl-2 family of proteins regulate the occurrence of apoptotic cell death. Apoptosis is a feature of both acute and chronic renal diseases. Diabetes mellitus modulates renal growth; it induces acute tubuloepithelial cell hypertrophy, leads to chronic glomerulopathy
Dopamine- and L-beta-3,4-dihydroxyphenylalanine hydrochloride (L-Dopa)-induced cytotoxicity towards catecholaminergic neuroblastoma SH-SY5Y cells. Effects of oxidative stress and antioxidative factors.
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Enhanced oxidative stress has been suggested to be involved in the degeneration of nigrostriatal dopaminergic neurons in Parkinson's disease. The high turnover rate of dopamine and/or unsequestered dopamine may cause an increase of formation of hydrogen peroxide via either oxidative deamination of
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