Congenital hydrocephalus mimicking Dandy-Walker syndrome induced by 6-aminonicotinamide injection in pregnant rat.
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Fetal hydrocephalus was induced by single intraperitoneal injection of 8 mg/kg 6-aminonicotinamide (6-AN), a niacinamide antagonist, in Sprague-Dawley rat on day 13 of gestation. Materials for histological examination were obtained by uterotomy 1, 2, 4, and 8 days after injection, and untreated fetuses of the same ages were used as controls. Macrocephalus was clear at day 17 (4 days after injection), when cerebral dysgenesis was suggested by bromodeoxyuridine immunohistochemical study. The entire ventricular system was dilated, including the aqueduct and foramen of Monro, and hypoplasia of the cerebellum was also observed. On day 21, macrocephalus was remarkable, and considerable hypoplasia of the choroid plexus and cerebellum and agenesis of the corpus callosum were recognized. These results indicate that this experimental hydrocephalic model associated with various central nervous system anomalies mimics human Dandy-Walker syndrome, suggesting the pathogenesis of Dandy-Walker syndrome to be a feature of systemic metabolic deficits. (+info)
Phenotypic transformation of clonal myogenic cells to cells resembling chondrocytes.
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The nicotinamide analogue 6-aminonicotinamide and dibutyryl 3':5'-cAMP inhibit myogenesis in a clonal rat cell line from skeletal muscle. Both reagents produce a similar morphological response in the cells, and stimulate collagen and glycosaminoglycan synthesis. These data suggest that 6-aminonicotinamide and dibutyryl cAMP induce a phenotypic transformation of myogenic cells to cells that share many characteristics with chondrocytes. (+info)
A new strategy to improve the efficiency and sustainability of Candida parapsilosis catalyzing deracemization of (R,S)-1-phenyl-1,2-ethanediol under non-growing conditions: increase of NADPH availability.
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Microbial oxidoreductive systems have been widely used in asymmetric syntheses of optically active alcohols. However, when reused in multi-batch reaction, the catalytic efficiency and sustainability of non-growing cells usually decreased because of continuous consumption of required cofactors during the reaction process. A novel method for NADPH regeneration in cells was proposed by using pentose metabolism in microorganisms. Addition of D-xylose, L-arabinose, or D-ribose to the reaction significantly improved the conversion efficiency of deracemization of racemic 1-phenyl-1,2-ethanediol to (S)-isomer by Candida parapsilosis cells already used once, which afforded the product with high optical purity over 97%e.e. in high yield over 85% under an increased substrate concentration of 15 g/l. Compared with reactions without xylose, xylose added to multi-batch reactions had no influence on the activity of the enzyme catalyzing the key step in deracemization, but performed a promoting effect on the recovery of the metabolic activity of the non-growing cells with its consumption in each batch. The detection of activities of xylose reductase and xylitol dehydrogenase from cell-free extract of C. parapsilosis made xylose metabolism feasible in cells, and the depression of the pentose phosphate pathway inhibitor to this reaction further indicated that xylose facilitated the NADPH-required deracemization through the pentose phosphate pathway in C. parapsilosis. moreover, by investigating the cofactor pool, the xylose addition in reaction batches giving more NADPH, compared with those without xylose, suggested that the higher catalytic efficiency and sustainability of C. parapsilosis non-growing cells had resulted from xylose metabolism recycling NADPH for the deracemization. (+info)
Synergistic activation of glucose-6-phosphate dehydrogenase and NAD(P)H oxidase by Src kinase elevates superoxide in type 2 diabetic, Zucker fa/fa, rat liver.
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Reactive oxygen species-independent oxidation of thioredoxin in hypoxia: inactivation of ribonucleotide reductase and redox-mediated checkpoint control.
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Glucose is necessary for stabilization of hypoxia-inducible factor-1alpha under hypoxia: contribution of the pentose phosphate pathway to this stabilization.
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Dehydroepiandrosterone inhibits glucose flux through the pentose phosphate pathway in human and mouse endometrial stromal cells, preventing decidualization and implantation.
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