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sorbitol/atrofia

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Role of sorbitol-mediated cellular stress response in obesity-associated retinal degeneration.

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Obesity is a global health problem associated with several diseases including ocular complications. Earlier we reported progressive retinal degeneration because of obesity in a spontaneous obese rat (WNIN/Ob) model. In the current study, we examined the molecular mechanisms leading to

Nerve glucose, fructose, sorbitol, myo-inositol, and fiber degeneration and regeneration in diabetic neuropathy.

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We measured the alcohol sugars in sural nerves from 11 controls, 21 conventionally treated patients with diabetes and neuropathy, and 4 diabetics without neuropathy. The results were related to metabolic control and to clinical, neuropathological, and morphometric abnormalities in the nerves. The

Modelling cortical cataractogenesis: 1. In vitro effects of glucose, sorbitol and fructose on intact rat lenses in medium 199.

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After 2 days, lenses with intact capsules from adults rats remained clear when incubated in medium 199 with a normal glucose concentration but showed opacities when the level of glucose was increased up to 10 times normal. Scanning electron microscopy of the fixed lenses demonstrate globular

Reversible lactic acidosis associated with repeated intravenous infusions of sorbitol and ethanol.

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Infusions of fructose or sorbitol are used commonly in parenteral nutrition and may cause lactic acidosis. A case is reported in whom blood lactate concentration was monitored frequently over a 5-day period during intravenous feeding with a sorbitol-ethanol-amino acid mixture. During the first five

Mechanism of testicular atrophy induced by di-n-butyl phthalate in rats. Part 2. The effects on some testicular enzymes.

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A single oral dose of di-n-butyl phthalate (DBP) to male rats caused histologically a sloughing of the germ cells at 6 h. On Days 1 and 2 more severe sloughing was seen, followed by atrophy and the dissociation of the germ cells from the Sertoli cells and the spermatogonia. Biochemically, there was

Alpha-lipoic acid: effect on glucose uptake, sorbitol pathway, and energy metabolism in experimental diabetic neuropathy.

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The peripheral nerve of experimental diabetic neuropathy (EDN) is reported to be ischemic and hypoxic, with an increased dependence on anaerobic metabolism, requiring increased energy substrate stores. When glucose stores become reduced, fiber degeneration has been reported. We evaluated glucose

The sorbitol shunt in the retina and the optic nerve of mice with inherited and STZ-induced diabetes.

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Micromethods designed for studying the sorbitol shunt permitted studies of the retina and the optic nerve from mice. A significant accumulation of sorbitol was found in the retina of 5-months-old obese-hyper-glycaemic and severely STZ diabetic mice. The latter mice also showed increased sorbitol
A DNA fragment of approximately 1500 bp, harbouring the sorbitol transport gene (srlT), was amplified from the chromosomal DNA of Erwinia herbicola ATCC 21998 by PCR and cloned in Escherichia coli JM109. Degenerate oligonucleotide primers used were designed based on the conserved regions in the gene

Rapid determination of functional liver plasma flow in ICU patients by a modified hepatic D-sorbitol plasma clearance method.

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Changes in liver perfusion may have a substantial influence on the pharmacokinetics of drugs with flow-controlled metabolism. This may have important implications for drug dosage in patients in an intensive care unit (ICU). The hepatic D-sorbitol plasma clearance has been suggested as a non-invasive

Testicular atrophy induced by di(2-ethylhexyl)phthalate: changes in histology, cell specific enzyme activities and zinc concentrations in rat testis.

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Daily administration of 2g/kg/day di(2-ethylhexyl)phthalate (DEHP) to immature rats was found to cause testicular atrophy and reduce zinc concentration. Specific activities of testicular enzymes associated with postmeiotic spermatogenic cells, such as lactate dehydrogenase isozyme-X, hyaluronidase
OBJECTIVE Sorbitol and myo-inositol levels and morphology of sural nerve were compared with nerve function and clinical neuropathy in men with diabetic, impaired (IGT), and normal glucose tolerance. METHODS After neurography of sural nerve and determinations of sensory thresholds for vibration, warm

Increased sorbitol levels in the hypertrophic ligamentum flavum of diabetic patients with lumbar spinal canal stenosis.

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The pathomechanism of the ligamentum flavum (LF) hypertrophy in diabetic patients with lumbar spinal canal stenosis (LSCS) remains unclear. A cross-sectional study was undertaken to investigate the mechanism of LF hypertrophy in these patients. Twenty-four diabetic and 20 normoglycemic patients with

Sorbitol in the accessory glands of the diabetic male rat.

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Diabetes was induced in rats by i.v. injection of streptozotocin (60 mg/kg body weight). Diabetes was accompanied by infertility and atrophy of the male accessory glands. Blood glucose rose above 500 mg% (post-prandial) and blood testosterone decreased to 14% of the level found in normoglycemic

Degenerate PCR method for identification of an antiapoptotic gene in BHV-1.

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To investigate on the hypothetical presence of an antiapoptotic gene, we utilized the CODEHOP (COnsensus-DEgenerate Hybrid Oligonucleotide Primers) strategy amplifying unknown sequences from a background of genomic (bovine herpesvirus type-1) BHV-1 DNA. An alignment of carboxyl-terminal domains
BACKGROUND Charcot-Marie-Tooth type 1A disease (CMT1A) is a rare orphan inherited neuropathy caused by an autosomal dominant duplication of a gene encoding for the structural myelin protein PMP22, which induces abnormal Schwann cell differentiation and dysmyelination, eventually leading to axonal
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