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Bladzijde 1 van 257 resultaten
Galactose and its Metabolites Deteriorate Metaphase II Mouse Oocyte Quality and Subsequent Embryo Development by Disrupting the Spindle Structure.
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Premature ovarian insufficiency (POI) is a frequent long-term complication of classic galactosemia. The majority of women with this disorder develop POI, however rare spontaneous pregnancies have been reported. Here, we evaluate the effect of D-galactose and its metabolites, galactitol and galactose
Age-dependent retinal capillary pericyte degeneration in galactose-fed dogs.
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The galactose-fed beagle develops diabetes-like microvascular changes that are histologically and clinically similar in appearance to all stages of human diabetic retinopathy. This animal model is extremely useful for evaluating drugs for the treatment of diabetic retinopathy; however, the time
Selective pericyte degeneration in the retinal capillaries of galactose-fed dogs results from apoptosis linked to aldose reductase-catalyzed galactitol accumulation.
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Galactose-fed dogs develop retinal capillary changes similar to diabetic retinopathy with pericyte degeneration as the initial lesion. This is followed by the formation of microaneurysms, hemorrhages, and some areas of acellularity. To investigate the mechanisms for selective pericyte degeneration,
Hepatic functional deterioration after portacaval shunt in the rat. Effects on sulfobromophthalein transport-maximum, indocyanine green clearance and galactose elimination capacity.
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The consequences of a portacaval shunt on liver function were studied in male Sprague-Dawley rats. Fourteen days after an end-to-side portacaval anastomosis the galactose elimination capacity and the plasma clearance of indocyanine green were reduced in proportion to the approximately 50% loss in
Analysis of the deterioration rates of liver function in cirrhosis, based on galactose elimination capacity.
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The prognosis of cirrhotic patients may depend on their liver function, but very few data are available to predict life expectancy in individual subjects on the basis of their liver function tests. The yearly changes in liver function, based on galactose elimination capacity (GEC), were
D-galactose-induced aging does not cause further deterioration in brain pathologies and cognitive decline in the obese condition
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Largely as a consequence of changes in modern lifestyle, a significant proportion of global population have become obese. When obese people grow old, pathologies aggravate neurodegeneration. Several studies have demonstrated that both aging and obesity have deleterious impact on brain. However, the
Axonal caliber and neurofilaments are proportionately decreased in galactose neuropathy.
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Feeding galactose to rats induces nerve conduction abnormalities, increased levels of nerve galactitol, endoneurial edema, elevated pressure and hypoxia of endoneurial fluid, and pathological abnormalities of nerve fibers. To investigate the cellular mechanisms of the fiber lesions and their
Schwann cell changes and demyelination in chronic galactose neuropathy.
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Dystrophic changes of Schwann cells and demyelination occurred in rats with chronic nerve edema induced by feeding a galactose-rich diet for two years. The mechanism for edema is the sorbitol pathway which generates osmotically active polyols from galactose or glucose. The blood-nerve barrier
Impairments of tight junctions are involved in D-galactose-induced brain aging.
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Impairments of tight junctions are implicated in the course of various age-related neurodegenerative disorders. Chronic injection of D-galactose can cause a progressive deterioration in learning and memory capacity and serve as an animal model of aging. To investigate the involvement of tight
Effect of sodium iodate injection on the development of galactose cataract in the rat.
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The effect of sodium iodate injection on the development of galactose cataract in the rat was investigated clinically and biochemically. Galactose cataracts were induced in animals which had been injected with a single dose of sodium iodate and compared with those given a saline injection. The
Chronic systemic injection of D-galactose impairs the septohippocampal cholinergic system in rats.
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Accumulated evidence indicates chronic systemic injection of D-galactose mimics aging progress induced by oxidative stress. We addressed whether memory impairment in this model was associated with the cholinergic septohippocampal degeneration. Rats injected with D-galactose for 6 weeks showed
The cloning and sequencing of the UDP-galactose 4-epimerase gene (galE) from Avibacterium paragallinarum.
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The putative uridine diphosphate (UDP)-galactose 4-epimerase encoding gene, galE, was isolated from Avibacterium paragallinarum with the use of degenerate primers, colony hybridization and inverse PCR. The data revealed an open reading frame of 1017 bp encoding a protein of 338 amino acids with a
Preventive effects of taurine against d-galactose-induced cognitive dysfunction and brain damage.
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Oxidative stress arising from life processes or environmental influences and its resultant cellular dysfunctions are major causes of neurodegenerative disorders. The objectives of this study were to investigate whether taurine (Tau) can prevent d-galactose-induced cognitive dysfunction and brain
The Effects of Light and Moderate Intensity Exercise on the Femoral Bone and Cerebellum of d-Galactose-Exposed Rats.
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Aging causes the degeneration of organs of the locomotor system, including the cerebellum and bones. Exercise may reverse this deterioration. d-galactose has been frequently used in rodents to accelerate aging. The present study aimed at investigating the effects of exercise on cerebellar and serum
Kinetin inhibits apoptosis of aging spleen cells induced by D-galactose in rats.
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Kinetin (Kn) is a cytokinin growth factor that exerts several anti-aging and antioxidant effects on cells and organs. To investigate the mechanism underlying apoptotic events in aging cells induced by D-galactose (D-gal), we examined the effect of Kn delivered via nuchal subcutaneous injection on
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