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scrapie/затлъстяване
Линкът е запазен в клипборда
Страница 1 от 23 резултата
Analysis of host genetic control of scrapie-induced obesity.
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The potential for induction of obesity during the preclinical phase of scrapie disease in mice was previously shown to be a function of both the strain of scrapie and the strain of inbred mouse. In the present study, host control of obesity induction by a scrapie strain was examined to determine if
Analysis of the incubation periods, induction of obesity and histopathological changes in senescence-prone and senescence-resistant mice infected with various scrapie strains.
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The similarity in histopathological changes seen in scrapie-infected mice and in an uninfected senescence-accelerated mouse strain led to a study in which the mouse strain that is prone to senescence (SAMP8), a strain that is resistant to senescence (SAMR1) and a progenitor strain (AKR) of these two
Quantitative immunogold study of glucose transporter (GLUT-1) in five brain regions of scrapie-infected mice showing obesity and reduced glucose tolerance.
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Distribution of glucose transporter (GLUT-1) in the microvascular endothelium of scrapie-infected SJL/J hyperglycemic mice showing clinical signs of scrapie, obesity and reduced glucose tolerance was studied in five brain regions: cerebral cortex, hippocampus, thalamus, cerebellum and olfactory
Scrapie-induced obesity in mice.
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Immunogold study of altered expression of some interendothelial junctional molecules in the brain blood microvessels of diabetic scrapie-infected mice.
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Quantitative immunogold procedure was used to study the distribution of molecular components of interendothelial junctions in blood-brain barrier (BBB) microvessels of scrapie infected SJL/J hyperglycemic mice showing obesity and reduced glucose tolerance. Samples of brain (fronto-parietal cerebral
Hyperplasia and hypertrophy of B cells in the islets of Langerhans in hamsters infected with the 139H strain of scrapie.
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Previous studies showed that in hamsters the 139H, but not the 263K, scrapie strain caused a marked increase in pancreatic size and led to obesity, hypoglycaemia and striking hyperinsulinaemia. In the preceding paper (Ye et al., 1994), the islets of Langerhans in 139H-affected hamsters showed
Contribution of pathogens in human obesity.
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Obesity is increasing rapidly in the United States as well as in other countries. The World Health Organization considers obesity a worldwide epidemic that poses a major public health threat. In humans, obesity causes or exacerbates a number of other diseases and co-morbidities. Etiology of obesity
[Can obesity be infectious?].
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Currently the presence of obesity is increasing and it has become the basic civilisation illness of our times. Up to date no attention has been paid to the possibility of etiology of infectious obesity. Recently some publications have appeared whose authors suggest a possibility of an infectious
The pathological changes in peripheral organs of scrapie-infected animals.
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Scrapie is an unconventional neurodegenerative disease in sheep and goats that has been known in Europe for over 260 Years. The scrapie agents affect the brain and are transmissible from animal to animal. Key features of scrapie infections are abnormal behavior and deficits in motor function. These
Scrapie strains retain their distinctive characteristics following passages of homogenates from different brain regions and spleen.
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The molecular basis of differences among scrapie strains is unknown. The prion theory posits that there are differences in the conformation of the host protease-resistant protein (PrP) molecules and that these differences are responsible for scrapie strains. A corollary of this theory is that the
Histopathological changes in the islets of Langerhans in scrapie 139H-affected hamsters.
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Previous studies showed that the 139H strain of scrapie injected into hamsters caused obesity, a marked hypertrophy of the islets of Langerhans, generalized endocrinopathy and marked hypoglycaemia-hyperinsulinaemia. In the current study, female weanling Syrian hamsters (LVG/LAK strain) were
Abnormal periodic acid-Schiff (PAS)-positive substance in the islets of Langerhans, pituitaries and adrenal glands of 139H scrapie-infected hamsters.
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Previous studies showed that the 139H strain of scrapie injected intra-cerebrally in hamsters caused obesity, and extensive histopathological changes in islets of Langerhans and pituitaries. In the current study, we report that an abnormal granular substance, which stained positively with periodic
The 139H scrapie agent produces hypothalamic neurotoxicity and pancreatic islet histopathology: electron microscopic studies.
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Neuronal degeneration, along with astrocytosis, spongiform vacuolation, and amyloid (PrPSc) formation, have long been regarded as neuropathological hallmarks of transmissible spongiform encephalopathies (TSEs). In animals, these diseases include; scrapie, transmissible mink encephalopathy, chronic
Isolation of two distinct prion strains from a scrapie-affected sheep.
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We performed a transmission study using mice to clarify the characteristics of the most recent case of scrapie in Japan. The mice that were inoculated with the brain homogenate from a scrapie-affected sheep developed progressive neurological disease, and one of the scrapie-affected mice showed
Scrapie-induced alterations in glucose tolerance in mice.
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Certain scrapie strains cause obesity in several strains of mice. The potential association between obesity and altered glucose tolerance was assessed by monitoring body weight and glucose tolerance throughout the incubation period in scrapie strain-mouse strain combinations that do and do not
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