Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the immunocytochemical distribution of the prion or proteinase-resistant protein (PrP) during the evolution of experimental Creutzfeldt-Jakob disease (CJD) in mice. Fifty-one brains were collected up to 22 weeks following intracerebral inoculation with the Fujisaki strain of the CJD agent. Slides were also immunostained for apolipoprotein E (apoE) and glial fibrillary acidic protein. Vacuolar changes with focal astrocytosis first occurred around the needle track at week 2 and later spread along white matter tracks. Until week 12, changes were asymmetrical, affecting more the side of inoculation. Spongiform change and astrogliosis spread subsequently to the gray matter. Time course and intensity of spongiform change and immunocytochemistry for PrP were discrepant: in most brain regions, severe vacuolation preceded immunocytochemically detectable PrP accumulation. PrP deposits in form of small dots were first detectable at week 6 in the area surrounding the needle track. After week 7, plaque-like amorphous PrP deposits were observed in white matter pathways. Finally, PrP was detectable also in basal ganglia and in the dorsal hippocampus (week 13) and in the neocortex (week 17), as the synaptic type of PrP immunopositivity. In the hippocampus, diffuse PrP deposits paralleled spongiform change, while in the cortex severe vacuolation was accompanied only by weak synaptic PrP deposits. Immunocytochemically detectable apoE was restricted to compact plaque-type PrP deposits after week 15. We conclude that disease-specific neuropathology spreads from the needle track along white matter pathways towards the gray matter; in this model, there is some discrepancy between development of tissue pathology and immunocytochemically detectable deposition of PrP. Immunocytochemically detectable apoE deposition follows PrP accumulation.
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PMID:Deposition of the prion protein (PrP) during the evolution of experimental Creutzfeldt-Jakob disease. 1060 35

Entrapment of lipoprotein particles in the extracellular matrix of the arterial intima is a characteristic feature of the development of atherosclerosis, the disease behind myocardial infarction and stroke. In this study, sugars were exploited in the separation of lipoproteins by CE. Monosaccharides, disaccharides and one sugar alcohol used during ultracentrifugal isolation of lipoproteins prevented the strong and unfavorable adsorption of lipoprotein particles on the capillary wall, allowing their selective separation in uncoated fused silica capillary. The effect of ionic strength of the phosphate BGE solution on the separation at physiological pH was clarified. Asymmetrical flow field-flow fractionation and dynamic light scattering showed that sugars affected the structure of lipoproteins by decreasing their sizes. Although in molecular dynamics simulations, only a 19 amino acid peptide of apolipoprotein B-100 and a 15 amino acid peptide of apolipoprotein E were employed, the results also indicated a decrease in lipoprotein size, supporting the asymmetrical flow field-flow fractionation and dynamic light scattering results.
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PMID:Sugar treatment of human lipoprotein particles and their separation by capillary electrophoresis. 2060 41