358 resultados para AMK11A-1392


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Distributions of Mn, Fe, Cu, Cd, Cr, Co and Ni in sea water are investigated (42 samples, dissolved and particulate forms) in the vicinity of the underwater gas vent field on the northwestern slope of the Paramushir Island. While regular background distributions of the elements occur in the shore zone, there is a column of elevated concentrations of particulate matter, particulate Mn, and dissolved Mn, Fe, Cu, Cd, Cr, Co and Ni that coincides with location of the gas plume. This column can be traced as high as 780 m above the bottom. High metal concentrations in water of the plume are attributable to physico-chemical concentration at the phase interface; the source of elevated mineral concentrations is obviously flux of dissolved minerals from interstitial waters, which extends to considerable distances in vertical direction.

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Thesis (doctoral)--Friedrich-Wilhelms-Universitat zu Berlin.

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Objective: To compare proteins related to Alzheimer disease ( AD) in the frontal cortex and cerebellum of subjects with early-onset AD (EOAD) with or without presenilin 1 (PS1) mutations with sporadic late-onset AD ( LOAD) and nondemented control subjects. Methods: Immunohistochemistry, immunoblot analysis, and ELISA were used to detect and assess protein levels in brain. Results: In EOAD and to a lesser extent in LOAD, there was increased amyloid beta (Abeta) deposition (by immunohistochemistry), increased soluble Abeta (by immunoblot analysis), and specific increases in Abeta(40) and Abeta(42) ( by ELISA) in the frontal cortex and, in some cases, in the cerebellum. Surprisingly, immunoblot analysis revealed reduced levels of PS1 in many of the subjects with EOAD with or without PS1 mutations. In those PS1 mutation-bearing subjects with the highest Abeta, PS1 was barely, if at all, detectable. This decrease in PS1 was specific and not attributable solely to neuronal loss because amyloid precursor protein (APP) and the PS1-interacting protein beta-catenin levels were unchanged. Conclusions: This study shows that in the frontal cortex and cerebellum from Alzheimer disease patients harboring certain presenilin 1 mutations, high levels of amyloid beta are associated with low levels of presenilin 1. The study provides the premise for further investigation of mechanisms underlying the downregulation of presenilin 1, which may have considerable pathogenic and therapeutic relevance.