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71.
Properdin factor B and histocompatibility loci linked in the rhesus monkey.   总被引:1,自引:0,他引:1  
J B Ziegler  C A Alper  H Balner 《Nature》1975,254(5501):609-611
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7-day-cultured islets from pregnant Wistar rats released at 5.6 mM glucose significantly more insulin than islets from nonpregnant rats, whereas in vivo this heigthened glucose sensitivity is lost 48 h post partum.  相似文献   
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Summary It is suggested that insulin is capable of activating cerebral NaK-ATPase in a dose-dependent manner.Supported by grants from Ministerium für Hoch- und Fachschulwesen der DDR.  相似文献   
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This paper uses a meta‐analysis to survey existing factor forecast applications for output and inflation and assesses what causes large factor models to perform better or more poorly at forecasting than other models. Our results suggest that factor models tend to outperform small models, whereas factor forecasts are slightly worse than pooled forecasts. Factor models deliver better predictions for US variables than for UK variables, for US output than for euro‐area output and for euro‐area inflation than for US inflation. The size of the dataset from which factors are extracted positively affects the relative factor forecast performance, whereas pre‐selecting the variables included in the dataset did not improve factor forecasts in the past. Finally, the factor estimation technique may matter as well. Copyright © 2008 John Wiley & Sons, Ltd.  相似文献   
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The present study examined the effect of GLP-1(1-37) on chemokine-induced CD4-positive lymphocyte migration as an early and critical step in atherogenesis. Pretreatment with GLP-1(1-37) reduced the SDF-induced migration of isolated human CD4-positive lymphocytes in a concentration-dependent manner. Similar effects were seen when RANTES was used as a chemokine. GLP-1(1-37)’s effect on CD4-positive lymphocyte migration was mediated through an early inhibition of chemokine-induced PI-3 kinase activity. Downstream, GLP-1(1-37) inhibited SDF-induced phosphorylation of MLC and cofilin and limited f-actin formation as well as ICAM3 translocation. Furthermore, exendin-4 inhibited SDF-induced migration of CD4-positive lymphocytes similarly to GLP-1(1-37), and transfection of these cells with GLP-1 receptor siRNA abolished GLP-1(1-37)’s action on chemokine-induced ICAM3 translocation, suggesting an effect mediated via the GLP-1 receptor. Thus, GLP-1(1-37) inhibits chemokine-induced CD4-positive lymphocyte migration by inhibition of the PI3-kinase pathway and via the GLP-1 receptor. This effect provides a potential novel mechanism for how GLP-1(1-37) may modulate vascular disease.  相似文献   
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Derry LA  Kurtz AC  Ziegler K  Chadwick OA 《Nature》2005,433(7027):728-731
Silicon has a crucial role in many biogeochemical processes--for example, as a nutrient for marine and terrestrial biota, in buffering soil acidification and in the regulation of atmospheric carbon dioxide. Traditionally, silica fluxes to soil solutions and stream waters are thought to be controlled by the weathering and subsequent dissolution of silicate minerals. Rates of mineral dissolution can be enhanced by biological processes. But plants also take up considerable quantities of silica from soil solution, which is recycled into the soil from falling litter in a separate soil-plant silica cycle that can be significant in comparison with weathering input and hydrologic output. Here we analyse soil water in basaltic soils across the Hawaiian islands to assess the relative contributions of weathering and biogenic silica cycling by using the distinct signatures of the two processes in germanium/silicon ratios. Our data imply that most of the silica released to Hawaiian stream water has passed through the biogenic silica pool, whereas direct mineral-water reactions account for a smaller fraction of the stream silica flux. We expect that other systems exhibiting strong Si depletion of the mineral soils and/or high Si uptake rates by biomass will also have strong biological control on silica cycling and export.  相似文献   
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Genes and mechanisms involved in common complex diseases, such as the autoimmune disorders that affect approximately 5% of the population, remain obscure. Here we identify polymorphisms of the cytotoxic T lymphocyte antigen 4 gene (CTLA4)--which encodes a vital negative regulatory molecule of the immune system--as candidates for primary determinants of risk of the common autoimmune disorders Graves' disease, autoimmune hypothyroidism and type 1 diabetes. In humans, disease susceptibility was mapped to a non-coding 6.1 kb 3' region of CTLA4, the common allelic variation of which was correlated with lower messenger RNA levels of the soluble alternative splice form of CTLA4. In the mouse model of type 1 diabetes, susceptibility was also associated with variation in CTLA-4 gene splicing with reduced production of a splice form encoding a molecule lacking the CD80/CD86 ligand-binding domain. Genetic mapping of variants conferring a small disease risk can identify pathways in complex disorders, as exemplified by our discovery of inherited, quantitative alterations of CTLA4 contributing to autoimmune tissue destruction.  相似文献   
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