Saint Louis University

About: Saint Louis University is a education organization based out in St Louis, Missouri, United States. It is known for research contribution in the topics: Population & Poison control. The organization has 18927 authors who have published 34895 publications receiving 1267475 citations. The organization is also known as: SLU & St. Louis University.

IL-1 produced and released endogenously within human islets inhibits beta cell function.

Abstract: Resident macrophages have been suggested to participate in the initiation of beta cell damage during the development of autoimmune diabetes. The purpose of this study was to determine if the endogenous production and release of interleukin 1 (IL-1) in human islets of Langerhans by resident macrophages results in the inhibition of beta cell function. Treatment of human islets with a combination of tumor necrosis factor (TNF) + lipopolysaccharide (LPS) + interferon-gamma (IFN-gamma) stimulates inducible nitric oxide synthase (iNOS) expression, nitric oxide production, and inhibits glucose-stimulated insulin secretion. The IL-1 receptor antagonist protein (IRAP) prevents TNF + LPS + IFN-gamma-induced iNOS expression and nitrite production, and attenuates the inhibitory effects on glucose-stimulated insulin secretion by human islets. Inhibition of iNOS activity by aminoguanidine also attenuates TNF + LPS + IFN-gamma-induced inhibition of insulin secretion by human islets. These results indicate that the inhibitory effects of TNF + LPS + IFN-gamma are mediated by nitric oxide, produced by the actions of IL-1 released endogenously within human islets. Reverse transcriptase polymerase chain reaction was used to confirm that TNF + LPS + IFN-gamma stimulates the expression of both IL-1alpha and IL-1beta in human islets. Two forms of evidence indicate that resident macrophages are the human islet cellular source of IL-1: culture conditions that deplete islet lymphoid cells prevent TNF + LPS + IFN-gamma-induced iNOS expression, nitric oxide production, and IL-1 mRNA expression by human islets; and IL-1 and the macrophage surface marker CD69 colocalize in human islets treated with TNF + LPS + IFN-gamma as determined by immunohistochemical analysis. Lastly, nitric oxide production is not required for TNF + LPS + IFN-gamma-induced IL-1 release in human islets. However, cellular damage stimulates IL-1 release by islet macrophages. These findings support the hypothesis that activated islet macrophages may mediate beta cell damage during the development of insulin-dependent diabetes by releasing IL-1 in human islets followed by cytokine-induced iNOS expression by beta cells.

Geochemistry of Neoarchean (ca. 2.55–2.50 Ga) volcanic and ophiolitic rocks in the Wutaishan greenstone belt, central orogenic belt, North China craton: Implications for geodynamic setting and continental growth

Abstract: Geological investigation of the Neoarchean (2.55–2.50 Ga) Wutaishan greenstone belt in the central orogenic belt of the North China craton has provided new information on the geodynamic origin of this belt and its mineral deposits. Structural, geochronological, and geochemical characteristics of the Wutaishan greenstone belt suggest that it formed in a forearc tectonic environment at ca. 2.55 Ga and accreted to the Eastern continental block at ca. 2.50 Ga. A ridge subduction model is proposed to explain several unique geological features of the Wutaishan greenstone belt, such as the generation of dunites and chromitite-hosting harzburgites with U-shaped rare earth element (REE) patterns, formation of volcanogenic massive sulphides (VMS) and banded iron formations (BIF), extrusion of mafic to felsic volcanic rocks, and intrusion of tonalite-trondhjemite-granodiorite plutons (TTG). Anomalously high geothermal gradients in the subarc mantle-wedge beneath the Wutaishan forearc may have increased its buoyancy, resulting in its accretion to the continental crust. We propose that ridge subduction also played an important role in the growth of Archean continental crust. In this model, the origin of Archean TTG is genetically linked to eclogites through partial melting of accreted and/or underplated oceanic plateaus and normal oceanic crust under amphibolite to eclogite metamorphic conditions by upwelling of an anomalously hot asthenospheric mantle window resulting from ridge subduction. TTG suites intruding Archean accretionary complexes formed the nuclei of intra-oceanic island arcs; subsequent juxtaposition of these arcs resulted in the lateral growth of Archean continental crust.