Copper isotope evidence for sulfide fractionation and lower crustal foundering in making continental crust.

The continental crust is strongly depleted in copper compared with its building blocks-primary arc magmas-and this depletion is intrinsically associated with continental crust formation. However, the process by which Cu removal occurs remains enigmatic. Here we show, using Cu isotopes, that subduction-zone processes and mantle melting produce limited fractionation of Cu isotopes in arc magmas, and, instead, the heterogeneous Cu isotopic compositions of lower crustal rocks, which negatively correlate with Cu contents, suggest segregation or accumulation of isotopically light sulfides during intracrustal differentiation of arc magmas.

Dominance of felsic continental crust on Earth after 3 billion years ago is recorded by vanadium isotopes.

The transition from mafic to felsic upper continental crust (UCC) is crucial to habitability of Earth, and may be related to the onset of plate tectonics. Thus, defining when this crustal transition occurred has great significance for the evolution of Earth and its inhabitants. We demonstrate that V isotope ratios (reported as δV) provide insights into this transition because they correlate positively with SiO and negatively with MgO contents during igneous differentiation in both subduction zones and intraplate settings.

Complement Inhibitors in Clinical Trials for Glomerular Diseases.

Defective complement action is a cause of several human glomerular diseases including atypical hemolytic uremic syndrome (aHUS), anti-neutrophil cytoplasmic antibody mediated vasculitis (ANCA), C3 glomerulopathy, IgA nephropathy, immune complex membranoproliferative glomerulonephritis, ischemic reperfusion injury, lupus nephritis, membranous nephropathy, and chronic transplant mediated glomerulopathy. Here we summarize ongoing clinical trials of complement inhibitors in nine glomerular diseases and show which inhibitors are used in trials for these renal disorders (http://clinicaltrials.gov).

FHR5 Binds to Laminins, Uses Separate C3b and Surface-Binding Sites, and Activates Complement on Malondialdehyde-Acetaldehyde Surfaces.

Factor H related-protein 5 (CFHR5) is a surface-acting complement activator and variations in the CFHR5 gene are linked to CFHR glomerulonephritis. In this study, we show that FHR5 binds to laminin-521, the major constituent of the glomerular basement membrane, and to mesangial laminin-211. Furthermore, we identify malondialdehyde-acetaldehyde (MAA) epitopes, which are exposed on the surface of human necrotic cells (), as new FHR5 ligands.