Trace elements and minerals in fumarolic sulfur: the case of Ebeko Volcano, Kuriles

Native sulfur deposits on fumarolic fields at Ebeko volcano (Northern Kuriles, Russia) are enriched in chalcophile elements (As-Sb-Se-Te-Hg-Cu) and contain rare heavy metal sulfides (Ag2S, HgS, and CuS), native metal alloys (Au2Pd), and some other low-solubility minerals (CaWO4, BaSO4). Sulfur incrustations are impregnated with numerous particles of fresh and altered andesite groundmass and phenocrysts (pyroxene, magnetite) as well as secondary minerals, such as opal, alunite, and abundant octahedral pyrite crystals. The comparison of elemental abundances in sulfur and unaltered rocks (andesite) demonstrated that rock-forming elements (Ca, K, Fe, Mn, and Ti) and other lithophile and chalcophile elements are mainly transported by fumarolic gas as aerosol particles, whereas semimetals (As, Sb, Se, and Te), halogens (Br and I), and Hg are likely transported as volatile species, even at temperatures slightly above 100°C. The presence of rare sulfides (Ag2S, CuS, and HgS) together with abundant FeS2 in low-temperature fumarolic environments can be explained by the hydrochloric leaching of rock particles followed by the precipitation of low-solubility sulfides induced by the reaction of acid solutions with H2S at ambient temperatures. The elemental composition of native sulfur can be used to qualitatively estimate elemental abundances in low-temperature fumarolic gases

Synergy between Piezo1 and Piezo2 channels confers high-strain mechanosensitivity to articular cartilage.

Diarthrodial joints are essential for load bearing and locomotion. Physiologically, articular cartilage sustains millions of cycles of mechanical loading. Chondrocytes, the cells in cartilage, regulate their metabolic activities in response to mechanical loading. Pathological mechanical stress can lead to maladaptive cellular responses and subsequent cartilage degeneration. We sought to deconstruct chondrocyte mechanotransduction by identifying mechanosensitive ion channels functioning at injurious levels of strain. We detected robust expression of the recently identified mechanosensitive channels, PIEZO1 and PIEZO2. Combined directed expression of Piezo1 and -2 sustained potentiated mechanically induced Ca(2+) signals and electrical currents compared with single-Piezo expression. In primary articular chondrocytes, mechanically evoked Ca(2+) transients produced by atomic force microscopy were inhibited by GsMTx4, a PIEZO-blocking peptide, and by Piezo1- or Piezo2-specific siRNA. We complemented the cellular approach with an explant-cartilage injury model. GsMTx4 reduced chondrocyte death after mechanical injury, suggesting a possible therapy for reducing cartilage injury and posttraumatic osteoarthritis by attenuating Piezo-mediated cartilage mechanotransduction of injurious strains