Transient RF self-bias in electropositive and electronegative plasmas

The transient self-biasing of surfaces has been modelled to extend the utility of an isolated probe technique. The biasing is effected by the arrival of electrons drawn from the adjacent plasma but proceeds at a rate determined by the positive ion flux. Electron temperature and ion flux can be extracted from the initial stages of transient biasing. The model has been used to interpret data from a helicon plasma in argon.Shorter transients occur within the period of applied radio frequency (RF). Sheath reversal occurs during the initial stages of RF bias when the RF amplitude exceeds the normal DC floating potential. Very large RF bias signals, even after the primary transient phase, can reverse the sign of potential across the space charge sheath briefly during the cycle. The onset of this stage is mass dependent and may arise in hydrogen when the RF amplitude is only 47 times the electron temperature.The development of self-bias is also modelled for an electronegative plasma. Here, sheath reversal sets in at lower RF amplitude and the self-bias takes longer to establish than in equivalent electropositive plasmas. The model has been applied to data from a helicon plasma in sulphur hexafluoride, leading to a quantification of its electronegativity

The sheath criterion for a collisional plasma sheath at the presence of external magnetic field

The Bohm sheath criterion is modified for collisional plasma containing Boltzmann electrons and cold fluid ions at the presence of external magnetic field. Based on fluid model, the effects of the strength and the orientation of an external magnetic field on the upper and lower limits of Bohm sheath criterion have been studied by considering the collision frequency between ions and neutrals. The results show that the sheath criterion depends on the orientation and magnitude of magnetic field and the ion flow velocity at the sheath boundary

Thermoneutral housing exacerbates nonalcoholic fatty liver disease in mice and allows for sex-independent disease modeling.

Nonalcoholic fatty liver disease (NAFLD), a common prelude to cirrhosis and hepatocellular carcinoma, is the most common chronic liver disease worldwide. Defining the molecular mechanisms underlying the pathogenesis of NAFLD has been hampered by a lack of animal models that closely recapitulate the severe end of the disease spectrum in humans, including bridging hepatic fibrosis. Here we demonstrate that a novel experimental model employing thermoneutral housing, as opposed to standard housing, resulted in lower stress-driven production of corticosterone, augmented mouse proinflammatory immune responses and markedly exacerbated high-fat diet (HFD)-induced NAFLD pathogenesis. Disease exacerbation at thermoneutrality was conserved across multiple mouse strains and was associated with augmented intestinal permeability, an altered microbiome and activation of inflammatory pathways that are associated with the disease in humans. Depletion of Gram-negative microbiota, hematopoietic cell deletion of Toll-like receptor 4 (TLR4) and inactivation of the IL-17 axis resulted in altered immune responsiveness and protection from thermoneutral-housing-driven NAFLD amplification. Finally, female mice, typically resistant to HFD-induced obesity and NAFLD, develop full disease characteristics at thermoneutrality. Thus, thermoneutral housing provides a sex-independent model of exacerbated NAFLD in mice and represents a novel approach for interrogation of the cellular and molecular mechanisms underlying disease pathogenesis