QGP flow fluctuations and the characteristics of higher moments

The dynamical development of expanding Quark-gluon Plasma (QGP) flow is studied in a 3+1D fluid dynamical model with a globally symmetric, initial condition. We minimize fluctuations arising from complex dynamical processes at finite impact parameters and from fluctuating random initial conditions to have a conservative fluid dynamical background estimate for the statistical distributions of the thermodynamical parameters. We also avoid a phase transition in the equation of state, and we let the matter supercool during the expansion. Then central Pb+Pb collisions at $\sqrt{s_{NN}} = 2.76$ TeV are studied in an almost perfect fluid dynamical model, with azimuthally symmetric initial state generated in a dynamical flux-tube model. The general development of thermodynamical extensives are also shown for lower energies. We observe considerable deviations from a thermal equilibrium source as a consequence of the fluid dynamical expansion arising from a least fluctuating initial state

A922 Sequential measurement of 1 hour creatinine clearance (1-CRCL) in critically ill patients at risk of acute kidney injury (AKI)

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Quark Number Scaling in Fluid Dynamics and Hadronization via Quarkyonic Matter

NCQ scaling of elliptic flow is studied in a non-equilibrium hadronization and freeze-out model from ideal, deconfined and chirally symmetric Quark Gluon Plasma (QGP), to final non-interacting hadrons. In this transition the quarks gain constituent quark mass while the background Bag-field breaks up. The constituent quarks then recombine into simplified hadron states, while chemical, thermal and flow equilibrium break down. Then the resulting temperatures and flow velocities of baryons and mesons will be different. In a simplified model, we reproduce the constituent quark number scaling

Genetic identification of thiosulfate sulfurtransferase as an adipocyte-expressed antidiabetic target in mice selected for leanness

The discovery of genetic mechanisms for resistance to obesity and diabetes may illuminate new therapeutic strategies for the treatment of this global health challenge. We used the polygenic \u27lean\u27 mouse model, which has been selected for low adiposity over 60 generations, to identify mitochondrial thiosulfate sulfurtransferase (Tst; also known as rhodanese) as a candidate obesity-resistance gene with selectively increased expression in adipocytes. Elevated adipose Tst expression correlated with indices of metabolic health across diverse mouse strains. Transgenic overexpression of Tst in adipocytes protected mice from diet-induced obesity and insulin-resistant diabetes. Tst-deficient mice showed markedly exacerbated diabetes, whereas pharmacological activation of TST ameliorated diabetes in mice. Mechanistically, TST selectively augmented mitochondrial function combined with degradation of reactive oxygen species and sulfide. In humans, TST mRNA expression in adipose tissue correlated positively with insulin sensitivity in adipose tissue and negatively with fat mass. Thus, the genetic identification of Tst as a beneficial regulator of adipocyte mitochondrial function may have therapeutic significance for individuals with type 2 diabetes. Nat Med 2016 Jul; 22(7):771-9