A note on the application of the Prigogine theorem to rotation of tokamak-plasmas in absence of external torques.

Rotation of tokamak-plasmas, not at the mechanical equilibrium, is investigated using the Prigogine thermodynamic theorem. This theorem establishes that, for systems confined in rectangular boxes, the global motion of the system with barycentric velocity does not contribute to dissipation. This result, suitably applied to toroidally confined plasmas, suggests that the global barycentric rotations of the plasma, in the toroidal and poloidal directions, are pure reversible processes. In case of negligible viscosity and by supposing the validity of the balance equation for the internal forces, we show that the plasma, even not in the mechanical equilibrium, may freely rotate in the toroidal direction with an angular frequency, which may be higher than the neoclassical estimation. In addition, its toroidal rotation may cause the plasma to rotate globally in the poloidal direction at a speed faster than the expression found by the neoclassical theory. The eventual configuration is attained when the toroidal and poloidal angular frequencies reaches the values that minimize dissipation. The physical interpretation able to explain the reason why some layers of plasma may freely rotate in one direction while, at the same time, others may freely rotate in the opposite direction, is also provided. Invariance properties, herein studied, suggest that the dynamic phase equation might be of the second order in time. We then conclude that a deep and exhaustive study of the invariance properties of the dynamical and thermodynamic equations is the most correct and appropriate way for understanding the triggering mechanism leading to intrinsic plasma-rotation in toroidal magnetic configurations.

Family of probability distributions derived from maximal entropy principle with scale invariant restrictions.

Using statistical thermodynamics, we derive a general expression of the stationary probability distribution for thermodynamic systems driven out of equilibrium by several thermodynamic forces. The local equilibrium is defined by imposing the minimum entropy production and the maximum entropy principle under the scale invariance restrictions. The obtained probability distribution presents a singularity that has immediate physical interpretation in terms of the intermittency models. The derived reference probability distribution function is interpreted as time and ensemble average of the real physical one. A generic family of stochastic processes describing noise-driven intermittency, where the stationary density distribution coincides exactly with the one resulted from entropy maximization, is presented.

Soluble ST2 is regulated by p75 neurotrophin receptor and predicts mortality in diabetic patients with critical limb ischemia.

OBJECTIVE: The p75 neurotrophin receptor (p75(NTR)) contributes to diabetes mellitus-induced defective postischemic neovascularization. The interleukin-33 receptor ST2 is expressed as transmembrane (ST2L) and soluble (sST2) isoforms. Here, we studied the following: (1) the impact of p75(NTR) in the healing of ischemic and diabetic calf wounds; (2) the link between p75(NTR) and ST2; and (3) circulating sST2 levels in critical limb ischemia (CLI) patients. METHODS AND RESULTS: Diabetes mellitus was induced in p75(NTR) knockout (p75KO) mice and wild-type (WT) littermates by streptozotocin. Diabetic and nondiabetic p75KO and WT mice received left limb ischemia induction and a full-thickness wound on the ipsilateral calf. Diabetes mellitus impaired wound closure and angiogenesis and increased ST2 expression in WT, but not in p75KO wounds. In cultured endothelial cells, p75(NTR) promoted ST2 (both isoforms) expression through p38(MAPK)/activating transcription factor 2 pathway activation. Next, sST2 was measured in the serum of patients with CLI undergoing either revascularization or limb amputation and in the 2 nondiabetic groups (with CLI or nonischemic individuals). Serum sST2 increased in diabetic patients with CLI and was directly associated with higher mortality at 1 year from revascularization. CONCLUSIONS: p75(NTR) inhibits the healing of ischemic lower limb wounds in diabetes mellitus and promotes ST2 expression. Circulating sST2 predicts mortality in diabetic CLI patients.