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Geometry effects in confined space
In this paper we calculate some exact solutions of the grand partition
functions for quantum gases in confined space, such as ideal gases in two- and
three-dimensional boxes, in tubes, in annular containers, on the lateral
surface of cylinders, and photon gases in three-dimensional boxes. Based on
these exact solutions, which, of course, contain the complete information about
the system, we discuss the geometry effect which is neglected in the
calculation with the thermodynamic limit , and analyze the
validity of the quantum statistical method which can be used to calculate the
geometry effect on ideal quantum gases confined in two-dimensional irregular
containers. We also calculate the grand partition function for phonon gases in
confined space. Finally, we discuss the geometry effects in realistic systems.Comment: Revtex,15 pages, no figur
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Recovery from acidosis is a robust trigger for loss of force in murine hypokalemic periodic paralysis.
Periodic paralysis is an ion channelopathy of skeletal muscle in which recurrent episodes of weakness or paralysis are caused by sustained depolarization of the resting potential and thus reduction of fiber excitability. Episodes are often triggered by environmental stresses, such as changes in extracellular K+, cooling, or exercise. Rest after vigorous exercise is the most common trigger for weakness in periodic paralysis, but the mechanism is unknown. Here, we use knock-in mutant mouse models of hypokalemic periodic paralysis (HypoKPP; NaV1.4-R669H or CaV1.1-R528H) and hyperkalemic periodic paralysis (HyperKPP; NaV1.4-M1592V) to investigate whether the coupling between pH and susceptibility to loss of muscle force is a possible contributor to exercise-induced weakness. In both mouse models, acidosis (pH 6.7 in 25% CO2) is mildly protective, but a return to pH 7.4 (5% CO2) unexpectedly elicits a robust loss of force in HypoKPP but not HyperKPP muscle. Prolonged exposure to low pH (tens of minutes) is required to cause susceptibility to post-acidosis loss of force, and the force decrement can be prevented by maneuvers that impede Cl- entry. Based on these data, we propose a mechanism for post-acidosis loss of force wherein the reduced Cl- conductance in acidosis leads to a slow accumulation of myoplasmic Cl- A rapid recovery of both pH and Cl- conductance, in the context of increased [Cl]in/[Cl]out, favors the anomalously depolarized state of the bistable resting potential in HypoKPP muscle, which reduces fiber excitability. This mechanism is consistent with the delayed onset of exercise-induced weakness that occurs with rest after vigorous activity
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