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Vapor compression cycles are not an established technology for microgravity applications yet. One reason for the low technology readiness level in microgravity is the concern of liquid flooding from the evaporator, which could reduce the lifetime of the compressor. Liquid refrigerant can accumulate in the evaporator while the cycle is turned off and slug into the suction line upon the next compressor start-up. This paper describes experiments on parabolic flights, which investigated this issue. A test stand was designed to observe liquid flooding from the evaporator upon compressor start-up. The time from compressor start-up until flooding first occurred and the duration of flooding were recorded and used as quantifiers. They showed that the occurrence of liquid flooding is mainly a function of the refrigerant mass in the evaporator before start-up and that there is a mass threshold below which flooding does not occur. Test were conducted with an off the shelf and one similarly sized transparent evaporator. The hypothesis that the threshold would be significantly smaller in microgravity was not confirmed with the data collected on the parabolic flights. Instead, flooding typically occurred at the same charge level for both evaporators and both testing environments. Flow visualizations showed that mostly stratified flow during start-up in ground testing became mostly annular flow in microgravity. Both flow regimes keep liquid close to the wall so that vapor generated during the start-up process can escape through a void tunnel. [ABSTRACT FROM AUTHOR]

Leptin, a hormone that regulates appetite and energy expenditure, is increased in obese individuals, although these individuals often exhibit leptin resistance. Obesity is characterized by sleep/wake disturbances, such as excessive daytime sleepiness, increased REM sleep, increased nighttime arousals, and decreased percentage of total sleep time. Several studies have shown that short sleep duration is highly correlated with decreased leptin levels in both animal and human models. Arousal and rapid eye movement (REM) sleep are regulated by the cholinergic arm of the reticular activating system, the pedunculopontine nucleus (PPN). The goal of this project was to determine the role of leptin in the PPN, and thus in obesity-related sleep disorders. Whole-cell patch-clamp recordings were conducted on PPN neurons in 9- to 17-day-old rat brainstem slices. Leptin decreased action potential (AP) amplitude, AP frequency, and h-current ( I). These findings suggest that leptin causes a blockade of Na channels. Therefore, we conducted an experiment to test the effects of leptin on Na conductance. To determine the average voltage dependence of this conductance, results from each cell were equally weighted by expressing conductance as a fraction of the maximum conductance in each cell. I amplitude was decreased in a dose-dependent manner, suggesting a direct effect of leptin on these channels. The average decrease in Na conductance by leptin was ~40 %. We hypothesize that leptin normally decreases activity in the PPN by reducing I and I currents, and that in states of leptin dysregulation (i.e., leptin resistance) this effect may be blunted, therefore causing increased arousal and REM sleep drive, and ultimately leading to sleep-related disorders. [ABSTRACT FROM AUTHOR]