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This report documents evaluation of simultaneous estimation of multiple interfacial heat transfer coefficients (HTCs) using transient measurements from an experiment designed for steady-state operation. The design of a mirror system for directing X-rays under cryogenic conditions requires knowledge of the interfacialHTC (contact conductance) between silicon and indium. An experimental apparatus was constructed to measure temperatures in a stack of five 7.62-mm thick pucks of silicon separated by 0.1-mm thick sheets of indium, which is operated under cryogenic temperatures in vacuum. Multiple pucks and interfaces are incorporated into the apparatus to allow evaluation of HTCs for surfaces of different roughness from a single experiment. Analysis of the sensitivity of each of the measured temperatures to each of the unknown HTCs reveals lack of linear independence of these sensitivities and suggests the recovery of the HTCs will be challenging. Artificially noised "data" were created from two different computational models by solving for temperatures and adding random Gaussian noise with a specified standard deviation. These data are subsequently analyzed using two different iterative parameter estimation methods: a Levenberg scheme and a Tikhonov iterative scheme. The required sensitivity matrix is computed using forward finite difference approximations. The results for the heat transfer coefficients for this model problem suggest that coefficients cannot be estimated independently, but the ratios relative to one of the unknowns can be recovered. [ABSTRACT FROM AUTHOR]

Compelling evidence has demonstrated that estradiol and estrogen receptor α/β (ERα/β) play key roles in the central regulation of energy balance and glucose homeostasis. Our previous research showed that ERα in the medial amygdala (ERαMeA) mediates estrogenic actions to stimulate physical activity, therefore promotes energy expenditure and prevents diet-induced obesity (DIO). Interestingly, another estrogen receptor, ERβ, is also highly expressed in the MeA. To test the metabolic functions of ERβMeA, we generated a mouse model with ERβ selectively deleted in the MeA (ERβKOMeA) during adulthood using AAV virus-mediated Cre-Lox site-specific recombination. We found that, when fed on a high-fat diet but not on a normal chow diet, compared to the control mice, both male and female ERβKOMeA mice showed decreased body weight gain and fat deposition, which were associated with increased energy expenditure. We further showed that half of the ERαMeA neurons co-express ERβ. In these ERα&β co-expressing MeA neurons, ERα agonist propyl pyrazole trio (PPT) induced ERα-dependent depolarization, while ERβ agonist diarypropionitrile (DPN) induced ERβ-dependent hyperpolarization. Finally, we showed that chemogenetic activation of ERαMeA or ERβMeA neurons induces a similar increase in energy expenditure. Collectively, our results support a model that, estrogen acts on ERα/βMeA neurons to provide bidirectional regulation of body weight and resistance to DIO, whereas activating ERαMeA decreases and activating ERβMeA increases body weight. Disclosure: H. Ye: None. Y. He: None. L. Ibrahimi: None. S. Schaul: None. P. Luo: None. L. Carrillo-Sáenz: None. P. Lai: None. N. Patel: None. M. Kota: None. D. Dixit: None. P. Xu: None. Funding: National Institutes of Health (5R00DK107008-04) [ABSTRACT FROM AUTHOR]