Nanoporous and single phase α-alumina membranes with pore diameters tunable over a wide range of approximately 60-350 nm were successfully fabricated by optimizing the conditions for anodizing, subsequent detachment, and heat treatment. The pore diameter increased and the cell diameter shrunk upon crystallization to α-alumina by approximately 20% and 3%, respectively, in accordance with the 23% volume shrinkage resulting from the change in density associated with the transformation from the amorphous state to α-alumina. Nevertheless, flat α-alumina membranes, each with a diameter of 25 mm and a thickness of 50 μm, were obtained without thermal deformation. The α-alumina membranes exhibited high chemical resistance in various concentrated acidic and alkaline solutions as well as when exposed to high temperature steam under pressure. The Young's modulus and hardness of the single phase α-alumina membranes formed by heat treatment at 1250 °C were notably decreased compared to the corresponding amorphous membranes, presumably because of the nodular crystallite structure of the cell walls and the substantial increase in porosity. Furthermore, when used for filtration, the α-alumina membrane exhibited a level of flux higher than that of the commercial ceramic membrane.
A deficient pancreatic β-cell mass increases the risk of type 2 diabetes mellitus. Here, we investigated the effects of testosterone on the development of pancreatic β-cell mass in male rats. The β-cell mass of male rats castrated at 6 wk of age was reduced to ~30% of that of control rats at 16 wk of age, and castration caused glucose intolerance. Loss of β-cell mass occurred because of decreases in islet density per pancreas and β-cell cluster size. Castration was negatively associated with the number of Ki-67-positive β-cells and positively associated with the number of TUNEL-positive β-cells. These β-cell changes could be prevented by testosterone treatment. In contrast, castration did not affect β-cell mass in male mice. Androgen receptor (AR) localized differently in mouse and rat β-cells. Testosterone enhanced the viability of INS-1 and INS-1 #6, which expresses high levels of AR, in rat β-cell lines. siRNA-mediated AR knockdown or AR antagonism with hydroxyflutamide attenuated this enhancement. Moreover, testosterone did not stimulate INS-1 β-cell viability under high d-glucose conditions. In INS-1 β-cells, d-glucose dose dependently (5.5-22.2 mM) downregulated AR protein levels both in the presence and absence of testosterone. The intracellular calcium chelator (BAPTA-AM) could prevent this decrease in AR expression. AR levels were also reduced by a calcium ionophore (A23187), but not by insulin, in the absence of the proteasome inhibitor MG132. Our results indicate that testosterone regulates β-cell mass, at least in part, by AR activation in the β-cells of male rats and that the β-cell AR is degraded under hyperglycemic conditions.
Androgen receptor (AR) is known to bind to the same cis-element that glucocorticoid receptor (GR) binds to. However, the effects of androgen signaling on glucocorticoid signaling have not yet been elucidated. Here, we investigated the effects of testosterone on dexamethasone (DEX, a synthetic glucocorticoid)-induced apoptosis of pancreatic β-cells, which might be involved in the pathogenesis of type 2 diabetes mellitus in males. We used INS-1 #6 cells, which were isolated from the INS-1 pancreatic β-cell line and which express high levels of AR. Testosterone and dihydrotestosterone inhibited apoptosis induced by DEX in INS-1 #6 cells. AR knockdown and the AR antagonist hydroxyflutamide each diminished the anti-apoptotic effects of testosterone. AR was localized in the nucleus of both INS-1 #6 cells and pancreatic β-cells of male rats. Induction of thioredoxin-interacting protein (TXNIP) is known to cause pro-apoptotic effects in β-cells. Testosterone suppressed the DEX-induced increase of TXNIP at the transcriptional level. A Chromatin immunoprecipitation assays showed that both AR and GR competitively bound to the TXNIP promoter in ligand-dependent manners. Recombinant DNA-binding domain of AR bound to the same cis-element of the TXNIP promoter that GR binds to. Our results show that AR and GR competitively bind to the same cis-element of TXNIP promoter as a silencer and enhancer, respectively. These results indicate that androgen signaling functionally competes with glucocorticoid signaling in pancreatic β-cell apoptosis.
The development of an oscillator controller for a quadruped robot with antagonistic pairs of pneumatic actuators is reported. Periodic motions of the legs switch between the swinging and supporting stages based on the phase of the oscillators. The oscillators receive touch sensor signals at the end of the legs as feedback when the leg touches the ground and compose a steady limit cycle of the total periodic dynamics of quadruped locomotion. And also muscle tone is adaptively controlled according to the dynamic state of the main body. This system can generate gait transition from one to another by changing locomotion speed and muscle tone. The effectiveness and performance of the proposed controller were evaluated with numerical simulations and experiments with the hardware.
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