Vitamin D receptor (VDR), a nuclear receptor that regulates calcium homeostasis, has been found to function as a receptor for secondary bile acids. Because the in vivo role of VDR in bile acid metabolism remains unknown, we investigated the effect of VDR activation in a mouse model of cholestasis. We treated mice with 1␣-hydroxyvitamin D 3 [1␣(OH)D 3 ] after bile duct ligation (BDL) and examined mRNA expression and cytokine levels. 1␣(OH)D 3 treatment altered the expression of genes involved in bile acid synthesis and transport in the liver, kidney, and intestine but did not decrease bile acid levels in the plasma and liver of BDL mice. 1␣(OH)D 3 treatment suppressed mRNA expression of proinflammatory cytokines in the liver and strongly decreased the plasma levels of proinflammatory cytokines in BDL mice. These findings indicate that 1␣(OH)D 3 regulates a network of bile acid metabolic genes and represses proinflammatory cytokine expression in BDL mice. VDR ligands have the potential to prevent the cholestasis-induced inflammatory response.

We have investigated photoinduced spectral changes of excitons in inorganic-organic layered semiconductors, ͑C 6 H 5 C 2 H 4 NH 3 ͒ 2 PbI 4 ͑PhE-PbI 4 ͒ and ͑C 6 H 13 NH 3 ͒ 2 PbI 4 ͑C6-PbI 4 ͒, by means of the subpicosecond pump-probe spectroscopy. The two semiconductors consist of the same inorganic layers and different organic layers. In the two substances, the blueshift and the bleaching of the exciton are observed. It is found that both of the blueshift and the bleaching are considerably stronger in C6-PbI 4 than in PhE-PbI 4 . The weight of the blueshift relative to the bleaching is larger in PhE-PbI 4 than in C6-PbI 4 . These differences are qualitatively explained in terms of the stronger dielectric confinement in C6-PbI 4 than in PhE-PbI 4 due to the lower dielectric constant of the organic layers in C6-PbI 4 than in PhE-PbI 4 . Delay time dependences of the blueshift and the bleaching and their polarization dependences are understood as being due to the exciton relaxation in the angular momentum space with rates of 2.7 and 4.1 ps −1 for PhE-PbI 4 and C6-PbI 4 , respectively.

We demonstrate a high-efficiency solar-thermophotovoltaic system (STPV) using a monolithic, planar, and spectrally selective absorber/emitter. A complete STPV system using gallium antimonide (GaSb) cells was designed and fabricated to conduct power generation tests. To produce a high-efficiency STPV, it is important to match the thermal radiation spectrum with the sensitive region of the GaSb cells. Therefore, to reach high temperatures with low incident power, a planar absorber/emitter is incorporated for controlling the thermal radiation spectrum. This multilayer coating consists of thin-film tungsten sandwiched by yttria-stabilized zirconia. The system efficiency is estimated to be 16% when accounting for the optical properties of the fabricated absorber/emitter. Power generation tests using a high-concentration solar simulator show that the absorber/emitter temperature peaks at 1640 K with an incident power density of 45 W∕cm 2 , which can be easily obtained by low-cost optics such as Fresnel lenses. The conversion efficiency became 23%, exceeding the Shockley-Queisser limit for GaSb, with a bandgap of 0.67 eV. Furthermore, a total system efficiency of 8% was obtained with the view factor between the emitter and the cell assumed to be 1.

A high-efficiency solar thermophotovoltaic (STPV) system has been demonstrated using spectrally selective planar absorber/emitter systems and a GaSb TPV cell. In this study, a novel approach for designing the STPV system based on the efficiency of unidirectional radiative heat transfer has been introduced. To achieve high extraction and photovoltaic conversion efficiencies, the spectrally selective absorber/emitter based on a coherent perfect absorber composed of a thin molybdenum layer sandwiched between hafnium layers was applied. The extraction efficiency was further investigated with respect to the absorber/emitter area ratio. The experimental efficiency of STPV reached 5.1% with the area ratio of 2.3.

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Infants with transient neonatal hypothyroidism, in whom TSH binding inhibitor immunoglobulin G (IgG) (TBII) were sequentially measured, are described. Their mother had been taking thyroid replacement for hypothyroidism due to nongoitrous autoimmune thyroiditis. IgGs inhibiting TSH binding were detected in maternal sera by radioreceptor assay. These IgGs also inhibited the adenylate cyclase response to TSH in human thyroid membranes. Three infants had frank hypothyroidism immediately after birth, and TBII were detected in two of them. In the two surviving infants, hypothyroidism was transient and improved when TBII disappeared from their sera. The profile of TBII in one patient corresponded to the IgG disappearance curve. These findings suggest that the transient neonatal hypothyroidism reported was caused by transplacental transfer of TBII.