No abstract

We show herein fabrication and field-modulated thermopower for KTaO 3 single-crystal based field-effect transistors (FETs). The KTaO 3 FET exhibits field effect mobility of ~8 cm 2 V -1 s -1 , which is ~4 times larger than that of SrTiO 3 FETs. The thermopower of the KTaO 3 FET decreased from 600 to 220 µVK −1 by the application of gate electric field up to 1.5 MVcm -1 , ~400 µVK −1 below that of an SrTiO 3 FET, clearly reflecting the smaller carrier effective mass of KTaO 3 .

Silodosin, a highly selective α1A-adrenoceptor antagonist, produces greater improvements in premature ejaculation profiles and related symptoms along with intravaginal ejaculation latency time in acquired premature ejaculation patients with or without erectile dysfunction. This result supports the clinical use of silodosin as an alternative treatment for premature ejaculation.

The influence of surface pit shape on 4H-SiC double implanted MOSFETs (DMOSFETs) reliability under a high temperature drain bias test has been investigated. Threading dislocations formed two types of pit shapes (deep pit and shallow pit) on an epitaxial layer surface. The cause of the failure was revealed to be an oxide breakdown above the pit generated at the threading mixed dislocation in both pit shapes. Weibull distributions between two types of pits were different. Although the DMOSFETs on the epitaxial layer with the deep pit show longer lifetime than those with the shallow pit, the epitaxial layer with the shallow pit is suitable to estimate the lifetime of the DMOSFETs because of a linearity of the Weibull plot. The lifetime of the DMOSFETs with the shallow pit was dominated by an oxide electric field. The maximum oxide electric field required to obtain the lifetime of more than 10 years was estimated to be 2.7 MV/cm.

The ectopic expression of the glucose-dependent insulinotropic polypeptide receptor (GIPR) in the human adrenal gland causes significant hypercortisolemia after ingestion of each meal and leads to Cushing’s syndrome, implying that human GIPR activation is capable of robustly activating adrenal glucocorticoid secretion. In this study, we transiently transfected the human GIPR expression vector into cultured human adrenocortical carcinoma cells (H295R) and treated them with GIP to examine the direct link between GIPR activation and steroidogenesis. Using quantitative RT-PCR assay, we examined gene expression of steroidogenic related proteins, and carried out immunofluorescence analysis to prove that forced GIPR overexpression directly promotes production of steroidogenic enzymes CYP17A1 and CYP21A2 at the single cell level. Immunofluorescence showed that the transfection efficiency of the GIPR gene in H295R cells was approximately 5%, and GIP stimulation enhanced CYP21A2 and CYP17A1 expression in GIPR-introduced H295R cells (H295R-GIPR). Interestingly, these steroidogenic enzymes were also expressed in the GIPR (–) cells adjacent to the GIPR (+) cells. The mRNA levels of a cholesterol transport protein required for all steroidogenesis, StAR, and steroidogenic enzymes, HSD3β2, CYP11A1, CYP21A2, and CYP17A1 increased 1.2-2.1-fold in GIP-stimulated H295R-GIPR cells. These changes were reflected in the culture medium in which 1.5-fold increase in the cortisol concentration was confirmed. Furthermore, the levels of adenocorticotropic hormone (ACTH) receptor and ACTH precursor proopiomelanocortin (POMC) mRNA were upregulated 2- and 1.5-fold, respectively. Immunofluorescence showed that ACTH expression was detected in GIP-stimulated H295R-GIPR cells. An ACTH-receptor antagonist significantly inhibited steroidogenic gene expression and cortisol production. Immunostaining for both CYP17A1 and CYP21A2 was attenuated in cells treated with ACTH receptor antagonists as well as with POMC siRNA. These results demonstrated that GIPR activation promoted production and release of ACTH, and that steroidogenesis is activated by endogenously secreted ACTH following GIP administration, at least in part, in H295R cells.