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Anomalous Kink Effect in Low Dimensional Gate-Recessed Fully Depleted SOI MOSFET at Low Temperature
Avi Karsenty,Avraham Chelly 성균관대학교(자연과학캠퍼스) 성균나노과학기술원 2015 NANO Vol.10 No.7
Nanoscale MOSFETs Gate-Recessed Channel (GRC) device with a silicon channel thickness (tSI) as low as 2.2 nm was first tested at room temperature for functionality check, and then tested at low temperature (77 K) for I–V characterizations. In spite of its FD-SOI nanoscale thickness, the GRC device has surprisingly exhibited a Kink Effect in the output characteristics at 77 K. The anomalous Kink Effect can be explained by the increase of the lateral electric field in the drain junction with the channel extension zone when lowering the temperature.
Functional role of serotonin in insulin secretion in a diet-induced insulin-resistant state.
Kim, Kyuho,Oh, Chang-Myung,Ohara-Imaizumi, Mica,Park, Sangkyu,Namkung, Jun,Yadav, Vijay K,Tamarina, Natalia A,Roe, Michael W,Philipson, Louis H,Karsenty, Gerard,Nagamatsu, Shinya,German, Michael S,Kim The Endocrine Society 2015 Endocrinology Vol.156 No.2
<P>The physiological role of serotonin, or 5-hydroxytryptamine (5-HT), in pancreatic β-cell function was previously elucidated using a pregnant mouse model. During pregnancy, 5-HT increases β-cell proliferation and glucose-stimulated insulin secretion (GSIS) through the Gαq-coupled 5-HT2b receptor (Htr2b) and the 5-HT3 receptor (Htr3), a ligand-gated cation channel, respectively. However, the role of 5-HT in β-cell function in an insulin-resistant state has yet to be elucidated. Here, we characterized the metabolic phenotypes of β-cell-specific Htr2b(-/-) (Htr2b βKO), Htr3a(-/-) (Htr3a knock-out [KO]), and β-cell-specific tryptophan hydroxylase 1 (Tph1)(-/-) (Tph1 βKO) mice on a high-fat diet (HFD). Htr2b βKO, Htr3a KO, and Tph1 βKO mice exhibited normal glucose tolerance on a standard chow diet. After 6 weeks on an HFD, beginning at 4 weeks of age, both Htr3a KO and Tph1 βKO mice developed glucose intolerance, but Htr2b βKO mice remained normoglycemic. Pancreas perfusion assays revealed defective first-phase insulin secretion in Htr3a KO mice. GSIS was impaired in islets isolated from HFD-fed Htr3a KO and Tph1 βKO mice, and 5-HT treatment improved insulin secretion from Tph1 βKO islets but not from Htr3a KO islets. Tph1 and Htr3a gene expression in pancreatic islets was not affected by an HFD, and immunostaining could not detect 5-HT in pancreatic islets from mice fed an HFD. Taken together, these results demonstrate that basal 5-HT levels in β-cells play a role in GSIS through Htr3, which becomes more evident in a diet-induced insulin-resistant state.</P>