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Cold development of positive-tone resist ZEP520A (Nippon Zean) in electron-beam lithography needs quantitative analysis for further improvement in resolution. Contrast curves and groove widths in cold development of ZEP520A were analyzed using models, and resolution enhancement was confirmed experimentally. Although the contrast improved at the expense of sensitivity in cold development, the improvement of contrast became smaller when the development temperature became colder. The dependence of contrast curve on developing temperature can be explained assuming resist dissolution rates that have an activation energy. For resolution evaluation, circumferentially aligned line-and-space patterns were exposed using an electron-beam recorder with a rotary stage. The resolved groove widths were explained by using the resist dissolution model and an incident electron distribution that consists of three Gaussians. Using these models, groove widths after development can be easily calculated at arbitrary development and exposure conditions. The resolution improved in lower temperature, and dense line-and-space patterns of 35 nm pitch were resolved in -10 °C. [ABSTRACT FROM AUTHOR]

It is well-known that past knowledge affects color perception, as for example in the perception of familiar objects having richer colors. Although there have been many studies on human memory function with regard to color perception, it is not clear how color signals are treated in the early stages of human memory formation. Here, we tested whether in early memory color information is conserved without any interaction of other visual information. We found that performance of chromatic discrimination between a memorized color and a test color did not deteriorate under any contrast condition of dynamic luminance masking, and thus concluded that color signals were not disturbed by dynamic luminance signals. The results indicate that chromatic sensation per se is not modified at the early stages of the human memory system. © 2010 Wiley Periodicals, Inc. Col Res Appl, 2011 [ABSTRACT FROM AUTHOR]

Abstract: KCNQ1, located on 11p15.5, encodes a voltage-gated K+ channel with six transmembrane regions, and loss-of-function mutations in the KCNQ1 gene cause hereditary long QT syndrome. Recent genetic studies have identified that single nucleotide polymorphisms located in intron 15 of the KCNQ1 gene are strongly associated with type 2 diabetes and impaired insulin secretion. In order to understand the role of KCNQ1 in insulin secretion, we introduced KCNQ1 into the MIN6 mouse β-cell line using a retrovirus-mediated gene transfer system. In KCNQ1 transferred MIN6 cells, both the density of the KCNQ1 current and the density of the total K+ current were significantly increased. In addition, insulin secretion by glucose, pyruvate, or tolbutamide was significantly impaired by KCNQ1-overexpressing MIN6 cells. These results suggest that increased KCNQ1 protein expression limits insulin secretion from pancreatic β-cells by regulating the potassium channel current. [Copyright &y& Elsevier]

Insulin signaling is mediated via a network of protein phosphorylation. Dysregulation of this network is central to obesity, type 2 diabetes and metabolic syndrome. Here we investigate the role of phosphatase binding protein Alpha4 (α4) that is essential for the serine/threonine protein phosphatase 2A (PP2A) in insulin action/resistance in adipocytes. Unexpectedly, adipocyte-specific inactivation of α4 impairs insulin-induced Akt-mediated serine/threonine phosphorylation despite a decrease in the protein phosphatase 2A (PP2A) levels. Interestingly, loss of α4 also reduces insulin-induced insulin receptor tyrosine phosphorylation. This occurs through decreased association of α4 with Y-box protein 1, resulting in the enhancement of the tyrosine phosphatase protein tyrosine phosphatase 1B (PTP1B) expression. Moreover, adipocyte-specific knockout of α4 in male mice results in impaired adipogenesis and altered mitochondrial oxidation leading to increased inflammation, systemic insulin resistance, hepatosteatosis, islet hyperplasia, and impaired thermogenesis. Thus, the α4 /Y-box protein 1(YBX1)-mediated pathway of insulin receptor signaling is involved in maintaining insulin sensitivity, normal adipose tissue homeostasis and systemic metabolism., (© 2022. The Author(s).)

The present study investigated hemispheric symmetry of cortical functions, in terms of the chromatic motion mechanism. A series of experiments examined the visual sensitivities to chromatic and achromatic stimuli with or without motion, presented in either of the two (left or right) visual hemifields. Experiment 1 measured, individually, the subjective isoluminance of red/green stimuli for each visual field. Experiment 2 examined the visual field differences of the detection thresholds for static stimuli with the isoluminant color contrast and achromatic luminance contrast. Subsequent experiments measured contrast thresholds for motion detection (Experiment 3) and motion direction discrimination (Experiment 4) with both chromatic and achromatic stimuli. No visual field differences between thresholds were found in Experiments 1 and 2, whereas in Experiments 3 and 4, thresholds for the chromatic conditions were found to be lower in the left than in the right visual field, suggesting functional lateralization of the early motion mechanism with chromatic information in motion detection and direction discrimination., (Copyright © 2022 Elsevier Ltd. All rights reserved.)

Hepatocyte nuclear factor 1α (HNF1α) is a transcription factor required for normal insulin secretion and maintenance of β-cell number in the pancreas. HNF1α is also expressed in pancreatic α-cells, but its role in these cells is unknown. The aim of this study was to clarify the role of HNF1α in α-cells. Male Hnf1a+/- mice with a mixed background were backcrossed to outbred ICR mice. Glucose tolerance, glucagon and insulin secretion, islet histology, and gene expression were investigated in ICR Hnf1a-/- and Hnf1a+/+ mice. Regulation of Slc5a1 (encoding sodium glucose cotransporter 1 [SGLT1]) expression by HNF1α and the effect of SGLT1 inhibition on glucagon secretion were also explored. ICR Hnf1a-/- mice were glucose intolerant and exhibited impaired glucose-stimulated insulin secretion. The β-cell area of ICR mice was decreased in Hnf1a-/- mice, but the α-cell area in the pancreas was similar between Hnf1a-/- and Hnf1a+/+ mice. Hnf1a-/- mice showed higher fasting glucagon levels and exhibited inadequate suppression of glucagon after glucose load. In addition, glucagon release in response to hypoglycemia was impaired in Hnf1a-/- mice, and glucagon secretion after 1.1 mM glucose administration, was also decreased in Hnf1a-/- islets. Slc5a1 expression was decreased in Hnf1a-/- islets, while HNF1α activated the Slc5a1 promoter in αTC1-6 cells. Inhibition of SGLT1 suppressed 1.1 mM glucose-stimulated glucagon secretion in islets and αTC1-6 cells, but SGLT1 inhibition had no additional inhibitory effect in HNF1α-deficient cells. Our findings indicate that HNF1α modulates glucagon secretion in α-cells through the regulation of Slc5a1., Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interest or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Sirtuins are a family of evolutionally conserved nicotinamide adenine dinucleotide (NAD + )-dependent protein deacetylases/deacylases that regulate metabolism. The mammalian sirtuin family consists of seven sirtuins (SIRT1-7). Recent findings have identified critical roles for SIRT1 and SIRT7 in glucose/lipid metabolism in multiple tissues. This review focuses on the metabolic roles of these two sirtuins and the benefits of modulating the activity of sirtuins for the treatment of metabolic diseases such as type 2 diabetes., (© 2018 Elsevier Inc. All rights reserved.)

Nearly nine years ago, new mechanism that bone secretes a hormone called osteocalcin and regulates glucose/energy metabolism was discovered. To date the study of osteocalcin as the bone hormone was progressed well, and the new roles in various tissues, such as glucose metabolism, male fertility, and development of the brain, are demonstrated. On the other hand, signaling pathway of osteocalcin has not yet been fully understood, though its receptor was reported. This review focuses on the diverse roles of osteocalcin and also on the future task that should be solved.

Recently, we reported that insulin signaling in osteoblasts was a positive regulator of bone acquisition, but also of bone resorption. Interestingly, insulin signaling in osteoblasts activated osteocalcin embedded in bone ECM by stimulating resorption activity in osteoclast. It has been demonstrated that activated osteocalcin acts as hormone and regulates glucose metabolism through increasing insulin secretion from pancreas. The interaction of bone and glucose metabolism established by these studies will be important to a study of the two scientific fields in the future, particularly a clinical field.

It has been demonstrated that osteocalcin, osteoblast-derived molecule, regulates glucose/lipid metabolism through increasing insulin secretion from pancreas and insulin sensitivity in peripheral tissues. This finding established that bone is an important endocrine organ to regulate glucose/lipid metabolism. Recently, it has been reported that insulin signaling in osteoblasts was a positive regulator of bone acquisition, but also of bone resorption. Interestingly, insulin signaling in osteoblasts activated osteocalcin embedded in bone ECM by stimulating resorption activity in osteoclast. This finding indicated that the osteoblasts is an important target cells used by insulin which playing a central role in glucose/lipid metabolism. The bone/glucose metabolism interaction established by these studies will be important to a study of the two fields in the future, particularly a clinical field.

We previously demonstrated that tensile stress (TS)-induced osteoblast differentiation eventually led to osteogenesis in an organ culture of mouse calvarial sutures. In the present study, we employed RNA-fingerprinting using an arbitrarily primed polymerase chain reaction (RAP-PCR) to identify alpha-adaptin C, a component of the endocytosis machinery AP2, as a TS-inducible gene. Protein production, as well as the gene expression of alpha-adaptin C, was induced by TS as early as 3 h following the initiation of loading. In situ hybridization and immunohistochemical analysis revealed that the induction of alpha-adaptin C mostly occurred in fibroblastic cells in the sutures, suggesting that it precedes TS-induced osteoblast differentiation. Consistent with this result, TS significantly increased the number of coated pits (CPs) and coated vesicles (CVs) in the undifferentiated fibroblastic cells but not in the osteoblastic cells around calvarial bones. Further, TS-induced osteoblast differentiation was suppressed when endocytosis was inhibited by potassium depletion. These results, taken together, suggest that TS accelerates osteoblast differentiation and osteogenesis, possibly through the induction of the alpha-adaptin C expression and consequent activation of receptor-mediated endocytosis., (Copyright 2003 Wiley-Liss, Inc.)