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Previous studies have offered multiple explanations for the causality of color preference but no consensus has been reached. In this study, we propose an alternative explanation that the memory colors of familiar objects, especially food colors of humans can induce color preferences. We conducted two experiments. In Experiment 1, the memory color experiment, we asked participants to rate the similarity between presented color samples and memory colors of five familiar fruits and vegetables in Japan; we then calculated the location of the colors in the CIELAB color space that looked most similar to the remembered objects using the bivariate Gaussian function. In Experiment 2, the color preference experiment, color variations were created based on the memory colors obtained from Experiment 1. A different group of participants rated their preference for each color variation, then we applied regression analysis to these ratings. We observed two types of regressions between preference ratings and distance to memory colors: (1) for colors from red to green that represent the food colors for primates, color preference increased when the color was closer to the memory colors of the fruits and vegetables found in Experiment 1; and (2) for blue and purple colors, colors were preferred when they became bluer. We suggest that the evolutionarily acquired mechanism of color preference derives crucial cues from our ecological environment. Therefore, the mechanism produces the same color preference trend among people who grow up in similar environments, for example, environments containing the same fruits. [ABSTRACT FROM AUTHOR]

Sirtuins (SIRT1–7 in mammals) are a family of NAD+-dependent lysine deacetylases and deacylases that regulate diverse biological processes, including metabolism, stress responses, and aging. SIRT7 is the least well-studied member of the sirtuins, but accumulating evidence has shown that SIRT7 plays critical roles in the regulation of glucose and lipid metabolism by modulating many target proteins in white adipose tissue, brown adipose tissue, and liver tissue. This review focuses on the emerging roles of SIRT7 in glucose and lipid metabolism in comparison with SIRT1 and SIRT6. We also discuss the possible implications of SIRT7 inhibition in the treatment of metabolic diseases such as type 2 diabetes and obesity. [ABSTRACT FROM AUTHOR]

Hypoxia can occur in pancreatic β‐cells in type 2 diabetes. Although hypoxia exerts deleterious effects on β‐cell function, the associated mechanisms are largely unknown. Here, we show that the transcriptional repressor basic helix–loop–helix family member e40 (BHLHE40) is highly induced in hypoxic mouse and human β‐cells and suppresses insulin secretion. Conversely, BHLHE40 deficiency in hypoxic MIN6 cells or β‐cells of ob/ob mice reverses defects in insulin secretion. Mechanistically, BHLHE40 represses the expression of Mafa, encoding the transcription factor musculoaponeurotic fibrosarcoma oncogene family A (MAFA), by attenuating the binding of pancreas/duodenum homeobox protein 1 (PDX1) to its enhancer region. Impaired insulin secretion in hypoxic β‐cells was recovered by MAFA re‐expression. Collectively, our work identifies BHLHE40 as a key hypoxia‐induced transcriptional repressor in β‐cells that inhibit insulin secretion by suppressing MAFA expression. Synopsis: Hypoxia inhibits insulin secretion in pancreatic β‐cells, but the associated mechanism is unclear. This study shows that hypoxia induces the expression of the transcriptional repressor BHLHE40 in β‐cells and that BHLHE40 inhibits insulin secretion through transcriptional repression of Mafa. Hypoxia induces the expression of BHLHE40 in pancreatic β‐cells.BHLHE40 inhibits insulin secretion in pancreatic β‐cells in vitro and in vivo.BHLHE40 represses Mafa transcription by inhibiting PDX1 binding to the enhancer. [ABSTRACT FROM AUTHOR]

The recent demonstration that osteoblasts have a role in controlling energy metabolism suggests that they express cell-specific regulatory genes involved in this process. Activating transcription factor 4 (ATF4) is a transcription factor that accumulates predominandy in osteoblasts, where it regulates virtually all functions linked to the maintenance of bone mass. Since [Atf4.sup.[-/-]] mice have smaller fat pads than littermate controls, we investigated whether ATF4 also influences energy metabolism. Here, we have shown, through analysis of [Atf4.sup.[-/-]] mice, that ATF4 inhibits insulin secretion and decreases insulin sensitivity in liver, fat, and muscle. Several lines of evidence indicated that this function of ATF4 occurred through its osteoblastic expression. First, insulin sensitivity is enhanced in the liver of [Atf4.sup.[-/-]] mice, but not in cultured hepatocytes from these mice. Second, mice overexpressing ATF4 in osteoblasts only [termed here αl(I)Collagen-Atf4 mice] displayed a decrease in insulin secretion and were insulin insensitive. Third, the αl(I)Collagen-Atf4 transgene corrected the energy metabolism phenotype of [Atf4.sup.[-/-]] mice. Fourth, and more definitely, mice lacking ATF4 only in osteoblasts presented the same metabolic abnormalities as [Atf4.sup.[-/-]] mice. Molecularly, ATF4 favored expression in osteoblasts of Esp, which encodes a product that decreases the bioactivity of osteocalcin, an osteoblast-specific secreted molecule that enhances secretion of and sensitivity to insulin. These results provide a transcriptional basis to the observation that osteoblasts fulfill endocrine functions and identify ATF4 as a regulator of most functions of osteoblasts., Introduction The transcriptional control of osteoblast differentiation and function involves many players, some broadly expressed and others with a more restricted expression (1). At least 3 of these transcription factors [...]

Alzheimer's disease (AD) is an age-related neurodegenerative disease that is characterized by irreversible memory loss and cognitive decline. The deposition of amyloid-β (Aβ), especially aggregation-prone Aβ42, is considered to be an early event preceding neurodegeneration in AD. Sirtuins (SIRT1–7 in mammals) are nicotinamide adenine dinucleotide-dependent lysine deacetylases/deacylases, and several sirtuins play important roles in AD. However, the involvement of SIRT7 in AD pathogenesis is not known. Here, we demonstrate that SIRT7 mRNA expression is increased in the cortex, entorhinal cortex, and prefrontal cortex of AD patients. We also found that Aβ42 treatment rapidly increased NADPH oxidase 4 (NOX4) expression at the post-transcriptional level, and induced reactive oxygen species (ROS) production and apoptosis in neuronal SH-SY5Y cells. In contrast, SIRT7 knockdown inhibited Aβ42-induced ROS production and apoptosis by suppressing the upregulation of NOX4. Collectively, these findings suggest that the inhibition of SIRT7 may play a beneficial role in AD pathogenesis through the regulation of ROS production. [ABSTRACT FROM AUTHOR]

An investigation of the effects of a prolonged handling task within the helmet-mounted display (HMD) environment on visual functions revealed sluggishness in version eye movement and accommodative response during the 40-minute task. Both functions were also worsened by delayed presentation of display after head movement. However, the sluggishness of responses was not significantly affected by delayed presentation after hand movement. These results indicate that decreasing time delay after head movement is important in enhancing performance of handling tasks within the HMD environment.

Abstract Background Chondromodulin-1 (ChM1), an endogenous anti-angiogenic factor expressed in cartilage, has been suggested to inhibit invasion of endothelial cells into cartilage. In addition, the ectopic administration of ChM1 has been reported to suppress tumorigenesis in vivo. However, it is unclear whether the anti-tumor effect is due to not only the anti-vascularization effect of ChM1, but also its direct action against oncocytes. In the present study, we sought to determine whether ChM1 has a direct action on tumor cells. Methods BrdU incorporation assay was performed on human umbilical vein endothelial cells (HUVECs), normal human dermal fibroblasts (NHDFs), HepG2 cells and HeLa cells in the presence or absence of recombinant human ChM1 (rhChM1). An adenovirus that expresses ChM1, Ad-ChM1, was established and applied to the tumor xenografted in vivo, and to in vitro tumor cells cultured on plates or in soft agar. Cell cycle-related proteins and the phosphorylation of Erk, Akt, and GSK3β, the downstream molecules of the extracellular matrix-integrin signaling pathways, in HepG2 cells treated with or without Ad-ChM1 were detected by western blot analysis. Luciferase reporter assays of STAT, GAS, and ISRE, which participate in another cytokine signaling pathway, ware performed in HepG2, HeLa, and HUVEC cells. Results ChM1 suppressed BrdU incorporation in HUVECs and in HepG2 cells dose-dependently, but did not suppress BrdU incorporation in NHDFs and HeLa cells cultured on plates. In soft agar, however, ChM1 suppressed the growth of HeLa cells, as well as HepG2 cells. Western blot analyses demonstrated that ChM1 decreased the levels of cyclin D1, cyclin D3, and cdk6 and increased those of p21cip1 without affecting the phosphorylation levels of Erk, Akt, and GSK3β in HepG2 cells. The luciferase reporter assay demonstrated that ChM1 suppressed the transcriptional activities of STAT and GAS but not of ISRE. Conclusion ChM1 directly suppressed the proliferation of tumor cells in an anchorage-independent manner. However, ChM1 did not alter the phosphorylation of downstream molecules, at which the signaling pathways through growth factor and cytokine receptors converge with the anchorage-dependent pathway. Our results show that ChM1 has a direct anti-tumor effect; moreover, this effect occurs by inhibiting the STAT signaling pathway.

Deterministic lateral displacement (DLD) based microfluidic devices have been developed for capturing circulating tumor cells (CTCs) from the peripheral blood. There was frequent and problematic channel clogging around the micro-post array formed on a microchannel of the device. In this study, various agents were dispersed into the blood specimen to avoid clogging. At first, platelet aggregation was considered to be the cause of the clogging, but even plasmin, which was assumed to decompose platelet aggregations, did not show obvious inhibition of the clogging. Then, enzymes used for cell detachment from tissue were examined and decomposition of the clogging residue was observed. Finally, dispersion of deoxyribonuclease into a blood specimen was found to be effective for the inhibition of clogging. The existence of DNA in the clogging residue was also confirmed by propidium iodide (PI) staining, suggesting DNA adhering to the micro-post. [ABSTRACT FROM AUTHOR]