431 research outputs found

    Prevention of drowsy driving by means of warning sound

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    Traffic accidents occur due to inattentive driving such as drowsy driving. A variety of support systems that make an attempt to prevent inattentive driving are under development. The development of a system to prevent drowsy driving using auditory or tactile alarm system is undertaken. It is essential to detect the low arousal state and warn drivers of such a state so that drowsy can be prevented. EEG (Electroencephalography) was used to evaluate how an arousal level degraded with time for eight participants under a low arousal level. Mean power frequency (MPF) was calculated to evaluate an arousal level. The value of MPF was compared between high and low arousal levels. The difference of arousal effect among four warning sounds was examined. As a result, there was no significant difference of arousal effect among four alarm sounds. The alarm sound was found to temporarily heighten participants' arousal level

    FGF21 as an Endocrine Regulator in Lipid Metabolism: From Molecular Evolution to Physiology and Pathophysiology

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    The FGF family comprises twenty-two structurally related proteins with functions in development and metabolism. The Fgf21 gene was generated early in vertebrate evolution. FGF21 acts as an endocrine regulator in lipid metabolism. Hepatic Fgf21 expression is markedly induced in mice by fasting or a ketogenic diet. Experiments with Fgf21 transgenic mice and cultured cells indicate that FGF21 exerts pharmacological effects on glucose and lipid metabolism in hepatocytes and adipocytes via cell surface FGF receptors. However, experiments with Fgf21 knockout mice indicate that FGF21 inhibits lipolysis in adipocytes during fasting and attenuates torpor induced by a ketogenic diet but maybe not a physiological regulator for these hepatic functions. These findings suggest the pharmacological effects to be distinct from the physiological roles. Serum FGF21 levels are increased in patients with metabolic diseases having insulin resistance, indicating that FGF21 is a metabolic regulator and a biomarker for these diseases

    Conferring the ability to utilize inorganic polyphosphate on ATP-specific NAD kinase

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    ATP特異性の獲得メカニズムの解明 : 新薬と新しい物質生産系の開発に期待. 京都大学プレスリリース. 2013-09-11.NAD kinase (NADK) is a crucial enzyme for production of NADP(+). ATP-specific NADK prefers ATP to inorganic polyphosphate [poly(P)] as a phosphoryl donor, whereas poly(P)/ATP-NADK utilizes both ATP and poly(P), and is employed in industrial mass production of NADP(+). Poly(P)/ATP-NADKs are distributed throughout Gram-positive bacteria and Archaea, whereas ATP-specific NADKs are found in Gram-negative α- and γ-proteobacteria and eukaryotes. In this study, we succeeded in conferring the ability to utilize poly(P) on γ-proteobacterial ATP-specific NADKs through a single amino-acid substitution; the substituted amino-acid residue is therefore important in determining the phosphoryl-donor specificity of γ-proteobacterial NADKs. We also demonstrate that a poly(P)/ATP-NADK created through this method is suitable for the poly(P)-dependent mass production of NADP(+). Moreover, based on our results, we provide insight into the evolution of bacterial NADKs, in particular, how NADKs evolved from poly(P)/ATP-NADKs into ATP-specific NADKs

    1α,25-Dihydroxyvitamin D3 enhances cerebral clearance of human amyloid-β peptide(1-40) from mouse brain across the blood-brain barrier

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    <p>Abstract</p> <p>Background</p> <p>Cerebrovascular dysfunction has been considered to cause impairment of cerebral amyloid-β peptide (Aβ) clearance across the blood-brain barrier (BBB). Further, low levels of vitamin D are associated with increased risk of Alzheimer's disease, as well as vascular dysfunction. The purpose of the present study was to investigate the effect of 1α,25-dihydroxyvitamin D<sub>3 </sub>(1,25(OH)<sub>2</sub>D3), an active form of vitamin D, on cerebral Aβ clearance from mouse brain.</p> <p>Methods</p> <p>The elimination of [<sup>125</sup>I]hAβ(1-40) from mouse brain was examined by using the Brain Efflux Index method to determine the remaining amount of [<sup>125</sup>I]hAβ(1-40) radioactivity after injection into the cerebral cortex. [<sup>125</sup>I]hAβ(1-40) internalization was analyzed using conditionally immortalized mouse brain capillary endothelial cells (TM-BBB4).</p> <p>Results</p> <p>Twenty-four hours after intraperitoneal injection of 1,25(OH)<sub>2</sub>D3 (1 μg/mouse), [<sup>125</sup>I]hAβ(1-40) elimination from mouse brain was increased 1.3-fold, and the level of endogenous Aβ(1-40) in mouse brain was reduced. These effects were observed at 24 h after i.p. injection of 1,25(OH)<sub>2</sub>D3, while no significant effect was observed at 48 or 72 h. Vitamin D receptor (VDR) mRNA was detected in mouse brain capillaries, suggesting that 1,25(OH)<sub>2</sub>D3 has a VDR-mediated genomic action. Furthermore, forskolin, which activates mitogen-activated protein kinase kinase (MEK), enhanced [<sup>125</sup>I]hAβ(1-40) elimination from mouse brain. Forskolin also enhanced [<sup>125</sup>I]hAβ(1-40) internalization in TM-BBB4 cells, and this enhancement was inhibited by a MEK inhibitor, suggesting involvement of non-genomic action.</p> <p>Conclusions</p> <p>The active form of vitamin D, 1,25(OH)<sub>2</sub>D3, appears to enhance brain-to-blood Aβ(1-40) efflux transport at the BBB through both genomic and non-genomic actions. Compounds activating these pathways may be candidate agents for modulating Aβ(1-40) elimination at the BBB.</p

    Variable Gain Type PID Control Using PSO for Ultrasonic Motor

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    Ultrasonic motor exhibits non-linearity that relates the input (Phase difference) and output (Velocity). It also causes serious characteristic changes during operation. PID control has been widely used as the design scheme for USM. However, it is difficult for the conventional PID control to compensate such characteristic changes of the plant and non-linearity. To overcome this problem, we propose a variable gain type PID control in which PID gains are optimized using a particle swarm optimization (PSO)
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