Site-dependent Local Spin Susceptibility and Low-energy Excitation in a Weyl Semimetal WTe2_2

Site-dependent local spin susceptibility is investigated with $^{125}$Te nuclear magnetic resonance in a Weyl semimetal WTe$_2$. The nuclear spin-lattice relaxation rate $1/T_1T$ shows a dependence of the square of temperature $T$ at high temperatures, followed by a constant behavior below 50 K. The temperature dependence features Weyl fermions appearing around the linearly crossing bands. The Knight shift $K$ scales to the square root of $1/T_1T$, corroborating a predominant spin contribution in low-lying excitation. The observed dependence of $K$ and $1/T_1T$ on the four Te sites shows the site-dependent electron correlation and density of states. The angular profile of the NMR spectrum gives the anisotropic hyperfine coupling tensor, consistent with $5p$ hole occupations on Te sites.Comment: 6 pages, 5 figure

High-speed simulation of PCB emission and immunity with frequency-domain IC/LSI source models

Some recent results from research conducted in the EMC group at Okayama University are reviewed. A scheme for power-bus modeling with an analytical method is introduced. A linear macro-model for ICs/LSIs, called the LECCS model, has been developed for EMI and EMS simulation. This model has a very simple structure and is sufficiently accurate. Combining the LECCS model with analytical simulation techniques for power-bus resonance simulation provides a method for high-speed EMI simulation and decoupling evaluation related to PCB and LSI design. A useful explanation of the common-mode excitation mechanism, which utilizes the imbalance factor of a transmission line, is also presented. Some of the results were investigated by implementing prototypes of a high-speed EMI simulator, HISES. </p

90-kDa ribosomal S6 kinase 1 is inhibited by S-glutathionylation of its active-site cysteine residue during oxidative stress

AbstractPreviously, we reported that p90-RSK1 phosphorylates neuronal nitric oxide synthase (nNOS) at Ser847 in cells treated with mitogens, leading to the inhibition of NOS activity. Here, we show RSK1 Cys223 glutathionylation limits the activity of the enzyme following an oxidative stimulus and attenuates the nNOS phosphorylation. Treatment of RSK1 with diamide/glutathione results in inactivation of the enzyme in vitro. Mutagenesis studies confirmed that S-glutathionylation of Cys223 is both necessary and sufficient for this inhibition of RSK1. In transfected cells expressing RSK1 and nNOS, treatment with diamide caused a decrease in EGF-induced phosphorylation of nNOS at Ser847. Cells expressing mutant RSK1 (C223S) proved resistant in this regard. Thus, RSK1 Cys223 glutathionylation may contribute to regulate the levels of NO in the brain

Resource Upgrading in Advanced Supercritical Fluid (Supercritical Fluid with Catalyst and Cosolvent): Liquid Fuels from Biomass in Sub and Supercritical Water and Carbohydrate Up-Conversion in Ionic Liquid and Supercritical Fluids Mixtures

Liquid fuels from biomass and up-conversion of biomass in advanced supercritical fluid are reviewed in this chapter. Lignin can be converted into heavy hydrocarbons in subcritical water extraction. Lipid, which is triglyceride, is catalytically converted into straight-chain hydrocarbons of free fatty acid (decarboxylation) formed by hydrolysis. Carbohydrate is also hydrothermally converted into furan ring compound and fatty acids. Protein is converted into amino acids in hydrothermal water and depolymerization of protein is favored with rapid heating and denaturation agency such as alkaline earth metals. Free amino acids are further decomposed into carboxylic acid through deamination and into amine through decarboxylation. To inhibit Maillard reactions, which result in polymerization, the deamination of amino acid at low temperature was favored and a solid catalyst was quite active for deamination of free amino acids at quite low temperature hydrothermal water. Cellulose was dissolved in some ionic liquids with high mass percentages (5–20 wt%) and converted into monomers and useful components such as furan ring compounds and supercritical fluid cosolvent such as hydrothermal water in ionic liquids supported improvement of reaction efficiency. For hydrogenation of biomass, it was confirmed that hydrogen solubility was enhanced with supercritical carbon dioxide and it must be helpful for hydrogen reaction with biomass molecule

A novel technique for the measurement of the avalanche fluctuation of gaseous detectors

We have developed a novel technique for the measurement of the avalanche fluctuation of gaseous detectors using a UV laser. The technique is simple and requires a short data-taking time of about ten minutes. Furthermore, it is applicable for relatively low gas gains. Our experimental setup as well as the measurement principle, and the results obtained with a stack of Gas Electron Multipliers (GEMs) operated in several gas mixtures are presented.Comment: 7 pages, 7 figures. For the proceedings of VCI2016, to be published in Nucl. Instrum. Methods Phys. Res.

Increased [¹⁸F]FMISO accumulation under hypoxia by multidrug-resistant protein 1 inhibitors

BACKGROUND: [¹⁸F]Fluoromisonidazole ([¹⁸F]FMISO) is a PET imaging probe widely used for the detection of hypoxia. We previously reported that [¹⁸F]FMISO is metabolized to the glutathione conjugate of the reduced form in hypoxic cells. In addition, we found that the [¹⁸F]FMISO uptake level varied depending on the cellular glutathione conjugation and excretion ability such as enzyme activity of glutathione-S-transferase and expression levels of multidrug resistance-associated protein 1 (MRP1, an efflux transporter), in addition to the cellular hypoxic state. In this study, we evaluated whether MRP1 activity affected [¹⁸F]FMISO PET imaging. METHODS: FaDu human pharyngeal squamous cell carcinoma cells were pretreated with MRP1 inhibitors (cyclosporine A, lapatinib, or MK-571) for 1 h, incubated with [¹⁸F]FMISO for 4 h under hypoxia, and their radioactivity was then measured. FaDu tumor-bearing mice were intravenously injected with [¹⁸F]FMISO, and PET/CT images were acquired at 4 h post-injection (1st PET scan). Two days later, the same mice were pretreated with MRP1 inhibitors (cyclosporine A, lapatinib, or MK-571) for 1 h, and PET/CT images were acquired (2nd PET scan). RESULTS: FaDu cells pretreated with MRP1 inhibitors exhibited significantly higher radioactivity than those without inhibitor treatment (cyclosporine A: 6.91 ± 0.27, lapatinib: 10.03 ± 0.47, MK-571: 10.15 ± 0.44%dose/mg protein, p < 0.01). In the in vivo PET study, the SUVmean ratio in tumors [calculated as after treatment (2nd PET scan)/before treatment of MRP1 inhibitors (1st PET scan)] of the mice treated with MRP1 inhibitors was significantly higher than those of control mice (cyclosporine A: 2.6 ± 0.7, lapatinib: 2.2 ± 0.7, MK-571: 2.2 ± 0.7, control: 1.2 ± 0.2, p < 0.05). CONCLUSION: In this study, we revealed that MRP1 inhibitors increase [¹⁸F]FMISO accumulation in hypoxic cells. This suggests that [¹⁸F]FMISO-PET imaging is affected by MRP1 inhibitors independent of the hypoxic state

Tubular Injury in a Rat Model of Type 2 Diabetes Is Prevented by Metformin: A Possible Role of HIF-1α Expression and Oxygen Metabolism

http://dx.doi.org/10.2337/db10-0655OBJECTIVE : Chronic hypoxia has been recognized as a key regulator in renal tubulointerstitial fibrosis, as seen in diabetic nephropathy, which is associated with the activation of hypoxia-inducible factor (HIF)-1α. We assess here the effects of the biguanide, metformin, on the expression of HIF-1α in diabetic nephropathy using renal proximal tubular cells and type 2 diabetic rats. RESEARCH DESIGN AND METHODS : We explored the effects of metformin on the expression of HIF-1α using human renal proximal tubular epithelial cells (HRPTECs). Male Zucker diabetic fatty (ZDF; Gmi-fa/fa) rats were treated from 9 to 39 weeks with metformin (250 mg/kg^/day^) or insulin. RESULTS : Metformin inhibited hypoxia-induced HIF-1α accumulation and the expression of HIF-1–targeted genes in HRPTECs. Although metformin activated the downstream pathways of AMP-activated protein kinase (AMPK), neither the AMPK activator, AICAR, nor the mTOR inhibitor, rapamycin, suppressed hypoxia-induced HIF-1α expression. In addition, knockdown of AMPK-α did not abolish the inhibitory effects of metformin on HIF-1α expression. The proteasome inhibitor, MG-132, completely eradicated the suppression of hypoxia-induced HIF-1α accumulation by metformin. The inhibitors of mitochondrial respiration similarly suppressed hypoxia-induced HIF-1α expression. Metformin significantly decreased ATP production and oxygen consumption rates, which subsequently led to increased cellular oxygen tension. Finally, metformin, but not insulin, attenuated tubular HIF-1α expression and pimonidazole staining and ameliorated tubular injury in ZDF rats. CONCLUSIONS : Our data suggest that hypoxia-induced HIF-1α accumulation in diabetic nephropathy could be suppressed by the antidiabetes drug, metformin, through the repression of oxygen consumption

OCT で検出された冠動脈のlipid-richプラークに対する至適薬物療法施行後の臨床経過

Background: The aim of this study was to evaluate optical coherence tomography (OCT)-detected lipid-rich coronary plaques (LRCPs) with coronary computed tomography angiography (CCTA) 10 months after optimal medical therapy (OMT). Methods and Results: Baseline OCT detected 28 LRCPs in non-culprit lesions. High-risk plaque features (HRPFs), such as positive remodeling, very low attenuation plaques, napkin-ring sign, and spotty calcification, were observed in 67.9%, 67.9%, 21.4%, and 64.3% of LRCPs, respectively, at the 10-month follow-up CCTA. Lesions with ≥3 HRPFs were defined as high-risk LRCPs (n=12); the remaining were defined as low-risk LRCPs (n=16). The maximum lipid arc on baseline OCT was larger in high- than low-risk LRCPs (221±62° vs. 179±44°, respectively; P=0.04). Receiver operating characteristic curve analysis indicated that a maximum lipid arc >154° on baseline OCT was the optimal cut-off value to predict high-risk LRCPs 10 months after OMT. Patients with high-risk LRCPs had worse clinical outcomes, defined as a composite of cardiac death, target lesion-related myocardial infarction, and target lesion-related revascularization, during follow-up than those with low-risk LRCPs (33.3% vs. 0%; P=0.01). Conclusions: A high-risk LRCP at follow-up CCTA was correlated with a larger maximum lipid arc on baseline OCT. Further aggressive treatment for patients with large LRCPs may reduce vulnerable plaque features and prevent future cardiac events.博士（医学）・甲第869号・令和5年3月15