Current Limiting and Recovery Characteristics Under Load of Transformer Type SFCL with Rewound Structure Using BSCCO Wire in Model Power System

AbstractWe have proposed new design of a transformer type SFCL with primary and secondary superconducting coils which has rewound structure. For not so large fault current, the proposed SFCL limits the current by the inductive component by the normal transition of the flux shielding coil (secondary), and for larger fault current, it can give the resistive component additively by the normal transition of the primary coil. The recovery characteristics under load condition and repetitive limiting operation were experimentally investigated in a laboratory scale power system. The SFCL limited twice repetitive faults current and recovered quickly under load condition

TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice

Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6.Fil: Oda, Sayaka. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; JapónFil: Numaga Tomita, Takuro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; JapónFil: Kitajima, Naoyuki. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; JapónFil: Tomizaki, Takashi. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; Japón. University of Tsukuba; JapónFil: Harada, Eri. Ajinomoto Co.; Japón. EA Pharma Co.; JapónFil: Shimauchi, Tsukasa. Okazaki Institute for Integrative Bioscience; Japón. Kyushu University; JapónFil: Nishimura, Akiyuki. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Ajinomoto Co.; JapónFil: Ishikawa, Tatsuya. Kyushu University; Japón. Ajinomoto Co.; Japón. EA Pharma Co.; JapónFil: Kumagai, Yoshito. University of Tsukuba; JapónFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Nishida, Motohiro. Okazaki Institute for Integrative Bioscience; Japón. SOKENDAI; Japón. Kyushu University; Japón. PRESTO; Japó

TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential-dependent coupling with PTEN

Vascular smooth muscle cells (VSMCs) play critical roles in the stability and tonic regulation of vascular homeostasis. VSMCs can switch back and forth between highly proliferative synthetic and fully differentiated contractile phenotypes in response to changes in the vessel environment. Although abnormal phenotypic switching of VSMCs is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty, how control of VSMC phenotypic switching is dysregulated in pathologic conditions remains obscure. We found that inhibition of canonical transient receptor potential 6 (TRPC6) channels facilitated contractile differentiation of VSMCs through plasma membrane hyperpolarization. TRPC6-deficient VSMCs exhibited more polarized resting membrane potentials and higher protein kinase B (Akt) activity than wild-type VSMCs in response to TGF-β1 stimulation. Ischemic stress elicited by oxygen-glucose deprivation suppressed TGF-β1-induced hyperpolarization and VSMC differentiation, but this effect was abolished by TRPC6 deletion. TRPC6-mediated Ca2+ influx and depolarization coordinately promoted the interaction of TRPC6 with lipid phosphatase and tensin homolog deleted from chromosome 10 (PTEN), a negative regulator of Akt activation. Given the marked up-regulation of TRPC6 observed in vascular disorders, our findings suggest that attenuation of TRPC6 channel activity in pathologic VSMCs could be a rational strategy to maintain vascular quality control by fine-tuning of VSMC phenotypic switching.Fil: Numaga-Tomita, Takuro. No especifíca;Fil: Shimauchi, Tsukasa. Kyushu University; JapónFil: Oda, Sayaka. No especifíca;Fil: Tanaka, Tomohiro. No especifíca;Fil: Nishiyama, Kazuhiro. Kyushu University; JapónFil: Nishimura, Akiyuki. Kyushu University; JapónFil: Birnbaumer, Lutz. Pontificia Universidad Católica Argentina "Santa María de los Buenos Aires". Instituto de Investigaciones Biomédicas. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Investigaciones Biomédicas; ArgentinaFil: Mori, Yasuo. No especifíca;Fil: Nishida, Motohiro. Kyushu University; Japó

自然散策、温泉入浴が女性の自律神経機能へ及ぼす影響

日帰りのヘルスツーリズムの企画において自然散策と温泉入浴を参加者女性に体験してもらい、女性の自律神経機能へ及ぼす影響について科学的検証を行った。対象者は成人女性11 名である。結果、自然散策前後では身体的ストレス得点は自然散策後に散策前より有意に上昇した（p ＜ .01）。ストレス対処能力得点は有意に低下していた（ｐ＜ .01）。疲労度得点は自然散策後で低下していた（ｐ＜ .05）。温泉入浴の前後の自律神経活動において有意差はみられなかった。効果には個人差や女性ホルモンの影響も考慮する必要がある

Surface damage characterization of photodegraded low-density polyethylene by means of friction measurements

金沢大学理工研究域フロンティア工学系Friction measurements have been carried out to characterize surface damages during photodegradation of low-density polyethylene. The average and mean deviation of the friction coefficients increase with the irradiation time in the early stage of photodegradation processes, indicating the increase in the surface roughness, whereas the mechanical properties remain essentially unchanged. In the following stage, where the ductile-brittle transition takes place, the mean deviation of the friction coefficients shows an appreciable decrease with maintaining almost constant average values, suggesting that the surface becomes more homogeneous. Beyond the ductile-brittle transition, both of the average and mean deviation of the friction coefficients gradually increase with the irradiation time, indicating further enhancement of surface roughness, followed by formation of surface cracks. The soundness of the friction measurements is confirmed by comparing with optical measurements of the surface roughness, and it is suggested that the present method gives a convenient and sensitive method of detection for degradation in polymeric materials. © 2019 Walter de Gruyter GmbH, Berlin/Boston 2019.Embargo Period 12 month

T cell dysfunction in elderly ARDS patients based on miRNA and mRNA integration analysis

BackgroundAcute respiratory distress syndrome (ARDS) is respiratory failure that commonly occurs in critically ill patients, and the molecular mechanisms underlying its pathogenesis and severity are poorly understood. We evaluated mRNA and miRNA in patients with ARDS and elucidated the pathogenesis of ARDS after performing mRNA and miRNA integration analysis.MethodsIn this single-center, prospective, observational clinical study of patients with ARDS, peripheral blood of each patient was collected within 24 hours of admission. Sequencing of mRNA and miRNA was performed using whole blood from the ARDS patients and healthy donors.ResultsThirty-four ARDS patients were compared with 15 healthy donors. Compared with the healthy donors, 1233 mRNAs and 6 miRNAs were upregulated and 1580 mRNAs and 13 miRNAs were downregulated in the ARDS patients. For both mRNA and miRNA-targeted mRNA, canonical pathway analysis showed that programmed death-1 (PD-1) and programmed cell death ligand 1 (PD-L1) cancer immunotherapy pathway was most activated and the Th2 pathway was most suppressed. For mRNA, the Th1 pathway was most suppressed. miR-149-3p and several miRNAs were identified as upstream regulators.ConclusionmiRNAs regulated the PD-1 and PD-L1 cancer immunotherapy pathway and Th2 pathway through miRNA interference action of mRNA. Integrated analysis of mRNAs and miRNAs showed that T cells were dysfunctional in ARDS patients

Different histological types of non-small cell lung cancer have distinct folate and DNA methylation levels

金沢大学がん研究所分子標的がん医療研究開発センターAberrant DNA methylation is a commonly observed epigenetic change in lung cancer. Folate has been suggested to play a role in the homeostasis of DNA methylation and has also been implicated in cancer chemotherapy. We investigated a possible role for folate in DNA methylation by measuring folate concentrations in tumors and adjacent normal tissues from 72 non-small cell lung cancer (NSCLC) patients. These were compared to DNA methylation levels and to clinicopathological features. Folate concentrations were determined as the sum of 5,10-methylenetetrahydrofolate and tetrahydrofolate. The MethyLight assay was used to quantitate methylation in promoter regions of P16(CDKN2A), APC, CDH13, RARB, RASSF1, RUNX3, and MYOD1. Methylation of LINE-1 repeats was used as a surrogate for global methylation. Folate levels in tumors correlated positively with LINE-1, CDH13, and RUNX3 methylation. Folate concentrations and methylation of LINE-1, RASSF1, and RUNX3 were significantly higher in adenocarcinoma compared to squamous cell carcinoma (SCC). Two sets of array-based data retrieved from the Gene Expression Omnibus consistently showed that expression of FOLR1, a folate transport enzyme, and GGH, an enzyme that prevents folate retention, were higher and lower, respectively, in adenocarcinomas compared to SCC. This was independently validated by quantitative RT-PCR in 26 adenocarcinomas and 13 SCC. Our results suggest that folate metabolism plays a role in aberrant DNA methylation in NSCLC. The histological subtype differences in folate concentration and DNA methylation observed here were associated with distinct expression patterns for folate metabolizing enzymes. These findings may have clinical applications for histology-directed chemotherapy with fluoropyrimidine and anti-folates in NSCLC. © 2009 Japanese Cancer Association

妊娠後期女性の自律神経活動が温泉入浴を含む ヘルスツーリズムにおいて改善を示した１例

2016年度からメンタルヘルス対策として，成人を対象に日帰りのヘルスツーリズムを企画・実施し，効果の検証を重ねてきた。今回，屋内型日帰りヘルスツーリズム（講話，食事，陶芸，温泉入浴の体験）を企画した。参加申し込みがあった妊娠後期女性において自律神経機能が改善したので報告する。分析対象者は，屋内型日帰りヘルスツーリズム（以後：ヘルスツーリズム）に家族とともに参加した現在産前産後休暇中の妊娠37週女性１名である。ヘルスツーリズム前の自律神経活動反応は安静CVRR 6.94％，着席 ccvHF 3.80％と過剰であり，安静 ccvL/H0.09％，⊿CVRR -1.41，⊿ccvL/H -0.01は低値を示していた。ヘルスツーリズム後は安静CVRR3.75％，⊿CVRR 1.89，⊿ccvL/H 0.08は標準に修正していた。安静ccvL/H 0.07％と着席ccvHF 3.87％に変化はみられなかった。平均心拍および瞬時心拍は測定においてヘルスツーリズム前後で大きな変化は見られなかった。CVRR はヘルスツーリズム前の安静座位で過剰であったが，起立・立位・着席には変化はみられなかった。本調査における１症例の結果，屋内型日帰りヘルスツーリズム（講話，食事，陶芸，温泉入浴の体験）は，妊娠後期女性の自律神経機能を改善に導く可能性が示唆された

TRPC3-Nox2 axis mediates nutritional deficiency-induced cardiomyocyte atrophy

Myocardial atrophy, characterized by the decreases in size and contractility of cardiomyocytes, is caused by severe malnutrition and/or mechanical unloading. Extracellular adenosine 5′-triphosphate (ATP), known as a danger signal, is recognized to negatively regulate cell volume. However, it is obscure whether extracellular ATP contributes to cardiomyocyte atrophy. Here, we report that ATP induces atrophy of neonatal rat cardiomyocytes (NRCMs) without cell death through P2Y2 receptors. ATP led to overproduction of reactive oxygen species (ROS) through increased amount of NADPH oxidase (Nox) 2 proteins, due to increased physical interaction between Nox2 and canonical transient receptor potential 3 (TRPC3). This ATP-mediated formation of TRPC3-Nox2 complex was also pathophysiologically involved in nutritional deficiency-induced NRCM atrophy. Strikingly, knockdown of either TRPC3 or Nox2 suppressed nutritional deficiency-induced ATP release, as well as ROS production and NRCM atrophy. Taken together, we propose that TRPC3-Nox2 axis, activated by extracellular ATP, is the key component that mediates nutritional deficiency-induced cardiomyocyte atrophy

TRPC6 counteracts TRPC3-Nox2 protein complex leading to attenuation of hyperglycemia-induced heart failure in mice

Excess production of reactive oxygen species (ROS) caused by hyperglycemia is a major risk factor for heart failure. We previously reported that transient receptor potential canonical 3 (TRPC3) channel mediates pressure overload-induced maladaptive cardiac fibrosis by forming stably functional complex with NADPH oxidase 2 (Nox2). Although TRPC3 has been long suggested to form hetero-multimer channels with TRPC6 and function as diacylglycerol-activated cation channels coordinately, the role of TRPC6 in heart is still obscure. We here demonstrated that deletion of TRPC6 had no impact on pressure overload-induced heart failure despite inhibiting interstitial fibrosis in mice. TRPC6-deficient mouse hearts 1 week after transverse aortic constriction showed comparable increases in fibrotic gene expressions and ROS production but promoted inductions of inflammatory cytokines, compared to wild type hearts. Treatment of TRPC6-deficient mice with streptozotocin caused severe reduction of cardiac contractility with enhancing urinary and cardiac lipid peroxide levels, compared to wild type and TRPC3-deficient mice. Knockdown of TRPC6, but not TRPC3, enhanced basal expression levels of cytokines in rat cardiomyocytes. TRPC6 could interact with Nox2, but the abundance of TRPC6 was inversely correlated with that of Nox2. These results strongly suggest that Nox2 destabilization through disrupting TRPC3-Nox2 complex underlies attenuation of hyperglycemia-induced heart failure by TRPC6