Seismic response analysis by subloading surface model

A lot of disaster by liquefaction have been reported in area along the shore of Japan. In particular, liquefaction has occurred in the wide area in the Great East Japan Earthquake of 2011. Various approaches for the liquefaction analysis have been proposed up to present. Among these approaches, the subloading surface model is formulated in the framework of the plasticity model and thus it is expected to provide a highly pertinent simulation of cyclic loading behaviour of materials. Further, the explicit constitutive equation of soils has been formulated to describe the cyclic loading behaviour with the cyclic mobility [1]. In this study, the validity of the liquefaction analysis by the subloading surface model is examined by comparing the simulation by the subloading surface model with the actual record for the acceleration wave in the ground surface to the input of the actual data of the acceleration wave in the soil ground base. The actual data used in the simulation was recorded in the Kushiro earthquake in 1993

Maximum tsunami height prediction using pressure gauge data by a Gaussian process at Owase in the Kii Peninsula, Japan

We constructed a model to predict the maximum tsunami height by a Gaussian process (GP) that uses pressure gauge data from the Dense Oceanfloor Network System for Earthquakes and Tsunamis (DONET) in the Nankai trough. We found a greatly improved generalization error of the maximum tsunami height by our prediction model. The error is about one third of that by a previous method, which tends to make larger predictions, especially for large tsunami heights (>10 m). These results indicate that GP enables us to get a more accurate prediction of tsunami height by using pressure gauge data

Implementation of Parallel Garbage Collection Using Fork System Call in Lisp System and Its Evaluation

We implemented the parallel garbage collector using fork system call for process generation supported in the multi-processes OS, suchas UNIX. The GC does not need a write barrier because the gc process performs marking the replica space generated by fork system call. Although Inter-Process Communication is needed in order tonotify garbagecells, the ordinary stop and collect mark-sweep GC can be easily changed to this method. We implemented the GC in the Lisp system and compared with the original mark-sweep GC

リポポリサッカライドの外因性投与はコリン欠乏 L-アミノ酸置換食誘発脂肪性肝炎モデルマウスにおいて肝線維化を促進する

Various rodent models have been proposed for basic research; however, the pathogenesis of human nonalcoholic steatohepatitis (NASH) is difficult to closely mimic. Lipopolysaccharide (LPS) has been reported to play a pivotal role in fibrosis development during NASH progression via activation of toll-like receptor 4 (TLR4) signaling. This study aimed to clarify the impact of low-dose LPS challenge on NASH pathological progression and to establish a novel murine NASH model. C57BL/6J mice were fed a choline-deficient l-amino-acid-defined (CDAA) diet to induce NASH, and low-dose LPS (0.5 mg/kg) was intraperitoneally injected thrice a week. CDAA-fed mice showed hepatic CD14 overexpression, and low-dose LPS challenge enhanced TLR4/NF-κB signaling activation in the liver of CDAA-fed mice. LPS challenge potentiated CDAA-diet-mediated insulin resistance, hepatic steatosis with upregulated lipogenic genes, and F4/80-positive macrophage infiltration with increased proinflammatory cytokines. It is noteworthy that LPS administration extensively boosted pericellular fibrosis with the activation of hepatic stellate cells in CDAA-fed mice. Exogenous LPS administration exacerbated pericellular fibrosis in CDAA-mediated steatohepatitis in mice. These findings suggest a key role for LPS/TLR4 signaling in NASH progression, and the authors therefore propose this as a suitable model to mimic human NASH.博士（医学）・甲第738号・令和2年3月16日© 2019 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/)

Initial In-Orbit Operation Result of Microsatellite HIBARI: Attitude Control by Driving Solar Array Paddles

We have developed a 50kg class microsatellite HIBARI . The mission of this satellite is to demonstrate a novel attitude control method for microsatellites which is called “Variable Shape Attitude Control (VSAC).” VSAC is a method using anti-torque by driving variable shape structures. HIBARI has four drivable solar array paddles, and will demonstrate VSAC. The development of HIBARI began in 2019, and it was injected into orbit in November 2021 under the Innovative Satellite Technology Demonstration Program led by JAXA. Currently, HIBARI has completed its critical phase and paddle deployment phase, and is conducting paddle drive experiments in orbit. In paddle drive experiments, the paddles are driven according to the command values, and the accompanying attitude change is confirmed. These results indicate that the satellite can generate angular velocities of 4 deg/s or more and achieve the target agile maneuver of 30deg in 10seconds, which is comparable to that of CMG for microsatellite

アンギオテンシン受容体を遮断することによりYes関連蛋白質の発癌活性が阻害されて胆管癌細胞増殖が抑制される

Cholangiocarcinoma (CCA) is a destructive malignancy with limited responsiveness to conventional chemotherapy. Although angiotensin receptor blockers (ARBs) have gained attention for their potential anticancer activity, little is known about their effects on CCA. The transcriptional co-activator, Yes-associated protein (YAP) is a critical oncogene in several cancers, including CCA. Following recent evidence showing that YAP is regulated by angiotensin II (AT-II), we investigated the effects of an ARB, losartan, on two human CCA cell lines (KKU-M213 and HuCCT-1) with regards to YAP oncogenic regulation. Losartan suppressed AT-II-induced CCA cell proliferation in a dose-dependent manner, induced apoptosis, decreased YAP (Ser127), and downregulated the YAP target genes CTGF, CYR61, ANKRD1, and MFAP5. However, losartan did not affect epithelial-mesenchymal transition, differentiation, or stemness in the CCA cells. Xenograft tumor growth assay showed that oral administration of a low clinical dose of losartan considerably reduced subcutaneous tumor burden and attenuated intratumor vascularization in CCA cell-derived xenograft tumors in BALB/c nude mice. These results indicate that ARB therapy could serve as a potential novel strategy for CCA treatment.博士（医学）・甲第728号・令和2年3月16日Copyright © 2018 Elsevier B.V. All rights reserved

フルクトースの経口投与はラット脂肪性肝炎モデルにおいて腸管透過性亢進作用を介して肝線維化および肝発癌を悪化させる

Recent reports have revealed the impact of a western diet containing large amounts of fructose on the pathogenesis of non-alcoholic steatohepatitis (NASH). Fructose exacerbates hepatic inflammation in NASH by inducing increasing intestinal permeability. However, it is not clear whether fructose contributes to the progression of liver fibrosis and hepatocarcinogenesis in NASH. The aim of this study was to investigate the effect of fructose intake on NASH in a rat model. A choline-deficient/L-amino acid diet was fed to F344 rats to induce NASH. Fructose was administrated to one group in the drinking water. The development of liver fibrosis and hepatocarcinogenesis were evaluated histologically. Oral fructose administration exacerbated liver fibrosis and increased the number of preneoplastic lesions positive for glutathione S-transferase placental form. Fructose-treated rats had significantly higher expression of hepatic genes related to toll-like receptor-signaling, suggesting that fructose consumption increased signaling in this pathway, leading to the progression of NASH. We confirmed that intestinal permeability was significantly higher in fructose-treated rats, as evidenced by a loss of intestinal tight junction proteins. Fructose exacerbated both liver fibrosis and hepatocarcinogenesis by increasing intestinal permeability. This observation strongly supports the role of endotoxin in the progression of NASH.博士（医学）・乙第1432号・令和元年9月27日Copyright © 2018 Impact Journals, LLCCopyright © Seki et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (CC BY 3.0 https://creativecommons.org/licenses/by/3.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited