85 research outputs found

    Estimation of Shallow Water Flow Based on Kalman Filter FEM

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    In this chapter, we present numerical examples of an estimation of shallow water flow based on Kalman filter finite element method (Kalman filter FEM). Shallow water equations are adopted as the governing equations. The Galerkin method, using triangular elements, is employed to discretize the governing equation in space, and the selective lumping method is used to discretize time. We describe the influence on the numerical results of setting the observation points

    Magnolol Protects against MPTP/MPP+-Induced Toxicity via Inhibition of Oxidative Stress in In Vivo and In Vitro Models of Parkinson's Disease

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    The aim of this study is to investigate the role of magnolol in preventing 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP-) induced neurodegeneration in mice and 1-methyl-4-phenylpyridinium ion-(MPP+-) induced cytotoxicity to human neuroblastoma SH-SY5Y cells and to examine the possible mechanisms. Magnolol (30 mg/kg) was orally administered to C57BL/6N mice once a day for 4 or 5 days either before or after MPTP treatment. Western blot analysis revealed that MPTP injections substantially decreased protein levels of dopamine transporter (DAT) and tyrosine hydroxylase (TH) and increased glial fibrillary acidic protein (GFAP) levels in the striatum. Both treatments with magnolol significantly attenuated MPTP-induced decrease in DAT and TH protein levels in the striatum. However, these treatments did not affect MPTP-induced increase in GFAP levels. Moreover, oral administration of magnolol almost completely prevented MPTP-induced lipid peroxidation in the striatum. In human neuroblastoma SH-SY5Y cells, magnolol significantly attenuated MPP+-induced cytotoxicity and the production of reactive oxygen species. These results suggest that magnolol has protective effects via an antioxidative mechanism in both in vivo and in vitro models of Parkinson's disease

    Epitaxial graphene on SiC formed by the surface structure control technique

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    The thermal decomposition of silicon carbide (SiC) is a promising method for producing wafer-scale single-crystal graphene. The optimal growth condition for high-mobility epitaxial graphene fabricated by infrared rapid thermal annealing is discussed in this paper. The surface structures, such as step-terrace and graphene coverage structures, on a non-off-axis SiC(0001) substrate were well controlled by varying the annealing time in a range below 10 min. The mobility of graphene grown at 1620 ºC for 5 min in 100 Torr Ar ambient had a maximum value of 2089 cm2V-1s-1. We found that the causes of the mobility reduction were low graphene coverage, high sheet carrier density, and nonuniformity of the step structure

    Coordinately Co-opted Multiple Transposable Elements Constitute an Enhancer for wnt5a Expression in the Mammalian Secondary Palate

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    Acquisition of cis-regulatory elements is a major driving force of evolution, and there are several examples of developmental enhancers derived from transposable elements (TEs). However, it remains unclear whether one enhancer element could have been produced via cooperation among multiple, yet distinct, TEs during evolution. Here we show that an evolutionarily conserved genomic region named AS3_9 comprises three TEs (AmnSINE1, X6b_DNA and MER117), inserted side-by-side, and functions as a distal enhancer for wnt5a expression during morphogenesis of the mammalian secondary palate. Functional analysis of each TE revealed step-by-step retroposition/transposition and co-option together with acquisition of a binding site for Msx1 for its full enhancer function during mammalian evolution. The present study provides a new perspective suggesting that a huge variety of TEs, in combination, could have accelerated the diversity of cis-regulatory elements involved in morphological evolution

    Autoantibody-induced internalization of nicotinic acetylcholine receptor α3 subunit exogenously expressed in human embryonic kidney cells

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    Autoantibody against nicotinic acetylcholine receptor (nAChR) α3 subunit has been implicated in the pathogenesis of paraneoplastic neurological syndrome. To examine the effect of anti-α3 subunit autoantibody on cell-surface nAChRs, we established human embryonic kidney 293 cells stably co-expressing α3 and β4 subunits. Upon incubation with seropositive patient\u27s serum, this cell line showed co-accumulation of patient\u27s IgG and α3 subunits in the cytoplasm. These data support the hypothesis that anti-α3 subunit autoantibody induces internalization of cell-surface nAChRs and thereby impairs synaptic transmission. © 2012 Elsevier B.V. All rights reserved

    チョウ カイテン イジョウショウ オ トモナッタ オウコウ ケッチョウガン ニ タイシテ フククウキョウ ホジョカ ケッチョウ セツジョジュツ オ シコウ シタ 1レイ

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    A 64-year-old woman with complaint of intermittent abdominal pain for one year was admitted to our hospital. She had been diagnosed as transverse colon cancer by barium enema and colonoscopy at the former hospital. Abdominal enhanced CT showed that the duodenal third portion was not detected at the back of superior mesenteric vessel. She underwent laparoscopic surgery based on a diagnosis of transverse colon cancer with intestinal malrotation. We could perform laparoscopic-assisted transverse colectomy using abdominal enhanced CT which was effective for not only preoprerative diagnosis of accompany of intestinal malrotation but also anatomical anomalies of vessels. The right sided colon which was not fixed to the retroperitoneum in cases with intestinal malrotation could be pulled out easily from the small incision wound. We also considered that colectomy and dissection of its lymph nodes to these cases could be safety performed using by laparoscopy and through small laparotomy

    タンカンナイ シュヨウセン オ ミトメ ゲンパツセイ カンナイ タンカンガン トノ カンベツ オ ヨウシタ イジセイ ダイチョウガン カンテンイ ノ 1セツジョレイ

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    The patient was a 68-year-old man who had undergone right hemicolectomy for ascending colon cancer, and pulmonary resection for lung metastases. After 10 months of operations, abdominal computed tomograms revealed a liver tumor with a biliary tumor thrombus in the segment 5 and a localized dilation of the intrahepatic bile duct. Endoscopic retrograde cholangiopancreatography showed obstruction, 2cm long, of the intrahepatic bile duct (B5) and dilation of the peripheral duct. Cytological examination of extracted bile showed adenocarcinoma. A right hepatic lobectomy was performed under the diagnosis of metastatic liver tumor with tumor development in the intrahepatic bile duct or intrahepatic cholangiocarcinoma. The resected specimen showed massive infiltration of the tumor into intrahepatic bile duct (B5) with forming a tumor thrombus. Histologically, the tumor was moderately differentiated adenocarcinoma, similar to the ascending colon cancer. The final diagnosis was liver metastasis of ascending colon cancer with intrabiliary tumor growth

    Evodiamine Inhibits Insulin-Stimulated mTOR-S6K Activation and IRS1 Serine Phosphorylation in Adipocytes and Improves Glucose Tolerance in Obese/Diabetic Mice

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    Evodiamine, an alkaloid extracted from the dried unripe fruit of the tree Evodia rutaecarpa Bentham (Rutaceae), reduces obesity and insulin resistance in obese/diabetic mice; however, the mechanism underlying the effect of evodiamine on insulin resistance is unknown. This study investigated the effect of evodiamine on signal transduction relating to insulin resistance using obese/diabetic KK-Ay mice and an in vitro adipocyte culture. There is a significant decrease in the mammalian target of rapamycin (mTOR) and ribosomal S6 protein kinase (S6K) signaling in white adipose tissue (WAT) in KK-Ay mice treated with evodiamine, in which glucose tolerance is improved. In addition, reduction of insulin receptor substrate 1 (IRS1) serine phosphorylation, an indicator of insulin resistance, was detected in their WAT, suggesting suppression of the negative feedback loop from S6K to IRS1. As well as the stimulation of IRS1 and Akt serine phosphorylation, insulin-stimulated phosphorylation of mTOR and S6K is time-dependent in 3T3-L1 adipocytes, whereas evodiamine does not affect their phosphorylation except for an inhibitory effect on mTOR phosphorylation. Moreover, evodiamine inhibits the insulin-stimulated phosphorylation of mTOR and S6K, leading to down-regulation of IRS1 serine phosphorylation in the adipocytes. Evodiamine also stimulates phosphorylation of AMP-activated protein kinase (AMPK), an important regulator of energy metabolism, which may cause down-regulation of mTOR signaling in adipocytes. A similar effect on AMPK, mTOR and IRS1 phosphorylation was found in adipocytes treated with rosiglitazone. These results suggest evodiamine improves glucose tolerance and prevents the progress of insulin resistance associated with obese/diabetic states, at least in part, through inhibition of mTOR-S6K signaling and IRS1 serine phosphorylation in adipocytes
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