86 research outputs found

    Determination of Stress Intensity Factor for Interface Crack under Uniform Heat Flow by Crack Tip Stress Method

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    This paper deals with the analysis of the thermal stress intensity factor for interfacial crack in dissimilar materials under uniform heat flow by using the finite element method. This method is based on the fact that the singular stress field near the interface crack tip is controlled by the stress values at the crack tip node calculated by FEM. The calculation shows that the present method has the sufficient accuracy in the interface crack problems under thermal stress.23rd International Congress of Theoretical and Applied Mechanics, August 19-24, 2012, Beijing, Chin

    Triptolide, an active compound identified in a traditional Chinese herb, induces apoptosis of rheumatoid synovial fibroblasts

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    BACKGROUND: Extracts of Tripterygium wilfordii Hook F (TWHF), a traditional Chinese herb, have been reported to show efficacy in patients with rheumatoid arthritis (RA). Since RA is not only characterized by inflammation but also by synovial proliferation in the joints, we examined whether triptolide (a constituent of TWHF) could influence the proliferation of rheumatoid synovial fibroblasts (RSF) by induction of apoptosis. RESULTS: RSF were obtained from RA patients during surgery and were treated with triptolide under various conditions. The viability and proliferation of RSF were measured by the 4-[3-(4-iodophenyl)-2-(4-nitrophenyl)-2H-5-tetrazolio]-1,3-benzene disulfonate (WST-1) assay and by 5-bromo-2'-deoxyuridine incorporation, respectively. Apoptosis was identified by detection of DNA fragmentation using an enzyme-linked immunosorbent assay and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labelling (TUNEL). The role of caspases in apoptosis of RSF was analyzed by measuring caspase-3 activity. Activation of the peroxisome proliferator-activated receptor (PPAR) γ was assessed by a luciferase reporter gene assay using RSF transfected with a plasmid containing the peroxisome proliferator response element. Triptolide decreased viability, inhibited proliferation, and induced apoptosis of RSF in a concentration-dependent manner at very low (nM) concentrations. Caspase-3 activity was increased by treatment with triptolide and was suppressed by caspase inhibitors. Although PPARγ activation was induced by 15-deoxy-Δ(12,14)-prostaglandin J(2), triptolide did not induce it under the same experimental conditions. An extract of TWHF also induced DNA fragmentation in RSF. CONCLUSION: The mechanism of action remains to be studied; however, triptolide may possibly have a disease-modifying effect in patients with RA

    L-Ascorbate Biosynthesis Involves Carbon Skeleton Rearrangement in the Nematode Caenorhabditis elegans

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    Ascorbate (AsA) is required as a cofactor and is widely distributed in plants and animals. Recently, it has been suggested that the nematode Caenorhabditis elegans also synthesizes AsA. However, its biosynthetic pathway is still unknown. To further understand AsA biosynthesis in C. elegans, we analyzed the incorporation of the 13C atom into AsA using gas chromatography-mass spectrometry (GC-MS) in worms fed with D-Glc (1-13C)-labeled Escherichia coli. GC-MS analysis revealed that AsA biosynthesis in C. elegans, similarly to that in mammalian systems, involves carbon skeleton rearrangement. The addition of L-gulono-1,4-lactone, an AsA precursor in the mammalian pathway, significantly increased AsA level in C. elegans, whereas the addition of L-galactono-1,4-lactone, an AsA precursor in the plant and Euglena pathway, did not affect AsA level. The suppression of E03H4.3 (an ortholog of gluconolactonase) or the deficiency of F54D5.12 (an ortholog of L-gulono-1,4-lactone oxidase) significantly decreased AsA level in C. elegans. Although N2- and AsA-deficient F54D5.12 knockout mutant worm (tm6671) morphologies and the ratio of collagen to non-collagen protein did not show any significant differences, the mutant worms exhibited increased malondialdehyde levels and reduced lifespan compared with the N2 worms. In conclusion, our findings indicate that the AsA biosynthetic pathway is similar in C. elegans and mammals

    One-Step Detection of the 2009 Pandemic Influenza A(H1N1) Virus by the RT-SmartAmp Assay and Its Clinical Validation

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    <div><h3>Background</h3><p>In 2009, a pandemic (pdm) influenza A(H1N1) virus infection quickly circulated globally resulting in about 18,000 deaths around the world. In Japan, infected patients accounted for 16% of the total population. The possibility of human-to-human transmission of highly pathogenic novel influenza viruses is becoming a fear for human health and society.</p> <h3>Methodology</h3><p>To address the clinical need for rapid diagnosis, we have developed a new method, the “RT-SmartAmp assay”, to rapidly detect the 2009 pandemic influenza A(H1N1) virus from patient swab samples. The RT-SmartAmp assay comprises both reverse transcriptase (RT) and isothermal DNA amplification reactions in one step, where RNA extraction and PCR reaction are not required. We used an exciton-controlled hybridization-sensitive fluorescent primer to specifically detect the HA segment of the 2009 pdm influenza A(H1N1) virus within 40 minutes without cross-reacting with the seasonal A(H1N1), A(H3N2), or B-type (Victoria) viruses.</p> <h3>Results and Conclusions</h3><p>We evaluated the RT-SmartAmp method in clinical research carried out in Japan during a pandemic period of October 2009 to January 2010. A total of 255 swab samples were collected from outpatients with influenza-like illness at three hospitals and eleven clinics located in the Tokyo and Chiba areas in Japan. The 2009 pdm influenza A(H1N1) virus was detected by the RT-SmartAmp assay, and the detection results were subsequently compared with data of current influenza diagnostic tests (lateral flow immuno-chromatographic tests) and viral genome sequence analysis. In conclusion, by the RT-SmartAmp assay we could detect the 2009 pdm influenza A(H1N1) virus in patients' swab samples even in early stages after the initial onset of influenza symptoms. Thus, the RT-SmartAmp assay is considered to provide a simple and practical tool to rapidly detect the 2009 pdm influenza A(H1N1) virus.</p> </div

    The neural bases for valuing social equality

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    The neural basis of how humans value and pursue social equality has become a major topic in social neuroscience research. Although recent studies have identified a set of brain regions and possible mechanisms that are involved in the neural processing of equality of outcome between individuals, how the human brain processes equality of opportunity remains unknown. In this review article, first we describe the importance of the distinction between equality of outcome and equality of opportunity, which has been emphasized in philosophy and economics. Next, we discuss possible approaches for empirical characterization of human valuation of equality of opportunity vs. equality of outcome. Understanding how these two concepts are distinct and interact with each other may provide a better explanation of complex human behaviors concerning fairness and social equality

    Neural signals in amygdala predict implicit prejudice toward an ethnic outgroup.

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    Racial and ethnic prejudice is one of the most pressing problems in modern societies. Although previous social neuroscience research has suggested the amygdala as a key structure in racial prejudice, it still remains elusive whether the amygdala activity reflects negative attitudes toward an outgroup or other unrelated processes. The present study aims to rigorously test the role of the amygdala in negative prejudice toward an outgroup. Seventy Japanese individuals passively viewed images related to an ethnic outgroup (South Korea) inside a functional magnetic resonance imaging scanner. Using Multi-Voxel Pattern Analysis (MVPA), we found that Japanese individuals\u27 level of implicit (but not explicit) evaluations of South Korea could be predicted from neural signals in the left amygdala. Our result further suggested that the medial and lateral parts of amygdala play different roles in implicit evaluations. In contrast to the MVPA findings, conventional univariate analyses failed to find any reliable relationship between brain activation and both implicit and explicit evaluations. Our findings provide evidence for the amygdala\u27s role in representing an implicit form of prejudice and highlight the utility of the multivariate approach to reveal neural signatures of this complex social phenomenon
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