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Physics at the [FORMULA OMISSION] linear collider
Moortgat-Pick, G.,Baer, H.,Battaglia, M.,Belanger, G.,Fujii, K.,Kalinowski, J.,Heinemeyer, S.,Kiyo, Y.,Olive, K.,Simon, F.,Uwer, P.,Wackeroth, D.,Zerwas, P. M.,Arbey, A.,Asano, M.,Bagger, J.,Bechtle, Springer Berlin Heidelberg 2015 European Physical Journal C Vol.75 No.8
<P>A comprehensive review of physics at an [FORMULA OMISSION] linear collider in the energy range of [FORMULA OMISSION] GeV–3 TeV is presented in view of recent and expected LHC results, experiments from low-energy as well as astroparticle physics. The report focusses in particular on Higgs-boson, top-quark and electroweak precision physics, but also discusses several models of beyond the standard model physics such as supersymmetry, little Higgs models and extra gauge bosons. The connection to cosmology has been analysed as well.</P>
Suwa, Tomone,Nabara, Yoshihiro,Ozeki, Hidemasa,Hemmi, Tsutomu,Isono, Takaaki,Takahashi, Yoshikazu,Kawano, Katsumi,Oshikiri, Masayuki,Tsutsumi, Fumiaki,Shibutani, Kazuyuki,Nunoya, Yoshihiko,Okuno, Kiyo Institute of Electrical and Electronics Engineers 2015 IEEE transactions on applied superconductivity Vol.25 No.3
<P>Japan Atomic Energy Agency (JAEA) is procuring 100% of the ITER Central Solenoid (CS) conductors. The CS conductor is required to maintain the performance under 60000 pulsed electromagnetic cycles. JAEA tested two internal-tin Nb<SUB>3</SUB>Sn conductors for the CS at the SULTAN test facility. As a result of destructive examination, the twist pitches of both of the cables satisfied requirements of the ITER Organization (IO). The current sharing temperatures T<SUB>cs</SUB> of each sample were 6.6 and 6.8 K before cyclic operation, and the T<SUB>cs</SUB> values were 6.8 and 6.9 K after 9700 electromagnetic cycles, including three warm-up/cooldowns, respectively. The T<SUB>cs</SUB> performance of both samples satisfied the IO requirement. The ac losses of CSKO1-C and CSKO1-D were approximately half of typical bronze-route CS conductors at 2 and 9 T. The ac loss at 45.1 kA after the cycling was 1.5 times higher than that without the transport current. An almost constant strain of the jacket was observed after the test as a result of the residual strain measurement. Therefore, the deformation of the cable might have been homogeneous along the conductor axis. Because of the higher T<SUB>cs</SUB> of CSKO1-D than CSKO1-C, JAEA started the manufacturing of the CS conductor with the same specification as CSKO1-D.</P>
Inhibition of plasminogen activator inhibitor-1 attenuates against intestinal fibrosis in mice
( Jin Imai ),( Takashi Yahata ),( Hitoshi Ichikawa ),( Abd Aziz Ibrahim ),( Masaki Yazawa ),( Hideaki Sumiyoshi ),( Yutaka Inagaki ),( Masashi Matsushima ),( Takayoshi Suzuki ),( Tetsuya Mine ),( Kiyo 대한장연구학회 2020 Intestinal Research Vol.18 No.2
Background/Aims: Intestinal fibrosis is a major complication of Crohn’s disease (CD). The profibrotic protein transforming growth factor-β (TGF-β) has been considered to be critical for the induction of the fibrotic program. TGF-β has the ability to induce not only the expression of extracellular matrix (ECM) including collagen, but also the production of plasminogen activator inhibitor-1 (PAI-1) that prevents enzymatic degradation of the ECM during the onset of fibrotic diseases. However, the significance of PAI-1 in the developing intestinal fibrosis has not been fully understood. In the present study, we examined the actual expression of PAI-1 in fibrotic legion of intestinal inflammation and its correlation with the abnormal ECM deposition. Methods: Chronic intestinal inflammation was induced in BALB/c mice using 8 repeated intrarectal injections of 2,4,6-trinitrobenzene sulfonic acid (TNBS). TM5275, a PAI-1 inhibitor, was orally administered as a carboxymethyl cellulose suspension each day for 2 weeks after the sixth TNBS injection. Results: Using a publicly available dataset (accession number, GSE75214) and TNBS-treated mice, we observed increases in PAI-1 transcripts at active fibrotic lesions in both patients with CD and mice with chronic intestinal inflammation. Oral administration of TM5275 immediately after the onset of intestinal fibrosis upregulated MMP-9 (matrix metalloproteinase 9) and decreased collagen accumulation, resulting in attenuation of the fibrogenesis in TNBS-treated mice. Conclusions: PAI-1-mediated fibrinolytic system facilitates collagen degradation suppression. Hence, PAI-1 inhibitor could be applied as an anti-fibrotic drug in CD treatment. (Intest Res 2020;18:219-228)