柔道の国際化と日本柔道の今後の課題(第四報) : 国際柔道連盟試合審判規定と講道館柔道試合審判規定の比較を中心に

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Observation of D_s1(2536)^+ → D^+π^-K^+ and angular decomposition of D_s1(2536)^+ →D^*+K_S^0

Using 462 fb^{-1} of e^+e^- annihilation data recorded by the Belle detector, we report the first observation of the decay D_s1(2536)^+　→　D+π^-K^+. The ratio of branching fractions \frac{B(D_s1(2536)^+ → D^+π^- K^+}{B(D_s1(2536)^+ → D+K^0}is measured to be (3.27±0.18±0.37)%. We also study the angular distributions in the D_s1(2536)^+　→D*+K_S^0 decay and measure the ratio of D- and S-wave amplitudes. The S-wave dominates, with a partial width of Γ_S/Γtotal=0.72±0.05±0.01.journal articl

Evidence for Direct CP Violation in B0→K+π-Decays

journal articl

Additional file 1: Figures S1–S5. of Widespread activation of antisense transcription of the host genome during herpes simplex virus 1 infection

Figure S1 Coverage profiles of antisense transcripts. Figure S2 Validation of antisense transcripts. Figure S3 Antisense transcripts with PAA, knockout virus, and HSV-2 infection [67]. Figure S4 Antisense transcript promoters are already poised for transcription. Figure S5 Ectopically expressed BBC3as localizes outside the nucleus. (PDF 4275 kb

Additional file 1: of Long non-coding RNAs defining major subtypes of B cell precursor acute lymphoblastic leukemia

Table S1. RNA-seq data used for analysis and subtype-specific lncRNAs from three subtypes (XLSX 13450 kb

Image_3_Rapid Inflammasome Activation Is Attenuated in Post-Myocardial Infarction Monocytes.tif

Inflammasomes are crucial gatekeepers of the immune response, but their maladaptive activation associates with inflammatory pathologies. Besides canonical activation, monocytes can trigger non-transcriptional or rapid inflammasome activation that has not been well defined in the context of acute myocardial infarction (AMI). Rapid transcription-independent inflammasome activation induced by simultaneous TLR priming and triggering stimulus was measured by caspase-1 (CASP1) activity and interleukin release. Both classical and intermediate monocytes from healthy donors exhibited robust CASP1 activation, but only classical monocytes produced high mature interleukin-18 (IL18) release. We also recruited a limited number of coronary artery disease (CAD, n=31) and AMI (n=29) patients to evaluate their inflammasome function and expression profiles. Surprisingly, monocyte subpopulations isolated from blood collected during percutaneous coronary intervention (PCI) from AMI patients presented diminished CASP1 activity and abrogated IL18 release despite increased NLRP3 gene expression. This unexpected attenuated rapid inflammasome activation was accompanied by a significant increase of TNFAIP3 and IRAKM expression. Moreover, TNFAIP3 protein levels of circulating monocytes showed positive correlation with high sensitive troponin T (hsTnT), implying an association between TNFAIP3 upregulation and the severity of tissue injury. We suggest this monocyte attenuation to be a protective phenotype aftermath following a very early inflammatory wave in the ischemic area. Damage-associated molecular patterns (DAMPs) or other signals trigger a transitory negative feedback loop within newly recruited circulating monocytes as a mechanism to reduce post-injury tissue damage.</p