Lepton-flavor-violating Higgs decay h→μτh \to \mu\tau and muon anomalous magnetic moment in a general two Higgs doublet model

A two Higgs doublet model (2HDM) is one of the minimal extensions of the Standard Model (SM), and it is well-known that the general setup predicts the flavor-violating phenomena, mediated by neutral Higgs interactions. Recently the CMS collaboration has reported an excess of the lepton-flavor-violating Higgs decay in $h \rightarrow \mu \tau$ channel with a significance of 2.5 $\sigma$. We investigate the CMS excess in a general 2HDM with tree-level Flavor Changing Neutral Currents (FCNCs), and discuss its impact on the other physical observations. Especially, we see that the FCNCs relevant to the excess can enhance the neutral Higgs contributions to the muon anomalous magnetic moment, and can resolve the discrepancy between the measured value and the SM prediction. We also find that the couplings to be consistent with the muon g-2 anomaly as well as the CMS excess in $h\rightarrow \mu\tau$ predict the sizable rate of $\tau \rightarrow \mu \gamma$, which is within the reach of future B factory.Comment: 6 pages, 3 figures, revised Fig.3, corrected Eq. (12), added references, accepted for publication in JHE

Serum BAFF and APRIL levels in patients with IgG4-related disease and their clinical significance.

[Introduction]B cell-activating factor of the tumor necrosis factor family (BAFF) and a proliferation-inducing ligand (APRIL) play a crucial role in B cell development, survival, and antibody production. Here we analyzed the serum levels of BAFF and APRIL and their respective clinical associations in patients with an immunoglobulin (Ig) G4-related disease (IgG4-RD). [Methods]We measured serum levels of BAFF and APRIL in patients with IgG4-RD, primary Sjögren's syndrome (pSS), and healthy individuals. Serum BAFF and APRIL levels in IgG4-RD were assessed for correlations with serological parameters, including Ig, particularly IgG4, and the number of affected organs. Serum BAFF and APRIL levels in IgG4-RD were monitored during glucocorticoid (GC) therapy. [Results]Serum BAFF and APRIL levels in patients with IgG4-RD were significantly higher (P < 0.01) than in healthy individuals. The BAFF levels of patients with IgG4-RD were comparable to those of patients with pSS. Although clinical parameters, such as serum IgG4 and the number of affected organs, were not correlated with the levels of BAFF, serum APRIL levels were inversely correlated with serum IgG4 levels (r = -0.626, P < 0.05). While serum BAFF levels decreased following GC therapy, serum APRIL levels increased during follow-up. [Conclusion]These results indicate that BAFF and APRIL might be useful markers for predicting disease activity in IgG4-RD. Further studies are needed to elucidate the role of BAFF and APRIL in the pathogenesis of IgG4-RD

Development of bifacial inverted polymer solar cells using a conductivity-controlled transparent PEDOT: PSS and a striped Au electrode on the hole collection side

An inverted bifacial polymer solar cell was developed using a conductivity-controlled transparent poly(3,4-ethylenedioxylenethiophene):poly(4- styrene sulfonic acid) (PEDOT:PSS) as a hole collection layer and a striped Au electrode with a large open aperture ratio (Rap) as a hole collection electrode. We investigated the performance of the device by varying the interelectrode distance of the striped Au electrode and the sheet resistance of the PEDOT:PSS film. The device using untreated Clevios P (PEDOT:PSS) showed a maximum electric output (Pw) in the Rap range of 50 to 65%. When alcohol-treated Clevios P (Clevios P+) with a lower electrical resistance was used, the maximum Pw increased by 40% compared with that of the device using Clevios P. The maximum Pw was obtained in the R ap range of 84% as the hole collection efficiency of the striped Au electrode improved with the decreased sheet resistance of the PEDOT:PSS. © 2014 The Japan Society of Applied Physics

MMP-13 is constitutively produced in human chondrocytes and co-endocytosed with ADAMTS-5 and TIMP-3 by the endocytic receptor LRP1

Matrix metalloproteinase 13 (MMP-13) degrades collagenous extracellular matrix and its aberrant activity associates with diseases such as arthritis, cancer, atherosclerosis and fibrosis. The wide range of MMP-13 proteolytic capacity suggests that it is a powerful, potentially destructive proteinase and thus it has been believed that MMP-13 is not produced in most adult human tissues in the steady state. Present study has revealed that human chondrocytes isolated from healthy adults constitutively express and secrete MMP-13, but that it is rapidly endocytosed and degraded by chondrocytes. Both pro- and activated MMP-13 bind to clusters II and III of low-density lipoprotein (LDL) receptor-related protein 1 (LRP1). Domain deletion studies indicated that the hemopexin domain is responsible for this interaction. Binding competition between MMP-13 and ADAMTS-4, -5 or TIMP-3, which also bind to cluster II, further shown that the MMP-13 binding site within cluster II is different from those of ADAMTS-4, -5 or TIMP-3. MMP-13 is therefore co-endocytosed with ADAMTS-5 and TIMP-3 by human chondrocytes. These findings indicate that MMP-13 may play a role on physiological turnover of cartilage extracellular matrix and that LRP1 is a key modulator of extracellular levels of MMP-13 and its internalization is independent of the levels of ADAMTS-4, -5 and TIMP-3

Extracellular regulation of metalloproteinases

Matrix metalloproteinases (MMPs) and adamalysin-like metalloproteinase with thrombospondin motifs (ADAMTSs) belong to the metzincin superfamily of metalloproteinases and they play key roles in extracellular matrix catabolism, activation and inactivation of cytokines, chemokines, growth factors, and other proteinases at the cell surface and within the extracellular matrix. Their activities are tightly regulated in a number of ways, such as transcriptional regulation, proteolytic activation and interaction with tissue inhibitors of metalloproteinases (TIMPs). Here, we highlight recent studies that have illustrated novel mechanisms regulating the extracellular activity of these enzymes. These include allosteric activation of metalloproteinases by molecules that bind outside the active site, modulation of location and activity by interaction with cell surface and extracellular matrix molecules, and endocytic clearance from the extracellular milieu by low-density lipoprotein receptor-related protein 1 (LRP1)