Evidence for the suppression of intermediate anti-ferroelectric ordering and observation of hardening mechanism in Na1/2Bi 1/2TiO3 ceramics through cobalt substitution

Co-ion (5 mol %) substitution in Na1/2Bi1/2TiO 3 (NBT) host lattice and their effects on the structural, ferroelectric and dielectric behavior has been investigated thoroughly in this present study. The substituted Co-ion at Ti-site acts an acceptor type doping and hardens (i.e., increase in coercivity) the system without any noticeable change in the remanent polarization values. However, the intermediate antiferroelectric (AFE) ordering which exists between 200 C-280 C in NBT system has been suppressed due to Co-ion substitution, which is an interesting feature for device applications

Search for CP violation in D+→K−K+π+D^{+} \to K^{-}K^{+}\pi^{+} decays

A model-independent search for direct CP violation in the Cabibbo suppressed decay $D^+ \to K^- K^+\pi^+$ in a sample of approximately 370,000 decays is carried out. The data were collected by the LHCb experiment in 2010 and correspond to an integrated luminosity of 35 pb$^{-1}$. The normalized Dalitz plot distributions for $D^+$ and $D^-$ are compared using four different binning schemes that are sensitive to different manifestations of CP violation. No evidence for CP asymmetry is found.Comment: 13 pages, 8 figures, submitted to Phys. Rev.

Selumetinib in combination with dacarbazine in patients with metastatic uveal melanoma: a phase III, multicentre, randomised trial (SUMIT)

Purpose: Uveal melanoma is the most common primary intraocular malignancy in adults with no effective systemic treatment option in the metastatic setting. Selumetinib (AZD6244, ARRY-142886) is an oral, potent, and selective MEK1/2 inhibitor with a short half-life, which demonstrated single-agent activity in patients with metastatic uveal melanoma in a randomized phase II trial. Methods: The Selumetinib (AZD6244: ARRY-142886) (Hyd-Sulfate) in Metastatic Uveal Melanoma (SUMIT) study was a phase III, double-blind trial (ClinicalTrial.gov identifier: NCT01974752) in which patients with metastatic uveal melanoma and no prior systemic therapy were randomly assigned (3:1) to selumetinib (75 mg twice daily) plus dacarbazine (1,000 mg/m2 intravenously on day 1 of every 21- day cycle) or placebo plus dacarbazine. The primary end point was progression-free survival (PFS) by blinded independent central radiologic review. Secondary end points included overall survival and objective response rate. Results: A total of 129 patients were randomly assigned to receive selumetinib plus dacarbazine (n = 97) or placebo plus dacarbazine (n = 32). In the selumetinib plus dacarbazine group, 82 patients (85%) experienced a PFS event, compared with 24 (75%) in the placebo plus dacarbazine group (median, 2.8 v 1.8 months); the hazard ratio for PFS was 0.78 (95% CI, 0.48 to 1.27; two-sided P = .32). The objective response rate was 3% with selumetinib plus dacarbazine and 0% with placebo plus dacarbazine (two-sided P = .36). At 37% maturity (n = 48 deaths), analysis of overall survival gave a hazard ratio of 0.75 (95% CI, 0.39 to 1.46; two-sided P = .40). The most frequently reported adverse events (selumetinib plus dacarbazine v placebo plus dacarbazine) were nausea (62% v 19%), rash (57% v 6%), fatigue (44% v 47%), diarrhea (44% v 22%), and peripheral edema (43% v 6%). Conclusion: In patients with metastatic uveal melanoma, the combination of selumetinib plus dacarbazine had a tolerable safety profile but did not significantly improve PFS compared with placebo plus dacarbazine

First observation of Bs -> D_{s2}^{*+} X mu nu decays

Using data collected with the LHCb detector in proton-proton collisions at a centre-of-mass energy of 7 TeV, the semileptonic decays Bs -> Ds+ X mu nu and Bs -> D0 K+ X mu nu are detected. Two structures are observed in the D0 K+ mass spectrum at masses consistent with the known D^+_{s1}(2536) and $D^{*+}_{s2}(2573) mesons. The measured branching fractions relative to the total Bs semileptonic rate are B(Bs -> D_{s2}^{*+} X mu nu)/B(Bs -> X mu nu)= (3.3\pm 1.0\pm 0.4)%, and B(Bs -> D_{s1}^+ X munu)/B(Bs -> X mu nu)= (5.4\pm 1.2\pm 0.5)%, where the first uncertainty is statistical and the second is systematic. This is the first observation of the D_{s2}^{*+} state in Bs decays; we also measure its mass and width.Comment: 8 pages 2 figures. Published in Physics Letters

First observation of the decay Bˉs0→D0K∗0\bar{B}^0_s \to D^0 K^{*0} and a measurement of the ratio of branching fractions B(Bˉs0→D0K∗0)B(Bˉ0→D0ρ0)\frac{{\cal B}(\bar{B}^0_s \to D^0 K^{*0})}{{\cal B}(\bar{B}^0 \to D^0 \rho^0)}

The first observation of the decay $\bar{B}^0_s \to D^0 K^{*0}$ using $pp$ data collected by the LHCb detector at a centre-of-mass energy of 7 TeV, corresponding to an integrated luminosity of 36 pb$^{-1}$, is reported. A signal of $34.4 \pm 6.8$ events is obtained and the absence of signal is rejected with a statistical significance of more than nine standard deviations. The $\bar{B}^0_s \to D^0 K^{*0}$ branching fraction is measured relative to that of $\bar{B}^0 \to D^0 \rho^0$: $\frac{{\cal B}(\bar{B}^0_s \to D^0 K^{*0})}{{\cal B}(\bar{B}^0 \to D^0 \rho^0)} = 1.48 \pm 0.34 \pm 0.15 \pm 0.12$, where the first uncertainty is statistical, the second systematic and the third is due to the uncertainty on the ratio of the $B^0$ and $B^0_s$ hadronisation fractions.Comment: 10 pages, 3 figures, submitted to Phys. Lett. B; ISSN 0370-269

Essential Role of TGF-β/Smad Pathway on Statin Dependent Vascular Smooth Muscle Cell Regulation

BACKGROUND: The 3-hydroxy-3-methylglutaryl CoA reductase inhibitors (also called statins) exert proven beneficial effects on cardiovascular diseases. Recent data suggest a protective role for Transforming Growth Factor-beta (TGF-beta) in atherosclerosis by regulating the balance between inflammation and extracellular matrix accumulation. However, there are no studies about the effect of statins on TGF-beta/Smad pathway in atherosclerosis and vascular cells. METHODOLOGY: In cultured vascular smooth muscle cells (VSMCs) statins enhanced Smad pathway activation caused by TGF-beta. In addition, statins upregulated TGF-beta receptor type II (TRII), and increased TGF-beta synthesis and TGF-beta/Smad-dependent actions. In this sense, statins, through Smad activation, render VSMCs more susceptible to TGF-beta induced apoptosis and increased TGF-beta-mediated ECM production. It is well documented that high doses of statins induce apoptosis in cultured VSMC in the presence of serum; however the precise mechanism of this effect remains to be elucidated. We have found that statins-induced apoptosis was mediated by TGF-beta/Smad pathway. Finally, we have described that RhoA inhibition is a common intracellular mechanisms involved in statins effects. The in vivo relevance of these findings was assessed in an experimental model of atherosclerosis in apolipoprotein E deficient mice: Treatment with Atorvastatin increased Smad3 phosphorylation and TRII overexpression, associated to elevated ECM deposition in the VSMCs within atheroma plaques, while apoptosis was not detected. CONCLUSIONS: Statins enhance TGF-beta/Smad pathway, regulating ligand levels, receptor, main signaling pathway and cellular responses of VSMC, including apoptosis and ECM accumulation. Our findings show that TGF-beta/Smad pathway is essential for statins-dependent actions in VSMCs

Search for the lepton number violating decays B+→π−μ+μ+B^{+}\to \pi^- \mu^+ \mu^+ and B+→K−μ+μ+B^{+}\to K^- \mu^+ \mu^+

A search is performed for the lepton number violating decay $B^{+}\to h^- \mu^+ \mu^+$, where $h^-$ represents a $K^-$ or a $\pi^-$, using data from the LHCb detector corresponding to an integrated luminosity of $36pb^{-1}$. The decay is forbidden in the Standard Model but allowed in models with a Majorana neutrino. No signal is observed in either channel and limits of $B(B^{+} \to K^- \mu^+ \mu^+) < 5.4\times 10^{-8}$ and $B(B^{+} \to \pi^- \mu^+ \mu^+) < 5.8\times 10^{-8}$ are set at the 95% confidence level. These improve the previous best limits by factors of 40 and 30, respectively

Measurement of b hadron production fractions in 7 TeV pp collisions

Measurements of $b$ hadron production ratios in proton-proton collisions at a centre-of-mass energy of 7 TeV with an integrated luminosity of 3 pb$^{-1}$ are presented. We study the ratios of strange $B$ meson to light $B$ meson production $f_s/(f_u+f_d)$ and $\Lambda_b^0$ baryon to light $B$ meson production $f_{\Lambda_b}/(f_u+f_d)$ as a function of the charmed hadron-muon pair transverse momentum $p_T$ and the $b$ hadron pseudorapidity $\eta$, for $p_T$ between 0 and 14 GeV and $\eta$ between 2 and 5. We find that $f_s/(f_u+f_d)$ is consistent with being independent of $p_{\rm T}$ and $\eta$, and we determine $f_s/(f_u+f_d)$ = 0.134$\pm$ 0.004 $^{+0.011}_{-0.010}$, where the first error is statistical and the second systematic. The corresponding ratio $f_{\Lambda_b}/(f_u+f_d)$ is found to be dependent upon the transverse momentum of the charmed hadron-muon pair, $f_{\Lambda_b}/(f_u+f_d)=(0.404\pm 0.017 (stat) \pm 0.027 (syst) \pm 0.105 (Br))\times[1 -(0.031 \pm 0.004 (stat) \pm 0.003 (syst))\times p_T(GeV)]$, where Br reflects an absolute scale uncertainty due to the poorly known branching fraction Br(\Lambda_c^+ \to pK^-\pi^+)$. We extract the ratio of strange$B$meson to light neutral$B$meson production$f_s/f_d$by averaging the result reported here with two previous measurements derived from the relative abundances of$\bar{B}_s \to D_S^+ \pi ^-$to$\bar{B}^0 \to D^+K^-$and$\bar{B}^0 \to D^+\pi^-$. We obtain$f_s/f_d=0.267^{+0.021}_{-0.020}$.Comment: 28 pages, 12 figures, version accepted for publication in Physical Review D, few more detailed explanations on analysis methods adde