Measurement of the Gluino Mass via Cascade Decays for SPS 1a

If R-parity conserving supersymmetry is realised with masses below the TeV scale, sparticles will be produced and decay in cascades at the LHC. In the case of a neutral LSP, which will not be detected, decay chains cannot be fully reconstructed, complicating the mass determination of the new particles. In this paper we extend the method of obtaining masses from kinematical endpoints to include a gluino at the head of a five-sparticle decay chain. This represents a non-trivial extension of the corresponding method for the squark decay chain. We calculate the endpoints of the new distributions and assess their applicability by examining the theoretical distributions for a variety of mass scenarios. The precision with which the gluino mass can be determined by this method is investigated for the mSUGRA point SPS 1a. Finally we estimate the improvement obtained from adding a Linear Collider measurement of the LSP mass.Comment: 40 pages; extended discussion of error

Production and FCNC decay of supersymmetric Higgs bosons into heavy quarks in the LHC

We analyze the production and subsequent decay of the neutral MSSM Higgs bosons (h = h^0, H^0, A^0) mediated by flavor changing neutral currents (FCNC) in the LHC collider. We have computed the h-production cross-section times the FCNC branching ratio, \sigma(pp -> h -> qq') = \sigma(pp -> h) B(h -> qq'), in the LHC focusing on the strongly-interacting FCNC sector. Here qq' is an electrically neutral pair of quarks of different flavors, the dominant modes being those containing a heavy quark: tc or bs. We determine the maximum production rates for each of these modes and identify the relevant regions of the MSSM parameter space, after taking into account the severe restrictions imposed by low energy FCNC processes. The analysis of \sigma(pp -> h -> qq') singles out regions of the MSSM parameter space different from those obtained by maximizing only the branching ratio, due to non-trivial correlations between the parameters that maximize/minimize each isolated factor. The production rates for the bs channel can be huge for a FCNC process (0.1-1 pb), but its detection can be problematic. The production rates for the tc channel are more modest (10^{-3}-10^{-2} pb), but its detection should be easier due to the clear-cut top quark signature. A few thousand tc events could be collected in the highest luminosity phase of the LHC, with no counterpart in the SM.Comment: 25 pages, 9 figures, 2 tables, LaTeX 2e. Typos corrected. Version to appear in JHE

Constraining Supersymmetry

We review constraints on the minimal supersymmetric extension of the Standard Model (MSSM) coming from direct searches at accelerators such as LEP, indirect measurements such as b -> s gamma decay and the anomalous magnetic moment of the muon. The recently corrected sign of pole light-by-light scattering contributions to the latter is taken into account. We combine these constraints with those due to the cosmological density of stable supersymmetric relic particles. The possible indications on the supersymmetric mass scale provided by fine-tuning arguments are reviewed critically. We discuss briefly the prospects for future accelerator searches for supersymmetry.Comment: 21 LaTeX pages, 9 eps figures, Invited Contribution to the New Journal of Physics Focus Issue on Supersymmetr

Constraining Dark Matter in the MSSM at the LHC

In the event that R-Parity conserving supersymmetry (SUSY) is discovered at the LHC, a key issue which will need to be addressed will be the consistency of that signal with astrophysical and non-accelerator constraints on SUSY Dark Matter. This issue is studied for the SPA benchmark model based on measurements of end-points and thresholds in the invariant mass spectra of various combinations of leptons and jets. These measurements are used to constrain the soft SUSY breaking parameters at the electroweak scale in a general MSSM model. Based on these constraints, we assess the accuracy with which the Dark Matter relic density can be measured.Comment: 21 pages, 12 figure

Measurement of SUSY masses via cascade decays for SPS 1a

If R-parity conserving supersymmetry exists below the TeV-scale, new particles will be produced and decay in cascades at the LHC. The lightest supersymmetric particle will escape the detectors, thereby complicating the full reconstruction of the decay chains. In this paper we expand on existing methods for determining the masses of the particles in the cascade from endpoints of kinematical distributions. We perform scans in the mSUGRA parameter space to delimit the region where this method is applicable. From the examination of theoretical distributions for a wide selection of mass scenarios it is found that caution must be exerted when equating the theoretical endpoints with the experimentally obtainable ones. We provide analytic formulae for the masses in terms of the endpoints most readily available. Complications due to the composite nature of the endpoint expressions are discussed in relation to the detailed analysis of two points on the SPS 1a line. Finally we demonstrate how a Linear Collider measurement can improve dramatically on the precision of the masses obtained

RUBY-1: a randomized, double-blind, placebo-controlled trial of the safety and tolerability of the novel oral factor Xa inhibitor darexaban (YM150) following acute coronary syndrome

AIMS: To establish the safety, tolerability and most promising regimen of darexaban (YM150), a novel, oral, direct factor Xa inhibitor, for prevention of ischaemic events in acute coronary syndrome (ACS). METHODS: In a 26-week, multi-centre, double-blind, randomized, parallel-group study, 1279 patients with recent high-risk non-ST-segment or ST-segment elevation ACS received one of six darexaban regimens: 5 mg b.i.d., 10 mg o.d., 15 mg b.i.d., 30 mg o.d., 30 mg b.i.d., or 60 mg o.d. or placebo, on top of dual antiplatelet treatment. Primary outcome was incidence of major or clinically relevant non-major bleeding events. The main efficacy outcome was a composite of death, stroke, myocardial infarction, systemic thromboembolism, and severe recurrent ischaemia. RESULTS: Bleeding rates were numerically higher in all darexaban arms vs. placebo (pooled HR: 2.275; 95% CI: 1.13–4.60, P = 0.022). Using placebo as reference (bleeding rate 3.1%), there was a dose–response relationship (P = 0.009) for increased bleeding with increasing darexaban dose (6.2, 6.5, and 9.3% for 10, 30, and 60 mg daily, respectively), which was statistically significant for 30 mg b.i.d. (P = 0.002). There was no decrease (indeed a numerical increase in the 30 and 60 mg dose arms) in efficacy event rates with darexaban, but the study was underpowered for efficacy. Darexaban showed good tolerability without signs of liver toxicity. CONCLUSIONS: Darexaban when added to dual antiplatelet therapy after ACS produces an expected dose-related two- to four-fold increase in bleeding, with no other safety concerns but no signal of efficacy. Establishing the potential of low-dose darexaban in preventing major cardiac events after ACS requires a large phase III trial. ClinicalTrials.gov Identifier: NCT0099429

Global Biobank Meta-analysis Initiative : Powering genetic discovery across human disease

Funding Information: The work of the contributing biobanks was supported by numerous grants from governmental and charitable bodies. Biobank-specific acknowledgments and more detailed acknowledgments are included in Data S2. Initiative management, S.B.C. J.C. N.J.C. M.J.D. E.E.K. A.R.M. B.M.N. Y.O. A.V.P. D.A.v.H. R.G.W. C.J.W. W.Z. and S.Z.; individual biobank analysis, A.B. Y.B. B.M.B. C.D.B. S.C. T.-T.C. K.C. S.M.D. M.D. G.H.d.B. Y.D. N.J.D. M.-J.F. Y.-C.A.F. S.F. V.L.F. L.G.F. E.R.G. T.R.G. D.H.G. C.R.G. G.G.-A. S.E.G. L.A.G. C.H. J.B.H. W.E.H. H.H. K.H. N.I. A.I. R.J. M. Kurki, J.K. N.K. E.E.K. J.T.K. M. Kanai, T.L. K.L. M.H.L. S.L. K.L. Y.-F.L. V.L.F. R.J.F.L. E.A.L.-M. A.R.-M. S.M.-G. R.M. R.E.M. H.C.M. A.R.M. Y.M. H.M. S.E.M. I.Y.M. B.M. S.M. K.N. S.N. M.A.N.-A. K.N. Y.O. P.P. A.L.-P. A.P. B.P. S.P. M.H.P. D.J.R. N.R. M.D.R. A.R. C.S. S.S. S.S.S. J.A.S. P.S. I.S. T.T. R.T. K.T. J.U. D.A.v.H. B.V. M.V. Y.V. J.M.V. R.G.W. Y.W. S.J.W. B.N.W. K.-H.H.W. M.Z. X.Z. and S.Z.; individual biobank management, N.A. A.A.T. K.M.A.-D. P.A. K.C.B. M. Boehnke, M. Boezen, C.D.B. A.C. Z.C. C.-Y.C. J.C. N.J.C. S.M.D. S.F. Y.-C.A.F. S.F. E.F. T.G. C.R.G. C.J.G. Y.G. H.H. K.A.H. K.H. S.I.I. N.M.J. N.K. E.E.K. J.T.K. C.L. M.H.L. M.T.M.L. L.L. K.L. Y.-F.L. R.J.F.L. J.L. S.M. Y.M. K.M. I.Y.M. Y.O. C.M.O. A.V.P. B.P. D.J.P. D.J.R. M.D.R. S.S. J.W.S. H.S. K.S. T.T. U.T. R.C.T. D.A.v.H. M.V. R.G.W. D.C.W. C.W. J.W. M.Z. X.Z. and S.Z.; study design and interpretation of results, A.B. M. Boehnke, M. Boezen, B.M.B. T.-T.C. C.-Y.C. M.J.D. G.D.S. N.J.D. S.F. M.-J.F. H.K.F. E.R.G. A.G. T.G. J.B.H. J.H. K.H. R.J. M.K. E.E.K. T.K. C.M.L. V.L.F. E.A.L.-M. A.R.M. S.N. B.M.N. C.M.O. J.J.P. B.P. N.R. H.R. J.A.S. I.S. K.T. D.A.v.H. R.G.W. Y.W. D.C.W. S.J.W. C.J.W. B.N.W. J.W. K.-H.H.W. M.Z. H.Z. J.Z. W.Z. X.Z. and S.Z.; drafted and edited the paper, A.B. M. Boehnke, M. Boezen, M.J.D. G.H.d.B. N.J.D. T.R.G. J.B.H. N.I. N.M.J. M.K. V.L.F. S.M. A.R.M. H.M. S.N. B.M.N. C.M.O. B.P. H.R. C.S. J.A.S. J.W.S. K.T. Y.W. D.C.W. C.J.W. K.-H.H.W. H.Z. J.Z. W.Z. and S.Z.; primary meta-analysis and quality control, M.J.D. H.K.F. M. Kanai, J.K. J.T.K. M. Kurki, M.M. B.M.N. C.J.W. K.-H.H.W. and W.Z.; drug discovery: S.N. T.K. K.-H.H.W. W.Z. and Y.O.; fine mapping, M. Kanai, W.Z. M.J.D. and H.K.F.; polygenic risk score, Y.W. S.N. E.A.L.-M. S.K. K.T. K.L. M. Kanai, W.Z. K.W. M.-J.F. L.B. P.A. P.D. V.L.F. R.M. Y.M. B.B. S.S. J.U. E.R.G. N.J.C. I.S. Y.O. A.R.M. and J.B.H.; proteome-wide Mendelian randomization, H.Z. H.R. A.B. G.H. G.D.S. B.M.B. W.Z. B.M.N. T.R.G. and J.Z.; transcriptome-wide association study, A.B. J.B.H. W.Z. J.Z. M. Kanai, B.P. E.R.G. and N.J.C.; asthma, K.T. W.Z. Y.W. M. Kanai, S.N. Y.O. B.M.N. M.J.D. and A.R.M.; heart failure, K.-H.H.W. N.J.D. B.N.W. I.S. S.E.G. J.B.H. N.J.C. M.P. R.J.F.L. M.J.D. B.M.N. W.Z. W.E.H. and C.J.W.; idiopathic pulmonary fibrosis, J.J.P. W.Z. M.J.D. J.T.K. N.J.C. and J.B.H.; primary open-angle glaucoma, V.L.F. A.B. W.Z. Y.W. K.L. M. Kanai, E.A.L.-M. P.S. R.T. X.Z. S.N. S.S. Y.O. N.I. S.M. H.S. I.S. C.W. A.R.M. E.R.G. N.M.J. N.J.C. and J.B.H.; stroke, I.S. K.-H.H.W. W.H. B.N.W. W.Z. J.E.H. A.P. B.B. A.H.S. M.E.G. R.G.W. K.H. C.K. S.Z. M.J.D. B.M.N. and C.J.W.; venous thromboembolism, B.N.W. I.S. K.-H.H.W. B.B. V.L.F. K.T. M.D. B.N. W.Z. J.A.S. and C.J.W. All authors reviewed the manuscript. M.J.D. is a founder of Maze Therapeutics. B.M.N. is a member of the scientific advisory board at Deep Genomics and a consultant for Camp4 Therapeutics, Takeda Pharmaceutical, and Biogen. The spouse of C.J.W. works at Regeneron Pharmaceuticals. C.-Y.C. is employed by Biogen. C.R.G. owns stock in 23andMe, Inc. T.R.G. has received research funding from various pharmaceutical companies to support the application of Mendelian randomization to drug target prioritization. E.E.K. has received speaker fees from Regeneron, Illumina, and 23andMe and is a member of the advisory board for Galateo Bio. R.E.M. has received speaker fees from Illumina and is a scientific advisor to the Epigenetic Clock Development Foundation. G.D.S. has received research funding from various pharmaceutical companies to support the application of Mendelian randomization to drug target prioritization. K.S. and U.T. are employed by deCODE Genetics/Amgen, Inc. J.Z. has received research funding from various pharmaceutical companies to support the application of Mendelian randomization to drug target prioritization. S.M. is a co-founder of and holds stock in Seonix Bio. Publisher Copyright: © 2022Biobanks facilitate genome-wide association studies (GWASs), which have mapped genomic loci across a range of human diseases and traits. However, most biobanks are primarily composed of individuals of European ancestry. We introduce the Global Biobank Meta-analysis Initiative (GBMI)—a collaborative network of 23 biobanks from 4 continents representing more than 2.2 million consented individuals with genetic data linked to electronic health records. GBMI meta-analyzes summary statistics from GWASs generated using harmonized genotypes and phenotypes from member biobanks for 14 exemplar diseases and endpoints. This strategy validates that GWASs conducted in diverse biobanks can be integrated despite heterogeneity in case definitions, recruitment strategies, and baseline characteristics. This collaborative effort improves GWAS power for diseases, benefits understudied diseases, and improves risk prediction while also enabling the nomination of disease genes and drug candidates by incorporating gene and protein expression data and providing insight into the underlying biology of human diseases and traits.Peer reviewe

Major clinical research advances in gynecologic cancer in 2011

The annual review of 2011 comprised 11 themes of major research achievements in gynecologic oncology including breast cancer. A potential paradigm shift in the management of ovarian cancer was reviewed through comprehensive genomic analyses and a tumor-specific new intraoperative fluorescence imaging technique using folate receptor-α targeted agent, which is expected to improve intraoperative staging and more radical cytoreduction. In addition, updates of bevacizumab and poly (ADP-ribose) polymerase inhibitors, risk-reducing salpingo-oophorectomy, and risk evaluation of pelvic mass were discussed. Regarding cervical cancer, this review covered new findings on human papillomavirus vaccines and human papillomavirus tests as well as the current status of clinical trials on locally advanced cervical cancer. The promising role of sentinel lymph node biopsy in the management of early stage endometrial cancer was followed by two notable clinical researches on: exemestane, an aromatase inhibitor, for the prevention of breast cancer and eribulin, a non-taxane microtubule dynamics inhibitor for the treatment of metastatic breast cancer. Lastly, in premenopausal women with breast cancer, the effect of gonadotropin-releasing hormone analogue on the occurrence of chemotherapy-induced early menopause was discussed