The automatic computation for SUSY processes

We have constructed a system for the automatic computation of cross-sections for the processes of the SUSY QED by the extension of the GRACE system including a Majorana fermion. The system has also been applied to another model including Majorana fermions, MSSM, by the definition of the model file.Comment: total 4 page

e+e−→H+H−e^+e^-\to H^+H^- signals at LEP2 energies in the Minimal Supersymmetric Standard Model

In this paper we compare $H^+H^-$ and $W^+W^-$ into four-fermion production at centre-of-mass energies typical of LEP2 and somewhat larger. The theoretical framework considered is the Minimal Supersymmetric Standard Model. The interest in exploiting the $e^+e^-$ CERN collider at values of $\sqrt s$ greater than 192 GeV could come from the discovery of Supersymmetric signals during runs at lower energy. If these indicate that a charged Higgs boson exists in the mass range \MH\approx95-105 GeV, then a few years of running at $\sqrt s=205-215$ GeV and nominal luminosity could make the detection of such scalars feasible, in the purely leptonic channel $\tau\nu_\tau\tau\nu_\tau$ and, for small \tb's, also in the semi-hadronic(leptonic) one ${jj}\tau\nu_\tau$. Charged Higgs bosons of the above nature cannot be produced by the beam energies approved at present for LEP2. However, if runs beyond the so-called `192 GeV cryogenic limit' will be approved by the CERN Council, our selection procedure will enable us to establish the presence, or otherwise, of charged Higgs bosons in the mentioned mass rangeComment: 30 pages, latex, epsfig, 12 postscript figures, complete paper available at ftp://axpa.hep.phy.cam.ac.uk/stefano/cavendish_9615 and at http://www.hep.phy.cam.ac.uk/theory/papers

PHASE, a Monte Carlo event generator for six-fermion physics at the LHC

PHASE is a new event generator dedicated to the study of Standard Model processes with six fermions in the final state at the LHC. The code is intended for analyses of vector boson scattering, Higgs search, three gauge boson production, and top physics. This first version of the program describes final states characterized by the presence of one neutrino, $pp\to 4q +l\nu_l$, at O($\alpha^6$). PHASE is based on a new iterative-adaptive multichannel technique, and employs exact leading order matrix elements. The code can generate unweighted events for any subset of all available final states. The produced parton-level events carry full information on their colour and flavour structure, enabling the evolution of the partons into fully hadronised final states. An interface to hadronization packages is provided via the Les Houches Protocol.Comment: 27 pages, Latex, 6 figure

ALPGEN, a generator for hard multiparton processes in hadronic collisions

This paper presents a new event generator, ALPGEN, dedicated to the study of multiparton hard processes in hadronic collisions. The code performs, at the leading order in QCD and EW interactions, the calculation of the exact matrix elements for a large set of parton-level processes of interest in the study of the Tevatron and LHC data. The current version of the code describes the following final states: (W -> ffbar') QQbar+ N jets (Q being a heavy quark, and f=l,q), with N f fbar)+QQbar+Njets (f=l,nu), with N ffbar') + charm + N jets (f=l,q), N f fbar') + N jets (f=l,q) and (Z/gamma* -> f fbar)+ N jets (f=l,nu), with N<=6; nW+mZ+lH+N jets, with n+m+l+N<=8 and N<=3 including all 2-fermion decay modes of W and Z bosons, with spin correlations; Q Qbar+N jets (N b f fbar' decays and relative spin correlations included if Q=t; Q Qbar Q' Qbar'+N jets, with Q and Q' heavy quarks (possibly equal) and N b f fbar' decays and relative spin correlations included if Q=t; N jets, with N<=6. Parton-level events are generated, providing full information on their colour and flavour structure, enabling the evolution of the partons into fully hadronised final states.Comment: 1+38 pages, uses JHEP.cls. Documents code version 1.2: extended list of processes, updated documentation and bibliograph

Review of differential diagnosis and management of spasmodic dysphonia

Purpose of Review: The recent literature on spasmodic dysphonia is reviewed with regard to pathogenesis, differential diagnosis, treatment options, audits, and current methods of management. Recent Findings: Advances in technology have enabled clinicians to better understand the connection between brain and laryngeal function and dysfunction. Refinements in imaging and genetic investigation techniques have led to advances in the understanding of the underlying mechanism of this neuro-laryngeal disorder. Development of diagnostic assessment tools and measures of Quality of Life hold the potential to improve treatment and care. Summary: Fifty articles published between 2014 and 2015 were selected for this review. The sources were drawn from several clinical specialties: 54% come under the scope of laryngology, 32% from neurology, and 14% from other areas. It remains poorly understood, misdiagnosed and under diagnosed. Its identification, diagnosis, treatment selection, and coordination of care require an expert specialist multi-disciplinary team. More training is required to help people who have this chronic and psychosocially disabling voice disorder, which impinges on all aspects of their lives. Spasmodic dysphonia is now classified as a “rare” disease in the USA. This designation will assist in international standards of diagnosis, assessment, treatment, and management

Retrograde ERK activation waves drive base-to-apex multicellular flow in murine cochlear duct morphogenesis

うずまき管の伸⻑を司る分子活性と細胞群の波を発見 --綱引きによる細胞群の流れと臓器の成長--. 京都大学プレスリリース. 2021-03-09.A notable example of spiral architecture in organs is the mammalian cochlear duct, where the morphology is critical for hearing function. Genetic studies have revealed necessary signaling molecules, but it remains unclear how cellular dynamics generate elongating, bending, and coiling of the cochlear duct. Here, we show that extracellular signal-regulated kinase (ERK) activation waves control collective cell migration during the murine cochlear duct development using deep tissue live-cell imaging, Förster resonance energy transfer (FRET)-based quantitation, and mathematical modeling. Long-term FRET imaging reveals that helical ERK activation propagates from the apex duct tip concomitant with the reverse multicellular flow on the lateral side of the developing cochlear duct, resulting in advection-based duct elongation. Moreover, model simulations, together with experiments, explain that the oscillatory wave trains of ERK activity and the cell flow are generated by mechanochemical feedback. Our findings propose a regulatory mechanism to coordinate the multicellular behaviors underlying the duct elongation during development

Stalling interkinetic nuclear migration in curved pseudostratified epithelium of developing cochlea

The bending of epithelial tubes is a fundamental process in organ morphogenesis, driven by various multicellular behaviours. The cochlea in the mammalian inner ear is a representative example of spiral tissue architecture where the continuous bending of the duct is a fundamental component of its morphogenetic process. Although the cochlear duct morphogenesis has been studied by genetic approaches extensively, it is still unclear how the cochlear duct morphology is physically formed. Here, we report that nuclear behaviour changes are associated with the curvature of the pseudostratified epithelium during murine cochlear development. Two-photon live-cell imaging reveals that the nuclei shuttle between the luminal and basal edges of the cell is in phase with cell-cycle progression, known as interkinetic nuclear migration, in the flat region of the pseudostratified epithelium. However, the nuclei become stationary on the luminal side following mitosis in the curved region. Mathematical modelling together with perturbation experiments shows that this nuclear stalling facilitates luminal-basal differential growth within the epithelium, suggesting that the nuclear stalling would contribute to the bending of the pseudostratified epithelium during the cochlear duct development. The findings suggest a possible scenario of differential growth which sculpts the tissue shape, driven by collective nuclear dynamics

Randomised clinical trial: a leucine-metformin-sildenafil combination (NS-0200) vs placebo in patients with non-alcoholic fatty liver disease

BACKGROUND: Sirtuin 1 (Sirt1) is suppressed in non-alcoholic fatty liver disease (NAFLD), while its' stimulation or overexpression results in reduced disease severity in pre-clinical NAFLD models. Leucine allosterically activates Sirt1 and synergise with other Sirt/AMPK/NO pathway activators. We developed a triple combination of leucine, metformin and sildenafil (NS-0200), which was effective in a mouse model of non-alcoholic steatohepatitis (NASH). AIM: To report the results from a Phase 2, randomised clinical trial of of NS-0200 in 91 subjects with NAFLD (liver fat ≥15% by magnetic resonance imaging-proton-density fat fraction (MRI-PDFF)). METHODS: Subjects were randomised to placebo, low-dose (1.1 g leucine/0.5 g metformin/0.5 mg sildenafil) or high-dose NS-0200 (1.1 g leucine/0.5 g metformin/1.0 mg sildenafil) b.d. for 16 weeks; change in hepatic fat was assessed via MRI-PDFF, and lipid metabolism was assessed via changes in the lipidomic signature. Seventy subjects completed the trial and met a priori compliance criteria. Analyses were conducted on the full cohort and on those with alanine aminotransferase (ALT) values above median (50 U/L; n = 35). RESULTS: In the full cohort, active treatments did not separate from placebo. High dose NS-0200 reduced hepatic fat by 15.7% (relative change from baseline) in the high ALT group (P < 0.005) while low dose NS-0200 and placebo did not significantly change hepatic fat. Lipidomic analysis showed dose-responsive treatment effects in both overall and high ALT cohorts, with significant decreases in metabolically active lipids and up-regulation of fatty acid oxidation. CONCLUSION: These data support further evaluation of high-dose NS-0200 for treating NASH, especially in those with elevated ALT (NCT 02546609)