Measurement of J/ψJ/\psi production as a function of event multiplicity in pp collisions at s=13 TeV\sqrt{s} = 13\,\mathrm{TeV} with ALICE

The availability at the LHC of the largest collision energy in pp collisions allows a significant advance in the measurement of $J/\psi$ production as function of event multiplicity. The interesting relative increase observed with data at the LHC at $\sqrt{s} = 7\,\mathrm{TeV}$ and at RHIC at $\sqrt{s} = 0.2\,\mathrm{TeV}$ is studied now at unprecedented multiplicities at $\sqrt{s} = 13\,\mathrm{TeV}$. The measurement at mid-rapidity in the dielectron channel with ALICE is presented and discussed in comparison to predictions from available theoretical models and to data at lower energies.Comment: 4 pages, 4 figures, Proceedings of the XXVIth International Conference on Ultrarelativistic Nucleus-Nucleus Collisions, Quark Matter 2017, Chicago, February 6-11, 201

Measurement of J/{\psi} production in pp collisions at LHC energies with ALICE

An overview of ALICE results on the measurement of J/{\psi} production in pp collisions at $\sqrt{s}$ = 7 TeV collected during the LHC Run-1 period is presented, as well as first results at forward rapidity from pp collisions at $\sqrt{s}$ = 13 TeV collected during the LHC Run-2 period. In particular, the measurement of J/{\psi} production as a function of transverse momentum and charged-particle multiplicity are discussed and compared to theoretical model calculations.Comment: 4 pages, 4 figures, Proceedings of Hot Quarks September 12-17, 2016, South Padre Island, Texas, US

Elucidating the multiplicity dependence of J/ψ production in proton–proton collisions with PYTHIA8

A study of prompt and non-prompt J/ψ production as a function of charged-particle multiplicity in inelastic proton–proton (pp) collisions at a centre-of-mass energy of s√ = 13 TeV based on calculations using the PYTHIA8 Monte Carlo is reported. Recent experimental data shows an intriguing stronger-than-linear increase of the self-normalized J/ψ yield with multiplicity; several models, based on initial or final state effects, have been able to describe the observed behaviour. In this paper, the microscopic reasons for this behaviour, like the role of multiple parton interactions, colour reconnections and auto-correlations are investigated. It is observed that the stronger-than-linear increase and the transverse momentum (pT) dependence, contrary to what is predicted by the other available models, can be attributed to auto-correlation effects only. In absence of auto-correlation effects, the increase of the yield of J/ψ with multiplicity – and in general for all hard processes – is weaker than linear for multiplicities exceeding about three times the mean multiplicity. The possibility of disentangling auto-correlation effects from other physical phenomena by measuring the charged-particle multiplicity in different pseudo-rapidity and azimuthal regions relative to the J/ψ direction is investigated. In this regard, it is suggested to extend the experimental measurements of J/ψ production as a function of the charged-particle multiplicity by determining the multiplicity in several azimuthal regions and in particular in the Transverse region with respect to the direction of the J/ψ meson

PU.1 controls fibroblast polarization and tissue fibrosis

Fibroblasts are polymorphic cells with pleiotropic roles in organ morphogenesis, tissue homeostasis and immune responses. In fibrotic diseases, fibroblasts synthesize abundant amounts of extracellular matrix, which induces scarring and organ failure. By contrast, a hallmark feature of fibroblasts in arthritis is degradation of the extracellular matrix because of the release of metalloproteinases and degrading enzymes, and subsequent tissue destruction. The mechanisms that drive these functionally opposing pro-fibrotic and pro-inflammatory phenotypes of fibroblasts remain unknown. Here we identify the transcription factor PU.1 as an essential regulator of the pro-fibrotic gene expression program. The interplay between transcriptional and post-transcriptional mechanisms that normally control the expression of PU.1 expression is perturbed in various fibrotic diseases, resulting in the upregulation of PU.1, induction of fibrosis-associated gene sets and a phenotypic switch in extracellular matrix-producing pro-fibrotic fibroblasts. By contrast, pharmacological and genetic inactivation of PU.1 disrupts the fibrotic network and enables reprogramming of fibrotic fibroblasts into resting fibroblasts, leading to regression of fibrosis in several organs

The SARS-coronavirus-host interactome

Coronaviruses (CoVs) are important human and animal pathogens that induce fatal respiratory, gastrointestinal and neurological disease. The outbreak of the severe acute respiratory syndrome (SARS) in 2002/2003 has demonstrated human vulnerability to (Coronavirus) CoV epidemics. Neither vaccines nor therapeutics are available against human and animal CoVs. Knowledge of host cell proteins that take part in pivotal virus-host interactions could define broad-spectrum antiviral targets. In this study, we used a systems biology approach employing a genome-wide yeast-two hybrid interaction screen to identify immunopilins (PPIA, PPIB, PPIH, PPIG, FKBP1A, FKBP1B) as interaction partners of the CoV non-structural protein 1 (Nsp1). These molecules modulate the Calcineurin/NFAT pathway that plays an important role in immune cell activation. Overexpression of NSP1 and infection with live SARS-CoV strongly increased signalling through the Calcineurin/NFAT pathway and enhanced the induction of interleukin 2, compatible with late-stage immunopathogenicity and long-term cytokine dysregulation as observed in severe SARS cases. Conversely, inhibition of cyclophilins by cyclosporine A (CspA) blocked the replication of CoVs of all genera, including SARS-CoV, human CoV-229E and -NL-63, feline CoV, as well as avian infectious bronchitis virus. Non-immunosuppressive derivatives of CspA might serve as broad-range CoV inhibitors applicable against emerging CoVs as well as ubiquitous pathogens of humans and livestock

The SARS-Coronavirus-Host Interactome: Identification of Cyclophilins as Target for Pan-Coronavirus Inhibitors

Coronaviruses (CoVs) are important human and animal pathogens that induce fatal respiratory, gastrointestinal and neurological disease. The outbreak of the severe acute respiratory syndrome (SARS) in 2002/2003 has demonstrated human vulnerability to (Coronavirus) CoV epidemics. Neither vaccines nor therapeutics are available against human and animal CoVs. Knowledge of host cell proteins that take part in pivotal virus-host interactions could define broad-spectrum antiviral targets. In this study, we used a systems biology approach employing a genome-wide yeast-two hybrid interaction screen to identify immunopilins (PPIA, PPIB, PPIH, PPIG, FKBP1A, FKBP1B) as interaction partners of the CoV non-structural protein 1 (Nsp1). These molecules modulate the Calcineurin/NFAT pathway that plays an important role in immune cell activation. Overexpression of NSP1 and infection with live SARS-CoV strongly increased signalling through the Calcineurin/NFAT pathway and enhanced the induction of interleukin 2, compatible with late-stage immunopathogenicity and long-term cytokine dysregulation as observed in severe SARS cases. Conversely, inhibition of cyclophilins by cyclosporine A (CspA) blocked the replication of CoVs of all genera, including SARS-CoV, human CoV-229E and -NL-63, feline CoV, as well as avian infectious bronchitis virus. Non-immunosuppressive derivatives of CspA might serve as broad-range CoV inhibitors applicable against emerging CoVs as well as ubiquitous pathogens of humans and livestock

Mass Bounds on a Very Light Neutralino

Within the Minimal Supersymmetric Standard Model (MSSM) we systematically investigate the bounds on the mass of the lightest neutralino. We allow for non-universal gaugino masses and thus even consider massless neutralinos, while assuming in general that R-parity is conserved. Our main focus are laboratory constraints. We consider collider data, precision observables, and also rare meson decays to very light neutralinos. We then discuss the astrophysical and cosmological implications. We find that a massless neutralino is allowed by all existing experimental data and astrophysical and cosmological observations.Comment: 36 pages, 13 figures, minor modification in astro-physical bounds. EPJC versio