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The inclusive J/ψ transverse momentum spectra and nuclear modification factors are reported at midrapidity (|y| < 1.0) in Au+Au collisions at √sN N = 39, 62.4 and 200 GeV taken by the STAR experiment. A suppression of J/ψ production, with respect to the production in p + p scaled by the number of binary nucleon–nucleon collisions, is observed in central Au+Au collisions at these three energies. No significant energy dependence of nuclear modification factors is found within uncertainties. The measured nuclear modification factors can be described by model calculations that take into account both suppression of direct J/ψ production due to the color screening effect and J/ψ regeneration from recombination of uncorrelated charm–anticharm quark pairs.
The acceptance-corrected dielectron excess mass spectra, where the known hadronic sources have been subtracted from the inclusive dielectron mass spectra, are reported for the first time at mid-rapidity |yee|<1 in minimum-bias Au+Au collisions at sNN−−−−√ = 19.6 and 200 GeV. The excess mass spectra are consistently described by a model calculation with a broadened ρ spectral function for Mee<1.1 GeV/c2. The integrated dielectron excess yield at sNN−−−−√ = 19.6 GeV for 0.4<Mee<0.75 GeV/c2, normalized to the charged particle multiplicity at mid-rapidity, has a value similar to that in In+In collisions at sNN−−−−√ = 17.3 GeV. For sNN−−−−√ = 200 GeV, the normalized excess yield in central collisions is higher than that at sNN−−−−√ = 17.3 GeV and increases from peripheral to central collisions. These measurements indicate that the lifetime of the hot, dense medium created in central Au+Au collisions at sNN−−−−√ = 200 GeV is longer than those in peripheral collisions and at lower energies.
Di-hadron correlations with identified leading hadrons in 200 GeV Au+Au and d+Au collisions at STAR
(2015)
The STAR collaboration presents for the first time two-dimensional di-hadron correlations with identified leading hadrons in 200 GeV central Au+Au and minimum-bias d+Au collisions to explore hadronization mechanisms in the quark gluon plasma. The enhancement of the jet-like yield for leading pions in Au+Au data with respect to the d+Au reference and the absence of such an enhancement for leading non-pions (protons and kaons) are discussed within the context of a quark recombination scenario. The correlated yield at large angles, specifically in the \emph{ridge region}, is found to be significantly higher for leading non-pions than pions. The consistencies of the constituent quark scaling, azimuthal harmonic model and a mini-jet modification model description of the data are tested, providing further constraints on hadronization.
Dihadron angular correlations in d + Au collisions at √sNN = 200 GeV are reported as a function of the measured zero-degree calorimeter neutral energy and the forward charged hadron multiplicity in the Au-beam direction. A finite correlated yield is observed at large relative pseudorapidity (η) on the near side (i.e. relative azimuth φ ∼ 0). This correlated yield as a function of η appears to scale with the dominant, primarily jet-related, away-side (φ ∼ π) yield. The Fourier coefficients of the φ correlation, Vn = (cosnφ), have a strong η dependence. In addition, it is found that V1 is approximately inversely proportional to the mid-rapidity event multiplicity, while V2 is independent of it with similar magnitude in the forward (d-going) and backward (Au-going) directions.
Effect of event selection on jetlike correlation measurement in d+Au collisions at √sNN = 200 GeV
(2015)
Dihadron correlations are analyzed in √sNN = 200 GeV d + Au collisions classified by forward charged particle multiplicity and zero-degree neutral energy in the Au-beam direction. It is found that the jetlike correlated yield increases with the event multiplicity. After taking into account this dependence, the non-jet contribution on the away side is minimal, leaving little room for a back-to-back ridge in these collisions.
The transversity distribution, which describes transversely polarized quarks in transversely polarized nucleons, is a fundamental component of the spin structure of the nucleon, and is only loosely constrained by global fits to existing semi-inclusive deep inelastic scattering (SIDIS) data. In transversely polarized p↑+p collisions it can be accessed using transverse polarization dependent fragmentation functions which give rise to azimuthal correlations between the polarization of the struck parton and the final state scalar mesons.This letter reports on spin dependent di-hadron correlations measured by the STAR experiment. The new dataset corresponds to 25 pb−1 integrated luminosity of p↑+p collisions at s=500 GeV, an increase of more than a factor of ten compared to our previous measurement at s=200 GeV. Non-zero asymmetries sensitive to transversity are observed at a Q2 of several hundred GeV and are found to be consistent with the former measurement and a model calculation. We expect that these data will enable an extraction of transversity with comparable precision to current SIDIS datasets but at much higher momentum transfers where subleading effects are suppressed.
Famotidine inhibits toll-like receptor 3-mediated inflammatory signaling in SARS-CoV-2 infection
(2021)
Apart from prevention using vaccinations, the management options for COVID-19 remain limited. In retrospective cohort studies, use of famotidine, a specific oral H2 receptor antagonist (antihistamine), has been associated with reduced risk of intubation and death in patients hospitalized with COVID-19. In a case series, nonhospitalized patients with COVID-19 experienced rapid symptom resolution after taking famotidine, but the molecular basis of these observations remains elusive. Here we show using biochemical, cellular, and functional assays that famotidine has no effect on viral replication or viral protease activity. However, famotidine can affect histamine-induced signaling processes in infected Caco2 cells. Specifically, famotidine treatment inhibits histamine-induced expression of Toll-like receptor 3 (TLR3) in SARS-CoV-2 infected cells and can reduce TLR3-dependent signaling processes that culminate in activation of IRF3 and the NF-κB pathway, subsequently controlling antiviral and inflammatory responses. SARS-CoV-2-infected cells treated with famotidine demonstrate reduced expression levels of the inflammatory mediators CCL-2 and IL6, drivers of the cytokine release syndrome that precipitates poor outcome for patients with COVID-19. Given that pharmacokinetic studies indicate that famotidine can reach concentrations in blood that suffice to antagonize histamine H2 receptors expressed in mast cells, neutrophils, and eosinophils, these observations explain how famotidine may contribute to the reduced histamine-induced inflammation and cytokine release, thereby improving the outcome for patients with COVID-19.