Measurements of the kinematic distributions of J /ψ mesons produced in p-C, p-Ti and p-W collisions at √ s = 41.6 GeV in the Feynman-x region −0.34 < x F < 0.14 and for transverse momentum up to p T = 5.4 GeV/c are presented. The x F and p T dependencies of the nuclear suppression parameter, α, are also given. The results are based on 2.4 × 10 5 J /ψ mesons reconstructed in both the e + e − and μ + μ − decay channels. The data have been collected by the HERA-B experiment at the HERA proton ring of the DESY laboratory. The measurement explores the negative region of x F for the first time. The average value of α in the measured x F region is 0.981 ± 0.015. The data suggest that the strong nuclear suppression of J /ψ production previously observed at high x F turns into an enhancement at negative x F .

Ratios of the ψ ′ over the J/ψ production cross sections in the dilepton channel for C, Ti and W targets have been measured in 920 GeV proton-nucleus interactions with the HERA-B detector at the HERA storage ring. The ψ ′ and J/ψ states were reconstructed in both the µ + µ − and the e + e − decay modes. The measurements covered the kinematic range −0.35 ≤ xF ≤ 0.1 with transverse momentum pT ≤ 4.5 GeV/c. The ψ ′ to J/ψ production ratio is almost constant in the covered xF range and shows a slow increase with pT. The angular dependence of the ratio has been used to measure the difference of the ψ ′ and J/ψ polarization. All results for the muon and electron decay channels are in good agreement: their ratio, averaged over all events, is R ψ ′ (µ)/R ψ ′ (e) = 1.00 ± 0.08 ± 0.04. This result constitutes a new, direct experimental constraint on the double ratio of branching fractions, (B ′ (µ) • B(e)) / (B(µ) • B ′ (e)), of ψ ′ and J/ψ in the two channels.

Purpose Vascular inflammation and disturbed metabolism are observed in heart failure and type 2 diabetes mellitus. Glycolytic enzyme hexokinase II (HKII) is upregulated by inflammation. We hypothesized that SGLT2 inhibitors Canagliflozin (Cana), Empagliflozin (Empa) or Dapagliflozin (Dapa) reduces inflammation via HKII in endothelial cells, and that HKII-dependent inflammation is determined by ERK1/2, NF-κB. and/or AMPK activity in lipopolysaccharide (LPS)-stimulated human coronary artery endothelial cells (HCAECs). Methods HCAECs were pre-incubated with 3 μM or 10 μM Cana, 1 μM, 3 μM or 10 μM Empa or 0.5 μM, 3 μM or 10 μM Dapa (16 h) and subjected to 3 h LPS (1 μg/mL). HKII was silenced via siRNA transfection. Interleukin-6 (IL-6) release was measured by ELISA. Protein levels of HK I and II, ERK1/2, AMPK and NF-κB were detected using infra-red western blot. Results LPS increased IL-6 release and ERK1/2 phosphorylation; Cana prevented these pro-inflammatory responses (IL-6: pg/ml, control 46 ± 2, LPS 280 ± 154 p < 0.01 vs. control, LPS + Cana 96 ± 40, p < 0.05 vs. LPS). Cana reduced HKII expression (HKII/GAPDH, control 0.91 ± 0.16, Cana 0.71 ± 0.13 p < 0.05 vs. control, LPS 1.02 ± 0.25, LPS + Cana 0.82 ± 0.24 p < 0.05 vs. LPS). Empa and Dapa were without effect on IL-6 release and HKII expression in the model used. Knockdown of HKII by 37% resulted caused partial loss of Cana-mediated IL-6 reduction (pg/ml, control 35 ± 5, LPS 188 ± 115 p < 0.05 vs. control, LPS + Cana 124 ± 75) and ERK1/2 activation by LPS. In LPS-stimulated HCAECs, Cana, but not Empa or Dapa, activated AMPK. AMPK activator A769662 reduced IL-6 release. Conclusion Cana conveys anti-inflammatory actions in LPS-treated HCAECs through 1) reductions in HKII and ERK1/2 phosphorylation and 2) AMPK activation. These data suggest a novel anti-inflammatory mechanism of Cana through HKII.

The inclusive production cross sections of the strange vector mesons K * 0 , K * 0 , and φ have been measured in interactions of 920 GeV protons with C, Ti, and W targets with the HERA-B detector at the HERA storage ring. Differential cross sections as a function of rapidity and transverse momentum have been measured in the central rapidity region and for transverse momenta up to pT = 3.5 GeV/c. The atomic number dependence is parametrised as σpA = σpN * A α , where σpN is the proton-nucleon cross section. Within the phase space accessible, α(K * 0) = 0.86 ± 0.03, α(K * 0) = 0.87 ± 0.03, and α(φ) = 0.96 ± 0.02. The total proton-nucleon cross sections, determined by extrapolating the differential measurements to full phase space, are σ pN→K * 0 = (5.06 ± 0.54) mb, σ pN→K * 0 = (4.02 ± 0.45) mb, and σ pN→φ = (1.17 ± 0.11) mb. For all resonances the Cronin effect is observed; compared to the measurements of Cronin et al. for K ± mesons, the measured values of α for φ mesons coincide with those of K + mesons for all transverse momenta, while the enhancement for K * 0 /K * 0 mesons is smaller.