Search for the baryon- and lepton-number violating decays B0 →pμ- and Bs0 →pμ

A search for the baryon- and lepton-number violating decays B0→pμ- and Bs0→pμ- is performed at the LHCb experiment using data collected in proton-proton collisions at s=7, 8 and 13 TeV, corresponding to integrated luminosities of 1, 2, and 6 fb-1, respectively. No significant signal for B0→pμ- and Bs0→pμ- decays is found and the upper limits on the branching fractions are determined to be B(B0→pμ-)<2.6(3.1)×10-9 and B(Bs0→pμ-)<12.1(14.0)×10-9, respectively, at 90% (95%) confidence level. These are the first limits on these decays to date

First observation of the B+ → Ds+ Ds- K+ decay

The B+→Ds+Ds-K+ decay is observed for the first time using proton-proton collision data collected by the LHCb detector at center-of-mass energies of 7, 8, and 13 TeV, corresponding to an integrated luminosity of 9 fb-1. Its branching fraction relative to that of the B+→D+D-K+ decay is measured to be B(B+→Ds+Ds-K+)B(B+→D+D-K+)=0.525±0.033±0.027±0.034, where the first uncertainty is statistical, the second systematic, and the third is due to the uncertainties on the branching fractions of the Ds±→K∓K±π± and D±→K∓π±π± decays. This measurement fills an experimental gap in the knowledge of the family of Cabibbo-favored b¯→c¯cs¯ transitions and opens the path for unique studies of spectroscopy in future. © 2023 CERN.<br/

First observation of the B+ → Ds+ Ds- K+ decay

The B+→Ds+Ds-K+ decay is observed for the first time using proton-proton collision data collected by the LHCb detector at center-of-mass energies of 7, 8, and 13 TeV, corresponding to an integrated luminosity of 9 fb-1. Its branching fraction relative to that of the B+→D+D-K+ decay is measured to be B(B+→Ds+Ds-K+)B(B+→D+D-K+)=0.525±0.033±0.027±0.034, where the first uncertainty is statistical, the second systematic, and the third is due to the uncertainties on the branching fractions of the Ds±→K∓K±π± and D±→K∓π±π± decays. This measurement fills an experimental gap in the knowledge of the family of Cabibbo-favored b¯→c¯cs¯ transitions and opens the path for unique studies of spectroscopy in future. © 2023 CERN.<br/

Acute Delta Hepatitis in Italy spanning three decades (1991–2019): Evidence for the effectiveness of the hepatitis B vaccination campaign

Updated incidence data of acute Delta virus hepatitis (HDV) are lacking worldwide. Our aim was to evaluate incidence of and risk factors for acute HDV in Italy after the introduction of the compulsory vaccination against hepatitis B virus (HBV) in 1991. Data were obtained from the National Surveillance System of acute viral hepatitis (SEIEVA). Independent predictors of HDV were assessed by logistic-regression analysis. The incidence of acute HDV per 1-million population declined from 3.2 cases in 1987 to 0.04 in 2019, parallel to that of acute HBV per 100,000 from 10.0 to 0.39 cases during the same period. The median age of cases increased from 27 years in the decade 1991-1999 to 44 years in the decade 2010-2019 (p &lt; .001). Over the same period, the male/female ratio decreased from 3.8 to 2.1, the proportion of coinfections increased from 55% to 75% (p = .003) and that of HBsAg positive acute hepatitis tested for by IgM anti-HDV linearly decreased from 50.1% to 34.1% (p &lt; .001). People born abroad accounted for 24.6% of cases in 2004-2010 and 32.1% in 2011-2019. In the period 2010-2019, risky sexual behaviour (O.R. 4.2; 95%CI: 1.4-12.8) was the sole independent predictor of acute HDV; conversely intravenous drug use was no longer associated (O.R. 1.25; 95%CI: 0.15-10.22) with this. In conclusion, HBV vaccination was an effective measure to control acute HDV. Intravenous drug use is no longer an efficient mode of HDV spread. Testing for IgM-anti HDV is a grey area requiring alert. Acute HDV in foreigners should be monitored in the years to come

Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P &lt; 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD4OL (Spearman's rank correlation coefficient [r(s)], -0.33; P &lt; 0.001), sNox2-dp (r(s), -0.57; P &lt; 0.0001), and urinary excretion of isoprostanes (r(s), -0.48; P &lt; 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2 alpha-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation