Increased prevalence of Human Polyomavirus JC viruria in Chronic Inflammatory Rheumatic Diseases patients in treatment with anti-TNF α: a 18 month follow-up study.

Chronic inflammatory rheumatic diseases (CIRDs) are immune-mediated pathologies involving joints. To date, TNFα-blocking agents administration is the most promising therapy, although these treatments are associated with an increased Polyomavirus JC (JCPyV) reactivation, the etiological agent of the Progressive Multifocal Leukoencephalopathy (PML). The aim of this study was the recruitment and the analysis of a CIRDs cohort in order to investigate a possible correlation between JCPyV presence and the influence of anti-TNF-α agents on viral loads. Blood and urine samples were collected from 34 CIRDs subjects prior the first anti-TNF-α infusion (T0) and after 3 (T3), 6 (T6), 12 (T12), and 18 (T18) months. Results showed persistent JC viruria significantly higher than JC viremia throughout the 18 month follow-up study (p=0.002). In JCPyV positive samples, the non-coding control region (NCCR) was analyzed. Results evidenced archetypal structures (type II-S) in all isolates with the exception of a sequence isolated from a plasma sample, that corresponds to the type II-R found in PML subjects. Finally, the viral protein 1 (VP1) genotyping was performed and results showed the prevalence of the European genotypes 1A, 1B, and 4. Since only few studies have been carried out to understand whether there is a PML risk in CIRDs population infected by JCPyV, this study contributes to enrich literature insight on JCPyV biology in this cluster. Further investigations are necessary in order to recognize the real impact of biologics on JCPyV life cycle and to identify possible and specific viral variants related to increased virulence in CIRDs patient

Precise mirror alignment and basic performance of the RICH detector of the NA62 experiment at CERN

The Ring Imaging Cherenkov detector is crucial for the identification of charged particles in the NA62 experiment at the CERN SPS. The detector commissioning was completed in 2016 by the precise alignment of mirrors using reconstructed tracks. The alignment procedure and measurement of the basic performance are described. Ring radius resolution, ring centre resolution, single hit resolution and mean number of hits per ring are evaluated for positron tracks. The contribution of the residual mirror misalignment to the performance is calculated.Comment: 13 pages, 10 figure

Measurement of the branching ratio of the decay Ξ0→Σ+μ−νˉμ\Xi^{0}\rightarrow \Sigma^{+} \mu^{-} \bar{\nu}_{\mu}

From the 2002 data taking with a neutral kaon beam extracted from the CERN-SPS, the NA48/1 experiment observed 97 $\Xi^{0}\rightarrow \Sigma^{+} \mu^{-} \bar{\nu}_{\mu}$ candidates with a background contamination of $30.8 \pm 4.2$ events. From this sample, the BR($\Xi^{0}\rightarrow \Sigma^{+} \mu^{-} \bar{\nu}_{\mu}$) is measured to be $(2.17 \pm 0.32_{\mathrm{stat}}\pm 0.17_{\mathrm{syst}})\times10^{-6}$

Observation of the rare decay K_S -> pi^0mu^+mu^-

A search for the decay K_S -> pi^0mu^+mu^- has been made by the NA48/1 Collaboration at the CERN SPS accelerator. The data were collected during 2002 with a high-intensity K_S beam. Six events were found with a background expectation of 0.22^+0.18_-0.11 event. Using a vector matrix element and unit form factor, the measured branching ratio is B(K_S -> pi^0mu^+mu^-)=[2.9^+1.5_-1.2(stat)+/-0.2(syst)]x10^{-9}.Comment: 19 pages, 8 figures, 4 tables. To be published in Physics Letters

Natalizumab affects T-cell phenotype in multiple sclerosis: implications for JCV reactivation

The anti-CD49d monoclonal antibody natalizumab is currently an effective therapy against the relapsing-remitting form of multiple sclerosis (RRMS). Natalizumab therapeutic efficacy is limited by the reactivation of the John Cunningham polyomavirus (JCV) and development of progressive multifocal leukoencephalopathy (PML). To correlate natalizumab-induced phenotypic modifications of peripheral blood T-lymphocytes with JCV reactivation, JCV-specific antibodies (serum), JCV-DNA (blood and urine), CD49d expression and relative abundance of peripheral blood T-lymphocyte subsets were longitudinally assessed in 26 natalizumab-treated RRMS patients. Statistical analyses were performed using GraphPad Prism and R. Natalizumab treatment reduced CD49d expression on memory and effector subsets of peripheral blood T-lymphocytes. Moreover, accumulation of peripheral blood CD8+ memory and effector cells was observed after 12 and 24 months of treatment. CD4+ and CD8+ T-lymphocyte immune-activation was increased after 24 months of treatment. Higher percentages of CD8+ effectors were observed in subjects with detectable JCV-DNA. Natalizumab reduces CD49d expression on CD8+ T-lymphocyte memory and effector subsets, limiting their migration to the central nervous system and determining their accumulation in peripheral blood. Impairment of central nervous system immune surveillance and reactivation of latent JCV, can explain the increased risk of PML development in natalizumab-treated RRMS subjects

First observation of the KS->pi0 gamma gamma decay

Using the NA48 detector at the CERN SPS, 31 KS->pi0 gamma gamma candidates with an estimated background of 13.7 +- 3.2 events have been observed. This first observation leads to a branching ratio of BR(KS->pi0 gamma gamma) = (4.9 +- 1.6(stat) +- 0.9(syst)) x 10^-8 in agreement with Chiral Perturbation theory predictions.Comment: 10 pages, 4 figures submitted to Phys. Lett.

A precision measurement of direct CP violation in the decay of neutral kaons into two pions

The direct CP violation parameter Re(epsilon'/epsilon) has been measured from the decay rates of neutral kaons into two pions using the NA48 detector at the CERN SPS. The 2001 running period was devoted to collecting additional data under varied conditions compared to earlier years (1997-99). The new data yield the result: Re(epsilon'/epsilon) = (13.7 +/- 3.1) times 10^{-4}. Combining this result with that published from the 1997, 98 and 99 data, an overall value of Re(epsilon'/epsilon) = (14.7 +/- 2.2) times 10^{-4} is obtained from the NA48 experiment.Comment: 19 pages, 5 figures, to be published in Physics Letters

Atmospheric Muon Flux at Sea Level, Underground, and Underwater

The vertical sea-level muon spectrum at energies above 1 GeV and the underground/underwater muon intensities at depths up to 18 km w.e. are calculated. The results are particularly collated with a great body of the ground-level, underground, and underwater muon data. In the hadron-cascade calculations, the growth with energy of inelastic cross sections and pion, kaon, and nucleon generation in pion-nucleus collisions are taken into account. For evaluating the prompt muon contribution to the muon flux, we apply two phenomenological approaches to the charm production problem: the recombination quark-parton model and the quark-gluon string model. To solve the muon transport equation at large depths of homogeneous medium, a semi-analytical method is used. The simple fitting formulas describing our numerical results are given. Our analysis shows that, at depths up to 6-7 km w. e., essentially all underground data on the muon intensity correlate with each other and with predicted depth-intensity relation for conventional muons to within 10%. However, the high-energy sea-level data as well as the data at large depths are contradictory and cannot be quantitatively decribed by a single nuclear-cascade model.Comment: 47 pages, REVTeX, 15 EPS figures included; recent experimental data and references added, typos correcte

Measurement of the branching ratios of the decays Xi0 --> Sigma+ e- nubar and anti-Xi0 --> anti-Sigma+ e+ nu

From 56 days of data taking in 2002, the NA48/1 experiment observed 6316 Xi0 --> Sigma+ e- nubar candidates (with the subsequent Sigma+ --> p pi0 decay) and 555 anti-Xi0 --> anti-Sigma+ e+ nu candidates with background contamination of 215+-44 and 136+-8 events, respectively. From these samples, the branching ratios BR(Xi0 --> Sigma+ e- nubar)= (2.51+-0.03stat+-0.09syst)E(-4) and BR(anti-Xi0 --> anti-Sigma+ e+ nu)= (2.55+-0.14stat+-0.10syst)E(-4) were measured allowing the determination of the CKM matrix element |Vus| = 0.209+0.023-0.028. Using the Particle Data Group average for |Vus| obtained in semileptonic kaon decays, we measured the ratio g1/f1 = 1.20+-0.05 of the axial-vector to vector form factors.Comment: 16 pages, 11 figures Submitted to Phys.Lett.