CAMCAT: an oil spill forecasting system for the Catalan-Balearic Sea based on the MFS products

International audienceThe Prestige oil spill crisis (2002?2003), one of the worst oil spills that affected the Atlantic Spanish coastal line, pointed out that some management tools are needed in the form of laws, regulations and technical procedures. In particular, the issues are contingency planning and prevention against marine pollution and prediction for a proper response. In that background, the Catalan local government approved the CAMCAT (2004), a Regional contingency plan against marine pollution, to be framed within the (Spanish) National Contingency Plan. The CAMCAT contemplated the implementation of a Regional Forecasting System for the North-Western Mediterranean area, intended to help Catalan Authorities during any pollution emergency. The Laboratory of Maritime Engineering (LIM/UPC) has been responsible for the implementation of this Regional CAMCAT Forecasting System that is based (nested) on existing larger Forecasting Systems/Products, and it integrates several coastal observational data. The present paper is aiming to make an overview of the several scientific and technical activities related to the implementation and validation of the CAMCAT System

Integrated test environment for a part of the LHCb calorimeter - TWEPP09

An integrated test environment for the data acquisition electronics of the Scintillator Pad Detector (SPD) from the calorimeter of the LHCb experiment is presented. It allows to test separately every single board or to perform global system tests, while being able to emulate every part of the system and debug it. This environment is foreseen to test the production of spare electronic boards and help the maintenance of the SPD electronics along the life of the detector. The heart of the system is an Altera Stratix II FPGA while the main board can be controlled over USB, Ethernet or WiFi

Observation of Z production in proton-lead collisions at LHCb

The first observation of Z boson production in proton-lead collisions at a centreof-mass energy per proton-nucleon pair of √ sNN = 5 TeV is presented. The data sample corresponds to an integrated luminosity of 1.6 nb−1 collected with the LHCb detector. The Z candidates are reconstructed from pairs of oppositely charged muons with pseudorapidities between 2.0 and 4.5 and transverse momenta above 20 GeV/c. The invariant dimuon mass is restricted to the range 60 − 120 GeV/c2 . The Z production cross-section is measured to be σZ→µ+µ− (fwd) = 13.5 +5.4 −4.0 (stat.) ± 1.2(syst.) nb in the direction of the proton beam and σZ→µ+µ− (bwd) = 10.7 +8.4 −5.1 (stat.) ± 1.0(syst.) nb in the direction of the lead beam, where the first uncertainty is statistical and the second systematic

Effect of ischemic preconditioning and a Kv7 channel blocker on cardiac ischemia-reperfusion injury in rats

Recently, we found cardioprotective effects of ischemic preconditioning (IPC), and from a blocker of KCNQ voltage-gated K+ channels (KV7), XE991 (10,10-bis(4-pyridinylmethyl)-9(10H)-anthracenone), in isolated rat hearts. The purpose of the present study was to investigate the cardiovascular effects of IPC and XE991 and whether they are cardioprotective in intact rats. In conscious rats, we measured the effect of the KV7 channel blocker XE991 on heart rate and blood pressure by use of telemetry. In anesthetized rats, cardiac ischemia was induced by occluding the left coronary artery, and the animals received IPC (2 × 5 min of occlusion), XE991, or a combination. After a 2 h reperfusion period, the hearts were excised, and the area at risk and infarct size were determined. In both anesthetized and conscious rats, XE991 increased blood pressure, and the highest dose (7.5 mg/kg) of XE991 also increased heart rate, and 44% of conscious rats died. XE991 induced marked changes in the electrocardiogram (e.g., increased PR interval and prolonged QTC interval) without changing cardiac action potentials. The infarct size to area at risk ratio was reduced from 53 ± 2% (n = 8) in the vehicle compared to 36 ± 3% in the IPC group (P < 0.05, n = 9). XE991 (0.75 mg/kg) treatment alone or on top of IPC failed to reduce myocardial infarct size. Similar to the effect in isolated hearts, locally applied IPC was cardioprotective in intact animals exposed to ischemia-reperfusion. Systemic administration of XE991 failed to protect the heart against ischemia-reperfusion injury suggesting effects on the autonomic nervous system counteracting the cardioprotection in intact animals. © 2019 Elsevier B.V.Aarhus Universitets ForskningsfondHjerteforeningen: 17-R116-A7616-22074K. Corydon was supported by a scholarship from Aarhus University Research Foundation , U. Simonsen and E.R. Hedegaard were supported by the Danish Heart Foundation (grant 17-R116-A7616-22074 ). The study was also supported by Jens Anker Andersens Foundation, Helge and Peter Kornings Foundation, Direktør Kurt Bønnelycke and wife Mrs Grethe Bønnelyckes Foundation, Helge Peetz and Verner Peetz and wife Vilma Peetz grant. Appendix

Immune-related gene expression profiling after PD-1 blockade in non–small cell lung carcinoma, head and neck squamous cell carcinoma, and melanoma

Antibody targeting of the immune checkpoint receptor PD1 produces therapeutic activity in a variety of solid tumors, but most patients exhibit partial or complete resistance to treatment for reasons that are unclear. In this study, we evaluated tumor specimens from 65 patients with melanoma, lung nonsquamous, squamous cell lung or head and neck cancers who were treated with the approved PD1-targeting antibodies pembrolizumab or nivolumab. Tumor RNA before anti-PD1 therapy was analyzed on the nCounter system using the PanCancer 730-Immune Panel, and we identified 23 immune-related genes or signatures linked to response and progression-free survival (PFS). In addition, we evaluated intra- and interbiopsy variability of PD1, PD-L1, CD8A, and CD4 mRNAs and their relationship with tumor-infiltrating lymphocytes (TIL) and PD-L1 IHC expression. Among the biomarkers examined, PD1 gene expression along with 12 signatures tracking CD8 and CD4 T-cell activation, natural killer cells, and IFN activation associated significantly with nonprogressive disease and PFS. These associations were independent of sample timing, drug used, or cancer type. TIL correlated moderately (~0.50) with PD1 and CD8A mRNA levels and weakly (~0.35) with CD4 and PD-L1. IHC expression of PD-L1 correlated strongly with PD-L1 (0.90), moderately with CD4 and CD8A, and weakly with PD1. Reproducibility of gene expression in intra- and interbiopsy specimens was very high (total SD <3%). Overall, our results support the hypothesis that identification of a preexisting and stable adaptive immune response as defined by mRNA expression pattern is reproducible and sufficient to predict clinical outcome, regardless of the type of cancer or the PD1 therapeutic antibody administered to patients

Search for CP violation in D+→ϕπ+ and D+s→K0Sπ+ decays

A search for CP violation in D + → ϕπ + decays is performed using data collected in 2011 by the LHCb experiment corresponding to an integrated luminosity of 1.0 fb−1 at a centre of mass energy of 7 TeV. The CP -violating asymmetry is measured to be (−0.04 ± 0.14 ± 0.14)% for candidates with K − K + mass within 20 MeV/c 2 of the ϕ meson mass. A search for a CP -violating asymmetry that varies across the ϕ mass region of the D + → K − K + π + Dalitz plot is also performed, and no evidence for CP violation is found. In addition, the CP asymmetry in the D+s→K0Sπ+ decay is measured to be (0.61 ± 0.83 ± 0.14)%

Differential branching fraction and angular analysis of the decay B0→K∗0μ+μ−

The angular distribution and differential branching fraction of the decay B 0→ K ∗0 μ + μ − are studied using a data sample, collected by the LHCb experiment in pp collisions at s√=7 TeV, corresponding to an integrated luminosity of 1.0 fb−1. Several angular observables are measured in bins of the dimuon invariant mass squared, q 2. A first measurement of the zero-crossing point of the forward-backward asymmetry of the dimuon system is also presented. The zero-crossing point is measured to be q20=4.9±0.9GeV2/c4 , where the uncertainty is the sum of statistical and systematic uncertainties. The results are consistent with the Standard Model predictions

Belle II Technical Design Report

The Belle detector at the KEKB electron-positron collider has collected almost 1 billion Y(4S) events in its decade of operation. Super-KEKB, an upgrade of KEKB is under construction, to increase the luminosity by two orders of magnitude during a three-year shutdown, with an ultimate goal of 8E35 /cm^2 /s luminosity. To exploit the increased luminosity, an upgrade of the Belle detector has been proposed. A new international collaboration Belle-II, is being formed. The Technical Design Report presents physics motivation, basic methods of the accelerator upgrade, as well as key improvements of the detector.Comment: Edited by: Z. Dole\v{z}al and S. Un

Search for the lepton-flavor-violating decays Bs0→e±μ∓ and B0→e±μ∓

A search for the lepton-flavor-violating decays Bs0→e±μ∓ and B0→e±μ∓ is performed with a data sample, corresponding to an integrated luminosity of 1.0  fb-1 of pp collisions at √s=7  TeV, collected by the LHCb experiment. The observed number of Bs0→e±μ∓ and B0→e±μ∓ candidates is consistent with background expectations. Upper limits on the branching fractions of both decays are determined to be B(Bs0→e±μ∓)101  TeV/c2 and MLQ(B0→e±μ∓)>126  TeV/c2 at 95% C.L., and are a factor of 2 higher than the previous bounds

Observation of the decay Bc→J/ψK+K−π+B_c \rightarrow J/\psi K^+ K^- \pi^+

The decay $B_c\rightarrow J/\psi K^+ K^- \pi^+$ is observed for the first time, using proton-proton collisions collected with the LHCb detector corresponding to an integrated luminosity of 3fb$^{-1}$. A signal yield of $78\pm14$ decays is reported with a significance of 6.2 standard deviations. The ratio of the branching fraction of \B_c \rightarrow J/\psi K^+ K^- \pi^+ decays to that of $B_c \rightarrow J/\psi \pi^+$ decays is measured to be $0.53\pm 0.10\pm0.05$, where the first uncertainty is statistical and the second is systematic.Comment: 18 pages, 2 figure