Tmetoceratidae (Ammonitina) fauna from the Gerecse Mts (Hungary)

Abstract Taxonomic and stratigraphic problems of the family Tmetoceratidae and the genera Dumortieria, Catulloceras, Cotteswoldia, Pleydellia and Tmetoceras included in it are briefly discussed. Fifteen species of Tmetoceratidae are described and illustrated from the Upper Toarcian-Aalenian ammonite assemblages of the Gerecse Mts (NE Transdanubian Range, Hungary). The fauna described here is closely allied to the Mediterranean Province of the Mediterranean-Caucasian Realm

Ammonite stratigraphy of a Toarcian (Lower Jurassic) section on Nagy-Pisznice Hill (Gerecse Mts, Hungary)

Abstract In the Jurassic rocks exposed in a small abandoned quarry on the northwestern edge of Nagy-Pisznice Hill in the Gerecse Mts, fairly well preserved parts of a crocodile skeleton was found in 1996. The bed which yielded the skeletal remains is the uppermost layer of the Kisgerecse Marl Formation exposed here and was determined as belonging to the Upper Toarcian Grammoceras thouarsense Zone. The beds of the sequence above and below were carefully sampled in the late 1990s, and the encountered ammonites were evaluated biostratigraphically. As a result, the Lower Toarcian Harpoceras serpentinum Zone, the Middle Toarcian Hildoceras bifrons and Merlaites gradatus Zones, and the Upper Toarcian Grammoceras thouarsense and Geczyceras speciosum Zones were identified. Within most of these zones the subzones and even the faunal horizons were successfully recognized. The lowermost beds above the underlying Pliensbachian red limestone did not yield any fossils; thus the lowermost Toarcian Dactylioceras tenuicostatum Zone could not be documented. The highest Toarcian ammonite zones also remained unidentified, because the beds of the Tölgyhát Limestone above were not sampled all the way up. This paper presents the lithostratigraphic and biostratigraphic details of the sequence, and the paleontological descriptions of the most important ammonites

Trapping in irradiated p-on-n silicon sensors at fluences anticipated at the HL-LHC outer tracker

The degradation of signal in silicon sensors is studied under conditions expected at the CERN High-Luminosity LHC. 200 $\mu$m thick n-type silicon sensors are irradiated with protons of different energies to fluences of up to $3 \cdot 10^{15}$ neq/cm$^2$. Pulsed red laser light with a wavelength of 672 nm is used to generate electron-hole pairs in the sensors. The induced signals are used to determine the charge collection efficiencies separately for electrons and holes drifting through the sensor. The effective trapping rates are extracted by comparing the results to simulation. The electric field is simulated using Synopsys device simulation assuming two effective defects. The generation and drift of charge carriers are simulated in an independent simulation based on PixelAV. The effective trapping rates are determined from the measured charge collection efficiencies and the simulated and measured time-resolved current pulses are compared. The effective trapping rates determined for both electrons and holes are about 50% smaller than those obtained using standard extrapolations of studies at low fluences and suggests an improved tracker performance over initial expectations

Precise determination of the mass of the Higgs boson and tests of compatibility of its couplings with the standard model predictions using proton collisions at 7 and 8 TeV

Peer reviewe

Observation of the diphoton decay of the Higgs boson and measurement of its properties

Peer reviewe

Search for Dark Matter and Supersymmetry with a Compressed Mass Spectrum in the Vector Boson Fusion Topology in Proton-Proton Collisions at root s=8 TeV

Peer reviewe

Antiinflammatory Therapy with Canakinumab for Atherosclerotic Disease

Background: Experimental and clinical data suggest that reducing inflammation without affecting lipid levels may reduce the risk of cardiovascular disease. Yet, the inflammatory hypothesis of atherothrombosis has remained unproved. Methods: We conducted a randomized, double-blind trial of canakinumab, a therapeutic monoclonal antibody targeting interleukin-1β, involving 10,061 patients with previous myocardial infarction and a high-sensitivity C-reactive protein level of 2 mg or more per liter. The trial compared three doses of canakinumab (50 mg, 150 mg, and 300 mg, administered subcutaneously every 3 months) with placebo. The primary efficacy end point was nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death. RESULTS: At 48 months, the median reduction from baseline in the high-sensitivity C-reactive protein level was 26 percentage points greater in the group that received the 50-mg dose of canakinumab, 37 percentage points greater in the 150-mg group, and 41 percentage points greater in the 300-mg group than in the placebo group. Canakinumab did not reduce lipid levels from baseline. At a median follow-up of 3.7 years, the incidence rate for the primary end point was 4.50 events per 100 person-years in the placebo group, 4.11 events per 100 person-years in the 50-mg group, 3.86 events per 100 person-years in the 150-mg group, and 3.90 events per 100 person-years in the 300-mg group. The hazard ratios as compared with placebo were as follows: in the 50-mg group, 0.93 (95% confidence interval [CI], 0.80 to 1.07; P = 0.30); in the 150-mg group, 0.85 (95% CI, 0.74 to 0.98; P = 0.021); and in the 300-mg group, 0.86 (95% CI, 0.75 to 0.99; P = 0.031). The 150-mg dose, but not the other doses, met the prespecified multiplicity-adjusted threshold for statistical significance for the primary end point and the secondary end point that additionally included hospitalization for unstable angina that led to urgent revascularization (hazard ratio vs. placebo, 0.83; 95% CI, 0.73 to 0.95; P = 0.005). Canakinumab was associated with a higher incidence of fatal infection than was placebo. There was no significant difference in all-cause mortality (hazard ratio for all canakinumab doses vs. placebo, 0.94; 95% CI, 0.83 to 1.06; P = 0.31). Conclusions: Antiinflammatory therapy targeting the interleukin-1β innate immunity pathway with canakinumab at a dose of 150 mg every 3 months led to a significantly lower rate of recurrent cardiovascular events than placebo, independent of lipid-level lowering. (Funded by Novartis; CANTOS ClinicalTrials.gov number, NCT01327846.