Single star progenitors of long gamma-ray bursts I: Model grids and redshift dependent GRB rate

We present grids of massive star evolution models at four different metallicities (Z=0.004, 0.002, 0.001, 0.00001). The effects of rotation on the stellar structure and the transport of angular momentum and chemical elements through the Spruit-Tayler dynamo and rotationally induced instabilities are considered. After discussing uncertainties involved with the adopted physics, we elaborate the final fate of massive stars as a function of initial mass and spin rate, at each considered metallicity. In particular, we investigate for which initial conditions long gamma-ray bursts (GRBs) are expected to be produced in the frame of the collapsar model. Then, using an empirical spin distribution of young massive metal-poor stars and a specified metallicity-dependent history of star-formation, we compute the expected GRB rate as function of metallicity and redshift based on our stellar evolution models. The GRB production in our models is limited to metallicities of Z \lsim 0.004, with the consequence that about 50 % of all GRBs are predicted to be found at redshifts above z = 4, with most supernovae occurring at redshifts below z\simeq 2.2. The average GRB/SN ratio predicted by our model is about 1/200 globally, and 1/1250 at low redshift. Future strategies for testing the considered GRB progenitor scenario are briefly discussed.Comment: 17 pages, 10 figures, 6 tables, accpeted by A&A, corrected, reference adde

The connection between Gamma-ray bursts and Supernovae Ib/c

It has been established that Gamma-Ray Bursts (GRBs) are connected to Supernovae (SNe) explosions of Type Ib/c. We intend to test whether the hypothesis of Type Ib/c SNe from different massive progenitors can reproduce the local GRB rate as well as the GRB rate as a function of redshift. We aim to predict the GRB rate at very high redshift under different assumptions about galaxy formation and star formation histories in galaxies. We assume different star formation histories in galaxies of different morphological type: ellipticals, spirals and irregulars. We explore different hypotheses concerning the progenitors of Type Ib/c SNe. We find an excellent agreement between the observed GRB local rate and the predicted Type Ib/c SN rate in irregular galaxies, when a range for single Wolf-Rayet stars of 40-100 M_sun is adopted. We also predict the cosmic Type Ib/c SN rate by taking into account all the galaxy types in an unitary volume of the Universe and we compare it with the observed cosmic GRB rate as a function of redshift. By assuming the formation of spheroids at high redshift, we predict a cosmic Type Ib/c SN rate, which is always higher than the GRB rate, suggesting that only a small fraction (0.1-1 %) of Type Ib/c SNe become GRBs. In particular, we find a ratio between the cosmic GRB rate and the cosmic Type Ib/c rate in the range 0.001-0.01, in agreement with previous estimates. Finally, due to the high star formation in spheroids at high redshift, which is our preferred scenario for galaxy formation, we predict more GRBs at high redshift than in the hierarchical scenario for galaxy formation, a prediction which awaits to be proven by future observations.Comment: A&A, in press, 15 pages, 11 figure

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.