The type II-plateau supernova 2017eaw in NGC 6946 and its red supergiant progenitor

We present extensive optical photometric and spectroscopic observations, from 4 to 482 days after explosion, of the Type II-plateau (II-P) supernova (SN) 2017eaw in NGC 6946. SN 2017eaw is a normal SN II-P intermediate in properties between, for example, SN 1999em and SN 2012aw and the more luminous SN 2004et, also in NGC 6946. We have determined that the extinction to SN 2017eaw is primarily due to the Galactic foreground and that the SN site metallicity is likely subsolar. We have also independently confirmed a tip-of-the-red-giant-branch (TRGB) distance to NGC 6946 of 7.73 ± 0.78 Mpc. The distances to the SN that we have also estimated via both the standardized candle method and expanding photosphere method corroborate the TRGB distance. We confirm the SN progenitor identity in pre-explosion archival Hubble Space Telescope (HST) and Spitzer Space Telescope images, via imaging of the SN through our HST Target of Opportunity program. Detailed modeling of the progenitor's spectral energy distribution indicates that the star was a dusty, luminous red supergiant consistent with an initial mass of ~15 M ⊙

Sn 2017fgc: A fast-expanding type ia supernova exploded in massive shell galaxy ngc 474

We present extensive optical photometric and spectroscopic observations of the high-velocity (HV) Type Ia supernova (SN Ia) 2017fgc, covering the phase from ~12 days before to ~389 days after maximum brightness. SN 2017fgc is similar to normal SNe Ia, with an absolute peak magnitude of MB max -19.32 ± 0.13 mag and a postpeak decline of ?m15(B) = 1.05 ± 0.07 mag. Its peak bolometric luminosity is derived as (1.32 ± 0.13) × 1043 erg s-1, corresponding to a 56Ni mass of 0.51 ± 0.03Me. The light curves of SN 2017fgc are found to exhibit excess emission in the UBV bands in the early nebular phase and pronounced secondary shoulder/maximum features in the RrIi bands. Its spectral evolution is similar to that of HV SNe Ia, with a maximum-light Si II velocity of 15,000 ± 150 km s-1 and a post-peak velocity gradient of ~120 ± 10 km s-1 day-1. The Fe II and Mg II lines blended near 4300 Å and the Fe II, Si II, and Fe III lines blended near 4800 Å are obviously stronger than those of normal SNe Ia. Inspecting a large sample reveals that the strength of the two blends in the spectra, and the secondary peak in the i/r-band light curves, are found to be positively correlated with the maximum-light Si II velocity. Such correlations indicate that HV SNe Ia may experience more complete burning in the ejecta and/or that their progenitors have higher metallicity. Examining the birthplace environment of SN 2017fgc suggests that it likely arose from a stellar environment with young and high-metallicity populations. © 2021 Institute of Physics Publishing. All rights reserved.Immediate accessThis item from the UA Faculty Publications collection is made available by the University of Arizona with support from the University of Arizona Libraries. If you have questions, please contact us at [email protected]

A randomised, blinded, trial of clopidogrel versus aspirin in patients at risk of ischaemic events (CAPRIE). CAPRIE Steering Committee

Many clinical trials have evaluated the benefit of long-term use of antiplatelet drugs in reducing the risk of clinical thrombotic events. Aspirin and ticlopidine have been shown to be effective, but both have potentially serious adverse effects. Clopidogrel, a new thienopyridine derivative similar to ticlopidine, is an inhibitor of platelet aggregation induced by adenosine diphosphate. METHODS: CAPRIE was a randomised, blinded, international trial designed to assess the relative efficacy of clopidogrel (75 mg once daily) and aspirin (325 mg once daily) in reducing the risk of a composite outcome cluster of ischaemic stroke, myocardial infarction, or vascular death; their relative safety was also assessed. The population studied comprised subgroups of patients with atherosclerotic vascular disease manifested as either recent ischaemic stroke, recent myocardial infarction, or symptomatic peripheral arterial disease. Patients were followed for 1 to 3 years. FINDINGS: 19,185 patients, with more than 6300 in each of the clinical subgroups, were recruited over 3 years, with a mean follow-up of 1.91 years. There were 1960 first events included in the outcome cluster on which an intention-to-treat analysis showed that patients treated with clopidogrel had an annual 5.32% risk of ischaemic stroke, myocardial infarction, or vascular death compared with 5.83% with aspirin. These rates reflect a statistically significant (p = 0.043) relative-risk reduction of 8.7% in favour of clopidogrel (95% Cl 0.3-16.5). Corresponding on-treatment analysis yielded a relative-risk reduction of 9.4%. There were no major differences in terms of safety. Reported adverse experiences in the clopidogrel and aspirin groups judged to be severe included rash (0.26% vs 0.10%), diarrhoea (0.23% vs 0.11%), upper gastrointestinal discomfort (0.97% vs 1.22%), intracranial haemorrhage (0.33% vs 0.47%), and gastrointestinal haemorrhage (0.52% vs 0.72%), respectively. There were ten (0.10%) patients in the clopidogrel group with significant reductions in neutrophils (< 1.2 x 10(9)/L) and 16 (0.17%) in the aspirin group. INTERPRETATION: Long-term administration of clopidogrel to patients with atherosclerotic vascular disease is more effective than aspirin in reducing the combined risk of ischaemic stroke, myocardial infarction, or vascular death. The overall safety profile of clopidogrel is at least as good as that of medium-dose aspirin

Vorapaxar in the secondary prevention of atherothrombotic events

Item does not contain fulltextBACKGROUND: Thrombin potently activates platelets through the protease-activated receptor PAR-1. Vorapaxar is a novel antiplatelet agent that selectively inhibits the cellular actions of thrombin through antagonism of PAR-1. METHODS: We randomly assigned 26,449 patients who had a history of myocardial infarction, ischemic stroke, or peripheral arterial disease to receive vorapaxar (2.5 mg daily) or matching placebo and followed them for a median of 30 months. The primary efficacy end point was the composite of death from cardiovascular causes, myocardial infarction, or stroke. After 2 years, the data and safety monitoring board recommended discontinuation of the study treatment in patients with a history of stroke owing to the risk of intracranial hemorrhage. RESULTS: At 3 years, the primary end point had occurred in 1028 patients (9.3%) in the vorapaxar group and in 1176 patients (10.5%) in the placebo group (hazard ratio for the vorapaxar group, 0.87; 95% confidence interval [CI], 0.80 to 0.94; P<0.001). Cardiovascular death, myocardial infarction, stroke, or recurrent ischemia leading to revascularization occurred in 1259 patients (11.2%) in the vorapaxar group and 1417 patients (12.4%) in the placebo group (hazard ratio, 0.88; 95% CI, 0.82 to 0.95; P=0.001). Moderate or severe bleeding occurred in 4.2% of patients who received vorapaxar and 2.5% of those who received placebo (hazard ratio, 1.66; 95% CI, 1.43 to 1.93; P<0.001). There was an increase in the rate of intracranial hemorrhage in the vorapaxar group (1.0%, vs. 0.5% in the placebo group; P<0.001). CONCLUSIONS: Inhibition of PAR-1 with vorapaxar reduced the risk of cardiovascular death or ischemic events in patients with stable atherosclerosis who were receiving standard therapy. However, it increased the risk of moderate or severe bleeding, including intracranial hemorrhage. (Funded by Merck; TRA 2P-TIMI 50 ClinicalTrials.gov number, NCT00526474.)