The contribution from stars stripped in binaries to cosmic reionization of hydrogen and helium

Massive stars are often found in binary systems and it has been argued that binary products boost the ionizing radiation of stellar populations. Accurate predictions for binary products are needed to understand and quantify their contribution to Cosmic Reionization. We investigate the contribution of stars stripped in binaries since (1) they are, arguably, the best-understood products of binary evolution, (2) we recently produced the first non-LTE radiative transfer calculations for the atmospheres of these stripped stars that predict their ionizing spectra, and (3) they are very promising sources since they boost the ionizing emission of stellar populations at late times. This allows stellar feedback to clear the surroundings such that a higher fraction of their photons can escape and ionize the intergalactic medium. Combining our detailed predictions for the ionizing spectra with a simple cosmic reionization model, we estimate that stripped stars contributed tens of percent of the photons that caused cosmic reionization of hydrogen, depending on the assumed escape fractions. More importantly, stripped stars harden the ionizing emission. We estimate that the spectral index for the ionizing part of the spectrum can increase to -1 compared to <-2 for single stars. At high redshift, stripped stars and massive single stars combined dominate the HeII-ionizing emission, but we expect active galactic nuclei drive cosmic helium reionization. Further observational consequences we expect are (1) high ionization states for the intergalactic gas surrounding stellar systems, such as CIV and SiIV and (2) additional heating of the intergalactic medium of up to a few thousand Kelvin. Quantifying these warrants the inclusion of accurate models for stripped stars and other binary products in full cosmological simulations.Comment: Under review in A&A, suggestions welcom

Spectral models for binary products: Unifying subdwarfs and Wolf-Rayet stars as a sequence of stripped-envelope stars

Stars stripped of their hydrogen-rich envelope through interaction with a binary companion are generally not considered when accounting for ionizing radiation from stellar populations, despite the expectation that stripped stars emit hard ionizing radiation, form frequently, and live 10–100 times longer than single massive stars. We compute the first grid of evolutionary and spectral models specially made for stars stripped in binaries for a range of progenitor masses (2–20 M⊙) and metallicities ranging from solar to values representative for pop II stars. For stripped stars with masses in the range 0.3–7 M⊙, we find consistently high effective temperatures (20 000–100 000 K, increasing with mass), small radii (0.2–1 R⊙), and high bolometric luminosities, comparable to that of their progenitor before stripping. The spectra show a continuous sequence that naturally bridges subdwarf-type stars at the low-mass end and Wolf-Rayet-like spectra at the high-mass end. For intermediate masses we find hybrid spectral classes showing a mixture of absorption and emission lines. These appear for stars with mass-loss rates of 10−8−10−6 M⊙ yr−1, which have semi-transparent atmospheres. At low metallicity, substantial hydrogen-rich layers are left at the surface and we predict spectra that resemble O-type stars instead. We obtain spectra undistinguishable from subdwarfs for stripped stars with masses up to 1.7 M⊙, which questions whether the widely adopted canonical value of 0.47 M⊙ is uniformly valid. Only a handful of stripped stars of intermediate mass have currently been identified observationally. Increasing this sample will provide necessary tests for the physics of interaction, internal mixing, and stellar winds. We use our model spectra to investigate the feasibility to detect stripped stars next to an optically bright companion and recommend systematic searches for their UV excess and possible emission lines, most notably HeII λ4686 in the optical and HeII λ1640 in the UV. Our models are publicly available for further investigations or inclusion in spectral synthesis simulations

The effects of surface fossil magnetic fields on massive star evolution: IV. Grids of models at Solar, LMC, and SMC metallicities

Magnetic fields can drastically change predictions of evolutionary models of massive stars via mass-loss quenching, magnetic braking, and efficient angular momentum transport, which we aim to quantify in this work. We use the MESA software instrument to compute an extensive main-sequence grid of stellar structure and evolution models, as well as isochrones, accounting for the effects attributed to a surface fossil magnetic field. The grid is densely populated in initial mass (3–60 M⊙), surface equatorial magnetic field strength (0–50 kG), and metallicity (representative of the Solar neighbourhood and the Magellanic Clouds). We use two magnetic braking and two chemical mixing schemes and compare the model predictions for slowly rotating, nitrogen-enriched (‘Group 2’) stars with observations in the Large Magellanic Cloud. We quantify a range of initial field strengths that allow for producing Group 2 stars and find that typical values (up to a few kG) lead to solutions. Between the subgrids, we find notable departures in surface abundances and evolutionary paths. In our magnetic models, chemical mixing is always less efficient compared to non-magnetic models due to the rapid spin-down. We identify that quasi-chemically homogeneous main sequence evolution by efficient mixing could be prevented by fossil magnetic fields. We recommend comparing this grid of evolutionary models with spectropolarimetric and spectroscopic observations with the goals of (i) revisiting the derived stellar parameters of known magnetic stars, and (ii) observationally constraining the uncertain magnetic braking and chemical mixing schemes

Treatment with the C5a receptor antagonist ADC-1004 reduces myocardial infarction in a porcine ischemia-reperfusion model

<p>Abstract</p> <p>Background</p> <p>Polymorphonuclear neutrophils, stimulated by the activated complement factor C5a, have been implicated in cardiac ischemia/reperfusion injury. ADC-1004 is a competitive C5a receptor antagonist that has been shown to inhibit complement related neutrophil activation. ADC-1004 shields the neutrophils from C5a activation before they enter the reperfused area, which could be a mechanistic advantage compared to previous C5a directed reperfusion therapies. We investigated if treatment with ADC-1004, according to a clinically applicable protocol, would reduce infarct size and microvascular obstruction in a large animal myocardial infarct model.</p> <p>Methods</p> <p>In anesthetized pigs (42-53 kg), a percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 minutes, followed by 4 hours of reperfusion. Twenty minutes after balloon inflation the pigs were randomized to an intravenous bolus administration of ADC-1004 (175 mg, n = 8) or saline (9 mg/ml, n = 8). Area at risk (AAR) was evaluated by ex vivo SPECT. Infarct size and microvascular obstruction were evaluated by ex vivo MRI. The observers were blinded to the treatment at randomization and analysis.</p> <p>Results</p> <p>ADC-1004 treatment reduced infarct size by 21% (ADC-1004: 58.3 ± 3.4 vs control: 74.1 ± 2.9%AAR, p = 0.007). Microvascular obstruction was similar between the groups (ADC-1004: 2.2 ± 1.2 vs control: 5.3 ± 2.5%AAR, p = 0.23). The mean plasma concentration of ADC-1004 was 83 ± 8 nM at sacrifice. There were no significant differences between the groups with respect to heart rate, mean arterial pressure, cardiac output and blood-gas data.</p> <p>Conclusions</p> <p>ADC-1004 treatment reduces myocardial ischemia-reperfusion injury and represents a novel treatment strategy of myocardial infarct with potential clinical applicability.</p

Apyrase treatment of myocardial infarction according to a clinically applicable protocol fails to reduce myocardial injury in a porcine model

<p>Abstract</p> <p>Background</p> <p>Ectonucleotidase dependent adenosine generation has been implicated in preconditioning related cardioprotection against ischemia-reperfusion injury, and treatment with a soluble ectonucleotidase has been shown to reduce myocardial infarct size (IS) when applied prior to induction of ischemia. However, ectonucleotidase treatment according to a clinically applicable protocol, with administration only after induction of ischemia, has not previously been evaluated. We therefore investigated if treatment with the ectonucleotidase apyrase, according to a clinically applicable protocol, would reduce IS and microvascular obstruction (MO) in a large animal model.</p> <p>Methods</p> <p>A percutaneous coronary intervention balloon was inflated in the left anterior descending artery for 40 min, in 16 anesthetized pigs (40-50 kg). The pigs were randomized to 40 min of 1 ml/min intracoronary infusion of apyrase (10 U/ml, n = 8) or saline (0.9 mg/ml, n = 8), twenty minutes after balloon inflation. Area at risk (AAR) was evaluated by <it>ex vivo </it>SPECT. IS and MO were evaluated by <it>ex vivo </it>MRI.</p> <p>Results</p> <p>No differences were observed between the apyrase group and saline group with respect to IS/AAR (75.7 ± 4.2% vs 69.4 ± 5.0%, p = NS) or MO (10.7 ± 4.8% vs 11.4 ± 4.8%, p = NS), but apyrase prolonged the post-ischemic reactive hyperemia.</p> <p>Conclusion</p> <p>Apyrase treatment according to a clinically applicable protocol, with administration of apyrase after induction of ischemia, does not reduce myocardial infarct size or microvascular obstruction.</p

Translating cardioprotection for patient benefit: Position paper from the Working Group of Cellular Biology of the Heart of the European Society of Cardiology

Coronary heart disease (CHD) is the leading cause of death and disability worldwide. Despite current therapy, the morbidity and mortality for patients with CHD remains significant. The most important manifestations of CHD arise from acute myocardial ischaemia-reperfusion injury (IRI) in terms of cardiomyocyte death and its long-term consequences. As such, new therapeutic interventions are required to protect the heart against the detrimental effects of acute IRI and improve clinical outcomes. Although a large number of cardioprotective therapies discovered in pre-clinical studies have been investigated in CHD patients, few have been translated into the clinical setting, and a significant number of these have failed to show any benefit in terms of reduced myocardial infarction and improved clinical outcomes. Because of this, there is currently no effective therapy for protecting the heart against the detrimental effects of acute IRI in patients with CHD. One major factor for this lack of success in translating cardioprotective therapies into the clinical setting can be attributed to problems with the clinical study design. Many of these clinical studies have not taken into consideration the important data provided from previously published pre-clinical and clinical studies. The overall aim of this ESC Working Group Cellular Biology of the Heart Position Paper is to provide recommendations for optimizing the design of clinical cardioprotection studies, which should hopefully result in new and effective therapeutic interventions for the future benefit of CHD patients

Safety of the Deferral of Coronary Revascularization on the Basis of Instantaneous Wave-Free Ratio and Fractional Flow Reserve Measurements in Stable Coronary Artery Disease and Acute Coronary Syndromes

OBJECTIVES The aim of this study was to investigate the clinical outcomes of patients deferred from coronary revascularization on the basis of instantaneous wave-free ratio (iFR) or fractional flow reserve (FFR) measurements in stable angina pectoris (SAP) and acute coronary syndromes (ACS). BACKGROUND Assessment of coronary stenosis severity with pressure guidewires is recommended to determine the need for myocardial revascularization. METHODS The safety of deferral of coronary revascularization in the pooled per-protocol population (n = 4,486) of the DEFINE-FLAIR (Functional Lesion Assessment of Intermediate Stenosis to Guide Revascularisation) and iFR-SWEDEHEART (Instantaneous Wave-Free Ratio Versus Fractional Flow Reserve in Patients With Stable Angina Pectoris or Acute Coronary Syndrome) randomized clinical trials was investigated. Patients were stratified according to revascularization decision making on the basis of iFR or FFR and to clinical presentation (SAP or ACS). The primary endpoint was major adverse cardiac events (MACE), defined as the composite of all-cause death, nonfatal myocardial infarction, or unplanned revascularization at 1 year. RESULTS Coronary revascularization was deferred in 2,130 patients. Deferral was performed in 1,117 patients (50%) in the iFR group and 1,013 patients (45%) in the FFR group (p <0.01). At 1 year, the MACE rate in the deferred population was similar between the iFR and FFR groups (4.12% vs. 4.05%; fully adjusted hazard ratio: 1.13; 95% confidence interval: 0.72 to 1.79; p = 0.60). A clinical presentation with ACS was associated with a higher MACE rate compared with SAP in deferred patients (5.91% vs. 3.64% in ACS and SAP, respectively; fully adjusted hazard ratio: 0.61 in favor of SAP; 95% confidence interval: 0.38 to 0.99; p = 0.04). CONCLUSIONS Overall, deferral of revascularization is equally safe with both iFR and FFR, with a low MACE rate of about 4%. Lesions were more frequently deferred when iFR was used to assess physiological significance. In deferred patients presenting with ACS, the event rate was significantly increased compared with SAP at 1 year. (C) 2018 The Authors. Published by Elsevier on behalf of the American College of Cardiology Foundation.Peer reviewe