The QSE-Reduced Nuclear Reaction Network for Silicon Burning

Iron and neighboring nuclei are formed by silicon burning in massive stars before core collapse and during supernova outbursts. Complete and incomplete silicon burning is responsible for the production of a wide range of nuclei with atomic mass numbers from 28 to 70. Because of the large number of nuclei involved, accurate modeling of these nucleosynthetic stages is computationally expensive. For this reason, hydrodynamic models of supernovae often employ a limited set of nuclei to track the nuclear energy generation until nuclear statistical equilibrium is reached. These limited approximations do not include many of the reaction channels important for the production of iron (Hix & Thielemann, 1996), making them a partial solution at best for energy generation during silicon burning (Timmes et al., 2000). Examination of the physics of silicon burning reveals that the nuclear evolution is dominated by large groups of nuclei in mutual chemical equilibrium before the global Nuclear Statistical Equilibrium (NSE) is reached and after temperatures drop below those needed to maintain NSE during explosive burning (Bodansky, Clayton, & Fowler, 1968). In this work a nuclear reaction network is built which takes advantage of Quasi Statistical Equilibrium (QSE) and NSE at the appropriate temperatures in order to reduce the number of independent variables calculated. This allows accurate prediction of the nuclear abundance evolution, deleptionization, and energy generation. Where conditions apply, the QSE-reduced network runs at least an order of magnitude faster and requires roughly a third as many variables as a standard nuclear reaction network without a significant loss of accuracy. These reductions in computational cost make this network well suited for inclusion within hydrodynamic simulations, particularly in multi-dimensional applications

Transportation challenges for persons aging with mobility disability: Qualitative insights and policy implications

Background Persons aging with mobility disability (PAwMD) experience transportation barriers, which can hinder their ability to fully participate in society. Despite a vast infrastructure of federal laws and programs designed to ensure access to transportation, PAwMD remain a transportation-disadvantaged population. Objectives This paper presents detailed insights on transportation challenges experienced by PAwMD along with recent Federal programmatic initiatives designed to enhance access and mobility for transportation for older adults and people with disabilities. To identify policy gaps and opportunities to improve transportation services, we compared individual-level challenges from PAwMD to national survey data about barriers associated with delivering transportation services at state and local levels. Methods To assess individual-level transportation challenges, we conducted in-depth, structured interviews with sixty older adult participants with self-identified mobility disabilities for at least 10 years. We also conducted a content analysis of end-user transportation challenges and agency-level transportation coordination barriers to identify correspondences. Results Participants reported challenges utilizing public and private modes of transportation, related to availability; accessibility; safety; advanced planning; as well as societal attitudes. Barriers to the availability, delivery, and coordination of access and mobility services are linked directly or indirectly to the PAwMD reports of experiencing a shortage of accessible transportation options. Conclusions Findings highlight the complexity of federal transportation policies and programmatic initiatives designed to support older adults and people with disabilities, which contribute to implementation barriers and transportation challenges. Results highlight the importance of integrating end-user and state and local provider input into transportation policy development and program implementation

Drowning risk and climate change: a state-of-the-art review

Drowning and climate change are both significant global health threats, yet little research links climate change to drowning risk. Research into the epidemiology, risk factors and preventive strategies for unintentional drowning in high-income and in low-income and middle-income countries has expanded understanding, but understanding of disaster and extreme weather-related drowning needs research focus. As nation states and researchers call for action on climate change, its impact on drowning has been largely ignored. This state-of-the-art review considers existing literature on climate change as a contributor to changes in drowning risks globally. Using selected climate change-related risks identified by the World Meteorological Organization and key risks to the Sustainable Development Goals as a framework, we consider the drowning risks associated with heat waves, hydrometeorological hazards, drought and water scarcity, damaged infrastructure, marine ecosystem collapse, displacement, and rising poverty and inequality. Although the degree of atmospheric warming remains uncertain, the impact of climate change on drowning risk is already taking place and can no longer be ignored. Greater evidence characterising the links between drowning and climate change across both high-income and low-income and middle-income contexts is required, and the implementation and evaluation of drowning interventions must reflect climate change risks at a local level, accounting for both geographical variation and the consequences of inequality. Furthermore, collaboration between the injury prevention, disaster risk reduction and climate change mitigation sectors is crucial to both prevent climate change from stalling progress on preventing drowning and further advocate for climate change mitigation as a drowning risk reduction mechanism

Simple mechanism for a positive exchange bias

We argue that the interface coupling, responsible for the positive exchange bias (HE) observed in ferromagnetic/compensated antiferromagnetic (FM/AF) bilayers, favors an antiferromagnetic alignment. At low cooling field this coupling polarizes the AF spins close to the interface, which spin configuration persists after the sample is cooled below the Neel temperature. This pins the FM spins as in Bean's model and gives rise to a negative HE. When the cooling field increases, it eventually dominates and polarizes the AF spins in an opposite direction to the low field one. This results in a positive HE. The size of HE and the crossover cooling field are estimated. We explain why HE is mostly positive for an AF single crystal, and discuss the role of interface roughness on the magnitude of HE, and the quantum aspect of the interface coupling.Comment: 10 pages, 2 figures, to be published on May 1 issue of PR

Virus-like particles identify an HIV V1V2 Apex-1 binding neutralizing antibody that lacks a protruding loop

Most HIV-1-specific neutralizing antibodies isolated to date exhibit unusual characteristics that complicate their elicitation. Neutralizing antibodies that target the V1V2 apex of the HIV-1 envelope (Env) trimer feature unusually long protruding loops, enabl them to penetrate the HIV-1 glycan shield. As antibodies with loops of requisite length are created through uncommon recombination events, an alternative mode of apex binding has been sought. Here, we isolated a lineage of Env apex-directed neutralizing antibodies, N90-VRC38.01-11, using virus-like particles and conformationally stabilized Env trimers as B cell probes. A crystal structure of N90-VRC38.01 with a scaffolded V1V2 revealed a binding mode involving side-chain to side-chain interactions that reduced the distance the antibody loop must traverse the glycan shield, facilitating V1V2 binding via a non-protruding loop. The N90-VRC38 lineage identifies a solution for V1V2apex binding that provides a more conventional B cell pathway for vaccine design

In-plane magnetic reorientation in coupled ferro- and antiferromagnetic thin films

By studying coupled ferro- (FM) and antiferromagnetic (AFM) thin film systems, we obtain an in-plane magnetic reorientation as a function of temperature and FM film thickness. The interlayer exchange coupling causes a uniaxial anisotropy, which may compete with the intrinsic anisotropy of the FM film. Depending on the latter the total in-plane anisotropy of the FM film is either enhanced or reduced. Eventually a change of sign occurs, resulting in an in-plane magnetic reorientation between a collinear and an orthogonal magnetic arrangement of the two subsystems. A canted magnetic arrangement may occur, mediating between these two extremes. By measuring the anisotropy below and above the N\'eel temperature the interlayer exchange coupling can be determined. The calculations have been performed with a Heisenberg-like Hamiltonian by application of a two-spin mean-field theory.Comment: 4 pages, 4 figure

Induced four fold anisotropy and bias in compensated NiFe/FeMn double layers

A vector spin model is used to show how frustrations within a multisublattice antiferromagnet such as FeMn can lead to four-fold magnetic anisotropies acting on an exchange coupled ferromagnetic film. Possibilities for the existence of exchange bias are examined and shown to exist for the case of weak chemical disorder at the interface in an otherwise perfect structure. A sensitive dependence on interlayer exchange is found for anisotropies acting on the ferromagnet through the exchange coupling, and we show that a wide range of anisotropies can appear even for a perfect crystalline structure with an ideally flat interface.Comment: 7 pages, 7 figure

The Candida albicans transcription factor Cas5 couples stress responses, drug resistance and cell cycle regulation

We thank Cowen lab members for helpful discussions. We also thank David Rogers (University of Tennessee) for sharing microarray analysis of the CAS5 homozygous mutant, and Li Ang (University of Macau) for assistance in optimizing the ChIP-Seq experiments. J.L.X. is supported by a Canadian Institutes of Health Research Doctoral award and M.D.L. is supported by a Sir Henry Wellcome Postdoctoral Fellowship (Wellcome Trust 096072). B.T.G. holds an Ontario Graduate Scholarship. C.B. and B.J.A. are supported by the Canadian Institutes of Health Research Foundation Grants (FDN-143264 and -143265). D.J.K. is supported by a National Institute of Allergy and Infectious Diseases grant (1R01AI098450) and J.D.L.C.D. is supported by the University of Rochester School of Dentistry and Medicine PREP program (R25 GM064133). A.S. is supported by the Creighton University and the Nebraska Department of Health and Human Services (LB506-2017-55). K.H.W. is supported by the Science and Technology Development Fund of Macau S.A.R. (FDCT; 085/2014/A2). L.E.C. is supported by the Canadian Institutes of Health Research Operating Grants (MOP-86452 and MOP-119520), the Natural Sciences and Engineering Council (NSERC) of Canada Discovery Grants (06261 and 462167), and an NSERC E.W.R. Steacie Memorial Fellowship (477598).Peer reviewedPublisher PD