Particle interactions with single or multiple 3D solar reconnecting current sheets

The acceleration of charged particles (electrons and protons) in flaring solar active regions is analyzed by numerical experiments. The acceleration is modelled as a stochastic process taking place by the interaction of the particles with local magnetic reconnection sites via multiple steps. Two types of local reconnecting topologies are studied: the Harris-type and the X-point. A formula for the maximum kinetic energy gain in a Harris-type current sheet, found in a previous work of ours, fits well the numerical data for a single step of the process. A generalization is then given approximating the kinetic energy gain through an X-point. In the case of the multiple step process, in both topologies the particles' kinetic energy distribution is found to acquire a practically invariant form after a small number of steps. This tendency is interpreted theoretically. Other characteristics of the acceleration process are given, such as the mean acceleration time and the pitch angle distributions of the particles.Comment: 18 pages, 9 figures, Solar Physics, in pres

Grain Surface Models and Data for Astrochemistry

AbstractThe cross-disciplinary field of astrochemistry exists to understand the formation, destruction, and survival of molecules in astrophysical environments. Molecules in space are synthesized via a large variety of gas-phase reactions, and reactions on dust-grain surfaces, where the surface acts as a catalyst. A broad consensus has been reached in the astrochemistry community on how to suitably treat gas-phase processes in models, and also on how to present the necessary reaction data in databases; however, no such consensus has yet been reached for grain-surface processes. A team of ∼25 experts covering observational, laboratory and theoretical (astro)chemistry met in summer of 2014 at the Lorentz Center in Leiden with the aim to provide solutions for this problem and to review the current state-of-the-art of grain surface models, both in terms of technical implementation into models as well as the most up-to-date information available from experiments and chemical computations. This review builds on the results of this workshop and gives an outlook for future directions

The Structure of a Rigorously Conserved RNA Element within the SARS Virus Genome

We have solved the three-dimensional crystal structure of the stem-loop II motif (s2m) RNA element of the SARS virus genome to 2.7-Å resolution. SARS and related coronaviruses and astroviruses all possess a motif at the 3′ end of their RNA genomes, called the s2m, whose pathogenic importance is inferred from its rigorous sequence conservation in an otherwise rapidly mutable RNA genome. We find that this extreme conservation is clearly explained by the requirement to form a highly structured RNA whose unique tertiary structure includes a sharp 90° kink of the helix axis and several novel longer-range tertiary interactions. The tertiary base interactions create a tunnel that runs perpendicular to the main helical axis whose interior is negatively charged and binds two magnesium ions. These unusual features likely form interaction surfaces with conserved host cell components or other reactive sites required for virus function. Based on its conservation in viral pathogen genomes and its absence in the human genome, we suggest that these unusual structural features in the s2m RNA element are attractive targets for the design of anti-viral therapeutic agents. Structural genomics has sought to deduce protein function based on three-dimensional homology. Here we have extended this approach to RNA by proposing potential functions for a rigorously conserved set of RNA tertiary structural interactions that occur within the SARS RNA genome itself. Based on tertiary structural comparisons, we propose the s2m RNA binds one or more proteins possessing an oligomer-binding-like fold, and we suggest a possible mechanism for SARS viral RNA hijacking of host protein synthesis, both based upon observed s2m RNA macromolecular mimicry of a relevant ribosomal RNA fold

Predicting diabetes risk among HIV-positive and HIV-negative women

Objective:To assess the performance of an adapted American Diabetes Association (ADA) risk score and the concise Finnish Diabetes Risk Score (FINRISC) for predicting type 2 diabetes development in women with and at risk of HIV infection.Design:Longitudinal analysis of the Women's Interagency HIV Study.Methods:The women's Interagency HIV Study is an ongoing prospective cohort study of women with and at risk for HIV infection. Women without prevalent diabetes and 3-year data on fasting blood glucose, hemoglobin A1c, self-reported diabetes medication use, and self-reported diabetes were included. ADA and FINRISC scores were computed at baseline and their ability to predict diabetes development within 3 years was assessed [sensitivity, specificity and area under the receiver operating characteristics (AUROC) curve].Results:A total of 1111 HIV-positive (median age 41, 60% African American) and 454 HIV-negative women (median age 38, 63% African-American) were included. ADA sensitivity did not differ between HIV-positive (77%) and HIV-negative women (81%), while specificity was better in HIV-negative women (42 vs. 49%, P = 0.006). Overall ADA discrimination was suboptimal in both HIV-positive [AUROC = 0.64 (95% CI: 0.58, 0.70)] and HIV-negative women [AUROC = 0.67 (95% CI: 0.57, 0.77)]. FINRISC sensitivity and specificity did not differ between HIV-positive (72 and 49%, respectively) and HIV-negative women (86 and 52%, respectively). Overall FINRISC discrimination was suboptimal in HIV-positive [AUROC = 0.68 (95% CI: 0.62, 0.75)] and HIV-negative women [AUROC = 0.78 (95% CI: 0.66, 0.90)].Conclusion:Model performance was suboptimal in women with and at risk of HIV, while greater misclassification was generally observed among HIV-positive women. HIV-specific risk factors known to contribute to diabetes risk should be explored in these models

Structure of 18Ne and the breakout from the hot CNO cycle

We used the 16O(3He,n)18Ne, 12C(12C,6He)18Ne, and 20Ne(p,t)18Ne reactions to study 18Ne states up to an excitation energy of 10 MeV, with emphasis on levels corresponding to 14O(α,p)17F and 17F(p,γ)18Ne resonances that could strongly affect these reaction rates in hot stellar environments. Excitation energies, widths, absolute cross sections, and angular distributions were measured. We found previously unidentified states at Ex=6.15±0.01 MeV, 7.12±0.02 MeV, 7.35±0.02 MeV, 7.62±0.02 MeV, 8.30±0.02 MeV, (8.45 ±0.03 MeV), 8.55±0.03 MeV, 8.94±0.02 MeV, and 9.58±0.02 MeV. We combined level width, cross section, and angular distribution data to infer Jπ values for a number of the new levels as well as for the previously known 5.1-MeV doublet. Using information from our experiments, we recalculated the 14O(α.p) 17F reaction rate, which constitutes a possible path out of the hot CNO cycle into the rp process and could play an important role in transforming nuclei involved in the hot CNO cycle into heavier nuclei with Z≥10

Regulation of intracellular free arachidonic acid in Aplysia nervous system

We have studied the regulation of arachidonic acid (AA) uptake, metabolism, and release in Aplysia nervous system. Following uptake of [ 3 H]AA, the distribution of radioactivity in intracellular and extracellular lipid pools was measured as a function of time in the presence or absence of exogenous AA. The greatest amount of AA was esterified into phosphatidylinositol (relative to pool size). We found that the intracellular free AA pool underwent rapid turnover, and that radioactive free AA and eicosanoids were released at a rapid rate into the extracellular medium, both in the presence and absence of exogenous AA. Most of the released radioactivity originated from phosphatidylinositol.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/48020/1/232_2005_Article_BF01868464.pd

Large-scale discovery of novel genetic causes of developmental disorders

Despite three decades of successful, predominantly phenotype-driven discovery of the genetic causes of monogenic disorders1, up to half of children with severe developmental disorders of probable genetic origin remain without a genetic diagnosis. Particularly challenging are those disorders rare enough to have eluded recognition as a discrete clinical entity, those with highly variable clinical manifestations, and those that are difficult to distinguish from other, very similar, disorders. Here we demonstrate the power of using an unbiased genotype-driven approach2 to identify subsets of patients with similar disorders. By studying 1,133 children with severe, undiagnosed developmental disorders, and their parents, using a combination of exome sequencing3,4,5,6,7,8,9,10,11 and array-based detection of chromosomal rearrangements, we discovered 12 novel genes associated with developmental disorders. These newly implicated genes increase by 10% (from 28% to 31%) the proportion of children that could be diagnosed. Clustering of missense mutations in six of these newly implicated genes suggests that normal development is being perturbed by an activating or dominant-negative mechanism. Our findings demonstrate the value of adopting a comprehensive strategy, both genome-wide and nationwide, to elucidate the underlying causes of rare genetic disorders