Nucleosynthesis in Massive Stars With Improved Nuclear and Stellar Physics

We present the first calculations to follow the evolution of all stable nuclei and their radioactive progenitors in stellar models computed from the onset of central hydrogen burning through explosion as Type II supernovae. Calculations are performed for Pop I stars of 15, 19, 20, 21, and 25 M_sun using the most recently available experimental and theoretical nuclear data, revised opacity tables, neutrino losses, and weak interaction rates, and taking into account mass loss due to stellar winds. A novel ``adaptive'' reaction network is employed with a variable number of nuclei (adjusted each time step) ranging from about 700 on the main sequence to more than 2200 during the explosion. The network includes, at any given time, all relevant isotopes from hydrogen through polonium (Z=84). Even the limited grid of stellar masses studied suggests that overall good agreement can be achieved with the solar abundances of nuclei between 16O and 90Zr. Interesting discrepancies are seen in the 20 M_sun model and, so far, only in that model, that are a consequence of the merging of the oxygen, neon, and carbon shells about a day prior to core collapse. We find that, in some stars, most of the ``p-process'' nuclei can be produced in the convective oxygen burning shell moments prior to collapse; in others, they are made only in the explosion. Serious deficiencies still exist in all cases for the p-process isotopes of Ru and Mo.Comment: 53 pages, 17 color figures (3 as separate GIF images), slightly extended discussion and references, accepted by Ap

IAC-Star: a Code for Synthetic Color-Magnitude Diagram Computation

The code IAC-star is presented. It generates synthetic HR and color-magnitude diagrams (CMDs) and is mainly aimed to star formation history studies in nearby galaxies. Composite stellar populations are calculated on a star by star basis, by computing the luminosity, effective temperature and gravity of each star by direct bi-logarithmic interpolation in the metallicity and age grid of a library of stellar evolution tracks. Visual (broad band and HST) and infrared magnitudes are also provided for each star after applying bolometric corrections. The Padua (Bertelli et al. 1994, Girardi et al. 2000) and Teramo (Pietrinferni et al. 2004) stellar evolution libraries and various bolometric corrections libraries are used in the current version. A variety of star formation rate functions, initial mass functions and chemical enrichment laws are allowed and binary stars can be computed. Although the main motivation of the code is the computation of synthetic CMDs, it also provides integrated masses, luminosities and magnitudes as well as surface brightness fluctuation luminosities and magnitudes for the total synthetic stellar population, and therefore it can also be used for population synthesis research. The code is offered for free use and can be executed at the site {\tt http://iac-star.iac.es}, with the only requirement of referencing this paper and crediting as indicated in the site.Comment: Astronomical Journal, in pres

Methyl 4-(piperidin-1-ylcarbon­yl)benzoate

In the title compound, C14H17NO3, the piperidine ring has a chair conformation and an intra­molecular C—H⋯O inter­action stabilizes the mol­ecular conformation. In the crystal, weak inter­molecular C—H⋯O inter­actions occur

Description of the Scenario Machine

We present here an updated description of the "Scenario Machine" code. This tool is used to carry out a population synthesis of binary stars. Previous version of the description can be found at http://xray.sai.msu.ru/~mystery//articles/review/contents.htmlComment: 32 pages, 3 figures. Corrected typo

Discovery of a new class of inhibitors for the protein arginine deiminase type 4 (PAD4) by structure-based virtual screening

<p>Abstract</p> <p>Background</p> <p>Rheumatoid arthritis (RA) is an autoimmune disease with unknown etiology. Anticitrullinated protein autoantibody has been documented as a highly specific autoantibody associated with RA. Protein arginine deiminase type 4 (PAD4) is the enzyme responsible for catalyzing the conversion of peptidylarginine into peptidylcitrulline. PAD4 is a new therapeutic target for RA treatment. In order to search for inhibitors of PAD4, structure-based virtual screening was performed using LIDAEUS (Ligand discovery at Edinburgh university). Potential inhibitors were screened experimentally by inhibition assays.</p> <p>Results</p> <p>Twenty two of the top-ranked water-soluble compounds were selected for inhibitory screening against PAD4. Three compounds showed significant inhibition of PAD4 and their IC₅₀values were investigated. The structures of the three compounds show no resemblance with previously discovered PAD4 inhibitors, nor with existing drugs for RA treatment.</p> <p>Conclusion</p> <p>Three compounds were discovered as potential inhibitors of PAD4 by virtual screening. The compounds are commercially available and can be used as scaffolds to design more potent inhibitors against PAD4.</p

Therapeutic opportunities within the DNA damage response

The DNA damage response (DDR) is essential for maintaining the genomic integrity of the cell, and its disruption is one of the hallmarks of cancer. Classically, defects in the DDR have been exploited therapeutically in the treatment of cancer with radiation therapies or genotoxic chemotherapies. More recently, protein components of the DDR systems have been identified as promising avenues for targeted cancer therapeutics. Here, we present an in-depth analysis of the function, role in cancer and therapeutic potential of 450 expert-curated human DDR genes. We discuss the DDR drugs that have been approved by the US Food and Drug Administration (FDA) or that are under clinical investigation. We examine large-scale genomic and expression data for 15 cancers to identify deregulated components of the DDR, and we apply systematic computational analysis to identify DDR proteins that are amenable to modulation by small molecules, highlighting potential novel therapeutic targets

Re-examination of the Controversial Coexistence of Traumatic Brain Injury and Posttraumatic Stress Disorder: Misdiagnosis and Self-Report Measures

The coexistence of traumatic brain injury (TBI) and posttraumatic stress disorder (PTSD) remains a controversial issue in the literature. To address this controversy, we focused primarily on the civilian-related literature of TBI and PTSD. Some investigators have argued that individuals who had been rendered unconscious or suffered amnesia due to a TBI are unable to develop PTSD because they would be unable to consciously experience the symptoms of fear, helplessness, and horror associated with the development of PTSD. Other investigators have reported that individuals who sustain TBI, regardless of its severity, can develop PTSD even in the context of prolonged unconsciousness. A careful review of the methodologies employed in these studies reveals that investigators who relied on clinical interviews of TBI patients to diagnose PTSD found little or no evidence of PTSD. In contrast, investigators who relied on PTSD questionnaires to diagnose PTSD found considerable evidence of PTSD. Further analysis revealed that many of the TBI patients who were initially diagnosed with PTSD according to self-report questionnaires did not meet the diagnostic criteria for PTSD upon completion of a clinical interview. In particular, patients with severe TBI were often misdiagnosed with PTSD. A number of investigators found that many of the severe TBI patients failed to follow the questionnaire instructions and erroneously endorsed PTSD symptoms because of their cognitive difficulties. Because PTSD questionnaires are not designed to discriminate between PTSD and TBI symptoms or determine whether a patient's responses are accurate or exaggerated, studies that rely on self-report questionnaires to evaluate PTSD in TBI patients are at risk of misdiagnosing PTSD. Further research should evaluate the degree to which misdiagnosis of PTSD occurs in individuals who have sustained mild TBI