146 research outputs found

    Very low metallicity massive star models: Pre-SN evolution and primary nitrogen production

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    Two series of models were computed. The first series consists of 20 solar mass models with varying initial metallicity (Z=0.02 down to Z=10^{-8}) and rotation (V_{ini}=0-600 km/s). The second one consists of models with an initial metallicity of Z=10^{-8}, masses between 9 and 85 solar masses and fast initial rotation velocities (V_{ini}=600-800 km/s). The most interesting models are the models with Z=10^{-8} ([Fe/H]~-6.6). In the course of helium burning, carbon and oxygen are mixed into the hydrogen burning shell. This boosts the importance of the shell and causes a reduction of the CO core mass. Later in the evolution, the hydrogen shell deepens and produces large amount of primary nitrogen. For the most massive models (M>~60 solar masses), significant mass loss occurs during the red supergiant stage. This mass loss is due to the surface enrichment in CNO elements via rotational and convective mixing. The 85 solar mass model ends up as a WO type Wolf-Rayet star. Therefore the models predict SNe of type Ic and possibly long and soft GRBs at very low metallicities. The rotating 20 solar mass models can best reproduce the observed CNO abundances at the surface of extremely metal poor (EMP) stars and the metallicity trends when their angular momentum content is the same as at solar metallicity (and therefore have an increasing surface velocity with decreasing metallicity). The wind of the massive star models can also reproduce the CNO abundances of the most metal-poor carbon-rich star known to date, HE1327-2326.Comment: A&A accepted, 18 pages, 13 figures WEBLINK: http://quasar.physik.unibas.ch/~hirschi/work/lowz.pd

    Production and evolution of Li, Be and B isotopes in the Galaxy

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    We reassess the problem of the production and evolution of the light elements Li, Be and B and of their isotopes in the Milky Way, in the light of new observational and theoretical developments. The main novelty is the introduction of a new scheme for the origin of Galactic cosmic rays (GCR), which for the first time enables a self-consistent calculation of their composition during galactic evolution. The scheme accounts for key features of the present-day GCR source composition, it is based on the wind yields of the Geneva models of rotating, mass losing stars and it is fully coupled to a detailed galactic chemical evolution code. We find that the adopted GCR source composition accounts naturally for the observations of primary Be and helps understanding why Be follows closer Fe than O. We find that GCR produce ~70% of the solar B11/B10 isotopic ratio; the remaining 30% of B11 presumably result from neutrino-nucleosynthesis in massive star explosions. We find that GCR and primordial nucleosynthesis can make at most 30% of solar Li. At least half of solar Li has to originate in low-mass stellar sources (red giants, asymptotic giant branch stars or novae), but the required average yields of those sources are found to be much larger than obtained in current models of stellar nucleosynthesis. We also present radial profiles of LiBeB elemental and isotopic abundances in the Milky Way disc. We argue that the shape of those profiles - and the late evolution of LiBeB in general - reveals important features of the production of those light elements through primary and secondary processes.Comment: Final version, matches the one to appear in Astronomy and Astrophysics, typos corrected, references adde

    Implications of a non-universal IMF from C, N, and O abundances in very metal-poor Galactic stars and damped Lyman-alpha absorbers

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    Recently revealed C, N, and O abundances in the most metal-poor damped Lyman-alpha (DLA) absorbers are compared with those of extremely metal-poor stars in the Galactic halo, as well as extragalactic H II regions, to decipher nucleosynthesis and chemical enrichment in the early Universe. These comparisons surprisingly identify a relatively high C/O ratio and a low N/O ratio in DLA systems, which is hard to explain theoretically. We propose that if these features are confirmed by future studies, this effect occurs because the initial mass function in metal-poor DLA systems has a cut-off at the upper mass end at around 20-25 Msun, thus lacks the massive stars that provide the nucleosynthesis products leading to the low C/O and high N/O ratios. This finding is a reasonable explanation of the nature of DLA systems in which a sufficient amount of cold H I gas remains intact because of the suppression of ionization by massive stars. In addition, our claim strongly supports a high production rate of N in very massive stars, which might be acceptable in light of the recent nucleosynthesis calculations with fast rotation models. The updates of both abundance data and nucleosynthesis results will strengthen our novel proposition that the C/O and N/O abundances are a powerful tool for inferring the form of the initial mass function.Comment: 9 pages including 5 figures, accepted for publication in A&

    Tracing the Reionization-Epoch Intergalactic Medium with Metal Absorption Lines

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    IGM metal absorption lines observed in z>6 spectra offer the opportunity to probe early feedback processes, the nature of enriching sources, and the topology of reionization. We run high-resolution cosmological simulations including galactic outflows to study the observability and physical properties of 5 ions (C II, C IV, O I, Si II, Si IV) in absorption between z=8->5. We apply three cases for ionization conditions: Fully neutral, fully reionized, and a patchy model based on the flux from the nearest galaxy. We find that our simulations broadly fit available z~5-6 IGM metal-line data, although all observations cannot be accommodated with a single ionization condition. Variations in O I absorbers among sight lines seen by Becker et al. (2006) suggest significant neutral IGM patches down to z~6. Strong C IV absorbers at z~6 may be the result of ionization by their parent galaxy. Our outflows have typical speeds of ~200 km/s and mass loading factors of ~6. Such high mass loading is critical for enriching the IGM to the observed levels while curtailing star formation to match the observed z~6 rest-frame UV luminosity function. The volume filling factor of metals increases during this epoch, but only reaches ~1% for Z>10^(-3) Zsolar by z=5. C IV is an ideal tracer of IGM metals at z~5-6, with dropping global ionization fractions to either higher or lower redshifts. This results in a strongly increasing global Omega(C IV) from z=8->5, in contrast to its relative constancy from z=5->2. Our simulations do not support widespread early IGM enrichment from e.g. Pop III stars. High-z absorbers arise from metals on their first outward journey from galaxies, at distances less than 50 kpc. The galaxies responsible for early IGM enrichment have typical M*=10^(7.0-8.5) Msolar.Comment: Accepted to MNRAS, 34 pages, 24 figures, 1 table (Sections 5.5, 6.3.1, & 6.3.2 added as well as 5 figures and 1 table

    Increased Circulating Endothelial Microparticles and Carotid Atherosclerosis in Obstructive Sleep Apnea

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    Background and Purpose Endothelial impairment is a linking mechanism between obstructive sleep apnea (USA) and cardiovascular diseases Profiles of endothelial micropanicles (EMPs) and endothelial progenitor cells (EPCs) reflect the degree of endothelial impairment The aims of this study were to measure the levels of EMI`s and progenitor cells in USA, determine the correlations between these factors and USA severity and the deuce of atherosclerosis, and document any changes in these factors after therapy Methods Subjects with (n=82) and without (n=22) OSA were recruited prospectively We measured the number of colony-forming units (CM) in cell cultuie as the endothelial progenitor cell index, and the number of EMPs using flow cytometry with CD31 [platelet endothelial cell adhesion molecule (PECAM)], CD42 (platelet glycoprotem), annexm V, and CD62E (E-selectin) antibodies at baseline and Act 4-6 weeks of continuous positive airway pressure (CPA P) therapy Carotid int ima-media thickness (IMT) was regarded as a marker of atherosclerosis Results The levels of PECAM(+)CD42(-) (p<0 001). PECAM(+)annexin V(+) (p<0 001), and E-selectin(+) micropamcles (p=0 001) were higher in USA subjects than in non-USA subjects The number of CRJ did not differ between the two groups OSA severity independently predicted the levels of PECAM(+)CD42(-) (p=0 02) and PECA(+)annexin V(+) (p=0 004) Carotid IMT was correlated with USA severity (p<0 001), PECAM(+)CD42: (p=0 03), and PECAM(+)annexin (p=0 01) Neither USA severity nor carotid IMT was correlated with either the number of CFI) or E-selectin(+) CPAP therapy decreased the occurrence of E-selecte (p<0 001) in 21 of the USA subjects, but had no effect on the other micioparticles of the number CFU Conclusions USA led to the overproduction of EMI`s, which moderately correlated with USA seventy and the degree of atherosclerosis, and partly responded to therapy The endothelial impairment might contribute to future cardiovascular events J Clin Neurol 2010;6`89-98This research was supported by the Stem Cell Research Center of the 21st Century Frontier Research Program funded by the Ministry of Science and Technology, Republic of Korea (#SC4120).de Lima AMJ, 2010, RESPIRATION, V79, P370, DOI 10.1159/000227800Jung KH, 2009, ANN NEUROL, V66, P191, DOI 10.1002/ana.21681Ayers L, 2009, EUR RESPIR J, V33, P574, DOI 10.1183/09031936.00107408Akinnusi ME, 2009, AM J RESP CRIT CARE, V179, P328Christou K, 2009, SLEEP MED, V10, P87, DOI 10.1016/j.sleep.2007.10.011Barcelo A, 2008, THORAX, V63, P946, DOI 10.1136/thx.2007.093740Dorkova Z, 2008, CHEST, V134, P686, DOI 10.1378/chest.08-0556Robinson GV, 2008, THORAX, V63, P855, DOI 10.1136/thx.2007.088096Somers VK, 2008, CIRCULATION, V118, P1080, DOI 10.1161/CIRCULATIONAHA.107.189375Hirschi KK, 2008, ARTERIOSCL THROM VAS, V28, P1584, DOI 10.1161/ATVBAHA.107.155960Daniel L, 2008, NEPHROL DIAL TRANSPL, V23, P2129, DOI 10.1093/ndt/gfn029Martin K, 2008, LUNG, V186, P145, DOI 10.1007/s00408-008-9073-yAmabile N, 2008, AM J RESP CRIT CARE, V177, P1268, DOI 10.1164/rccm.200710-1458OCHeiss C, 2008, J AM COLL CARDIOL, V51, P1760, DOI 10.1016/j.jacc.2008.01.040Chu K, 2008, STROKE, V39, P1441, DOI 10.1161/STROKEAHA.107.499236Jelic S, 2008, CIRCULATION, V117, P2270, DOI 10.1161/CIRCULATIONAHA.107.741512Lee ST, 2008, NEUROLOGY, V70, P1510Bakouboula B, 2008, AM J RESP CRIT CARE, V177, P536, DOI 10.1164/rccm.200706-840OCLopez-Jimenez F, 2008, CHEST, V133, P793, DOI 10.1378/chest.07-0800de la Pena M, 2008, RESPIRATION, V76, P28, DOI 10.1159/000109643WON CHJ, 2008, P AM THORAC SOC, V5, P193Kloner RA, 2007, CIRCULATION, V116, P1306, DOI 10.1161/CIRCULATIONAHA.106.678375El Solh AA, 2007, AM J RESP CRIT CARE, V175, P1186, DOI 10.1164/rccm.200611-1598OCIBER C, 2007, AASM MANUAL SCORINGMONTSERRAT JM, 2007, AM J RESP CRIT CARE, V176, P6Pirro M, 2006, ARTERIOSCL THROM VAS, V26, P2530, DOI 10.1161/01.ATV.0000243941.72375.15Ryan S, 2006, AM J RESP CRIT CARE, V174, P824, DOI 10.1164/rccm.200601-066OCBoulanger CM, 2006, HYPERTENSION, V48, P180, DOI 10.1161/01.HYP.0000231507.00962.b5Arteaga RB, 2006, AM J CARDIOL, V98, P70, DOI 10.1016/j.amjcard.2006.01.054Robinson GV, 2006, EUR RESPIR J, V27, P1229, DOI 10.1183/09031936.06.00062805Werner N, 2005, NEW ENGL J MED, V353, P999Mezentsev A, 2005, AM J PHYSIOL-HEART C, V289, pH1106, DOI 10.1152/ajpheart.00265.2005Minoguchi K, 2005, AM J RESP CRIT CARE, V172, P625, DOI 10.1164/rccm.200412-1652OCMassa M, 2005, BLOOD, V105, P199, DOI 10.1182/blood-2004-05-1831Kim J, 2004, AM J RESP CRIT CARE, V170, P1108, DOI 10.1164/rccm.200404-519OCJy W, 2004, J THROMB HAEMOST, V2, P1842Tramontano AF, 2004, BIOCHEM BIOPH RES CO, V320, P34, DOI 10.1016/j.bbrc.2004.05.127Ip MSM, 2004, AM J RESP CRIT CARE, V169, P348, DOI 10.1164/rccm.200306.767OCBarba C, 2004, LANCET, V363, P157Bernal-Mizrachi L, 2003, AM HEART J, V145, P962, DOI 10.1016/S0002-8703(03)00103-0Jimenez JJ, 2003, THROMB RES, V109, P175, DOI 10.1016/S0049-3848(03)00064-1Hill JM, 2003, NEW ENGL J MED, V348, P593Preston RA, 2003, HYPERTENSION, V41, P211, DOI 10.1161/01.HYP.0000049760.15764.2DSabatier F, 2002, DIABETES, V51, P2840, DOI 10.2337/diabetes.51.9.2840El-Solh AA, 2002, CHEST, V121, P1541Boulanger CM, 2001, CIRCULATION, V104, P2649Barbe F, 2001, ANN INTERN MED, V134, P1015Chin K, 2000, AM J MED, V109, P562Lusis AJ, 2000, NATURE, V407, P233Ohga E, 1999, J APPL PHYSIOL, V87, P10YOUNG T, 1993, NEW ENGL J MED, V328, P1230JOHNS MW, 1991, SLEEP, V14, P540

    High-Resolution Spectroscopy of Extremely Metal-Poor Stars from SDSS/SEGUE: I. Atmospheric Parameters and Chemical Compositions

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    Chemical compositions are determined based on high-resolution spectroscopy for 137 candidate extremely metal-poor (EMP) stars selected from the Sloan Digital Sky Survey (SDSS) and its first stellar extension, the Sloan Extension for Galactic Understanding and Exploration (SEGUE). High-resolution spectra with moderate signal-to-noise (S/N) ratios were obtained with the High Dispersion Spectrograph of the Subaru Telescope. Most of the sample (approximately 80%) are main-sequence turnoff stars, including dwarfs and subgiants. Four cool main-sequence stars, the most metal-deficient such stars known, are included in the remaining sample. Good agreement is found between effective temperatures estimated by the SEGUE stellar parameter pipeline, based on the SDSS/SEGUE medium-resolution spectra, and those estimated from the broadband (V – K)[subscript 0] and (g – r)[subscript 0] colors. Our abundance measurements reveal that 70 stars in our sample have [Fe/H] +0.7) among the 25 giants in our sample is as high as 36%, while only a lower limit on the fraction (9%) is estimated for turnoff stars. This paper is the first of a series of papers based on these observational results. The following papers in this series will discuss the higher-resolution and higher-S/N observations of a subset of this sample, the metallicity distribution function, binarity, and correlations between the chemical composition and kinematics of extremely metal-poor stars

    Traumatic Brain Injury: A potential cause of violent crime?

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    Traumatic Brain Injury (TBI) is the biggest cause of death and disability in children and young people. TBI compromises important neurological functions for self-regulation and social behavior and increases risk of behavioral disorder and psychiatric morbidity. Crime in young people is a major social issue. “Early starters” often continue for a lifetime. A substantial majority of young offenders are re-convicted soon after release. Multiple factors play a role in crime. We show how TBI is a risk factor for earlier, more violent, offending. TBI is linked to poorer engagement in treatment, in-custody infractions, and re-conviction. Schemes to assess and manage TBI are under development. These might improve engagement of offenders in forensic psychotherapeutic rehabilitation and reduce crime
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