666 research outputs found

    Ejecta and progenitor of the low-luminosity Type IIP supernova 2003Z

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    The origin of low-luminosity Type IIP supernovae is unclear: they have been proposed to originate either from massive (about 25 Msun) or low-mass (about 9 Msun) stars. We wish to determine parameters of the low-luminosity Type IIP supernova 2003Z, to estimate a mass-loss rate of the presupernova, and to recover a progenitor mass. We compute the hydrodynamic models of the supernova to describe the light curves and the observed expansion velocities. The wind density of the presupernova is estimated using a thin shell model for the interaction with circumstellar matter. We estimate an ejecta mass of 14 Msun, an explosion energy of 2.45x10^50 erg, a presupernova radius of 229 Rsun, and a radioactive Ni-56 amount of 0.0063 Msun. The upper limit of the wind density parameter in the presupernova vicinity is 10^13 g/cm, and the mass lost at the red/yellow supergiant stage is less than 0.6 Msun assuming the constant mass-loss rate. The estimated progenitor mass is in the range of 14.4-17.4 Msun. The presupernova of SN 2003Z was probably a yellow supergiant at the time of the explosion. The progenitor mass of SN 2003Z is lower than those of SN 1987A and SN 1999em, normal Type IIP supernovae, but higher than the lower limit of stars undergoing a core collapse. We propose an observational test based on the circumstellar interaction to discriminate between the massive (about 25 Msun) and moderate-mass (about 16 Msun) scenarios.Comment: 8 pages, 9 figures, 3 tables, accepted for publication in Astronomy & Astrophysics; one reference remove

    A Phenomenological Model for the Extended Zone Above AGB Stars

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    I suggest the existence of an extended zone above the surface of asymptotic giant branch (AGB), as well as similar stars experiencing high mass loss rates. In addition to the escaping wind, in this zone there are parcels of gas that do not reach the escape velocity. These parcels of dense gas rise slowly and then fall back. The wind and bound gas exist simultaneously to distances of ~100AU. I term this region the effervescent zone. In this phenomenological study I find that the density of the bound material in the effervescent zone falls as ~r^{-5/2}, not much faster than the wind density. The main motivation to propose the effervescent model is to allow wide binary companions to influence the morphology of the descendant planetary nebulae (PN) by accreting mass from the effervescent zone. Accretion from the effervescent zone is more efficient than accretion from the wind in forming an accretion disk around the companion. The companion might then blow two jets that will shape the descendant PN.Comment: New Astronomy, in pres

    Baltijas Psiholoģijas žurnāls

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    Contents: Viesturs Reņģe, Ivars Austers. Social Representations of Science and Psychology: Anchoring and Personification ; Aleksandrs Koļesovs. Gender Differences in Time Perspective of High School Students in Latvia ; Daina Škuškovnika. Comparison of State and Trait Anxiety of Latvians and Russians Residing in Latvia ; Mary Balaisis, Juris Dragūns, Solveiga Miezītis. Students’ Adjustment at Vilnius University: The Role of Self-Orientation, Locus of Control, Social Support and Demographic Variable

    Comparison of genetic association strategies in the presence of rare alleles

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    In the quest for the missing heritability of most complex diseases, rare variants have received increased attention. Advances in large-scale sequencing have led to a shift from the common disease/common variant hypothesis to the common disease/rare variant hypothesis or have at least reopened the debate about the relevance and importance of rare variants for gene discoveries. The investigation of modeling and testing approaches to identify significant disease/rare variant associations is in full motion. New methods to better deal with parameter estimation instabilities, convergence problems, or multiple testing corrections in the presence of rare variants or effect modifiers of rare variants are in their infancy. Using a recently developed semiparametric strategy to detect causal variants, we investigate the performance of the model-based multifactor dimensionality reduction (MB-MDR) technique in terms of power and family-wise error rate (FWER) control in the presence of rare variants, using population-based and family-based data (FAM-MDR). We compare family-based results obtained from MB-MDR analyses to screening findings from a quantitative trait Pedigree-based association test (PBAT). Population-based data were further examined using penalized regression models. We restrict attention to all available single-nucleotide polymorphisms on chromosome 4 and consider Q1 as the outcome of interest. The considered family-based methods identified marker C4S4935 in the VEGFC gene with estimated power not exceeding 0.35 (FAM-MDR), when FWER was kept under control. The considered population-based methods gave rise to highly inflated FWERs (up to 90% for PBAT screening)

    Coevolution of insulin-like growth factors, insulin and their receptors and binding proteins in new world monkeys

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    Previous work has shown that the evolution of both insulin-like growth factor 1 (IGF1) and insulin shows an episode of accelerated change on the branch leading to New World monkeys (NWM). Here the possibility that this is accompanied by a corresponding episode of accelerated evolution of IGF1 receptor (IGF1R), insulin receptor (IR) and/or IGF binding proteins (IGFBPs) was investigated. Analysis of receptor sequences from a range of primates and some non-primate mammals showed that accelerated evolution did indeed occur on this branch in the case of IGF1R and IR, but not for the similar insulin receptor-related receptor (IRRR) which does not bind insulin or IGF1. Marked accelerated evolution on this branch was also seen for some IGFBPs, but not the mannose 6-phosphate/IGF2 receptor or epidermal growth factor receptor. The rate of evolution slowed before divergence of the lineages leading to the NWM for which sequences are available (Callithrix and Saimiri). For the IGF1R and IR the accelerated evolution was most marked for the extracellular domains (ectodomains). Application of the branch-sites method showed dN/dS ratios significantly greater than 1.0 for both receptor ectodomains and for IGFBP1, and allowed identification of residues likely to have been subject to selection. These residues were concentrated in the N-terminal half of the IGF1R ectodomain but the C-terminal half of the IR ectodomain, which could have implications for the formation of hybrid receptors. Overall the results suggest that adaptive coevolution of IGF1, insulin and their receptors and some IGFBPs occurred during the evolution of NWM. For the most part, the residues that change on this branch could not be associated with specific functional aspects (ligand binding, receptor dimerization, glycosylation) and the physiological significance of this coevolution remains to be established

    The Gag Cleavage Product, p12, is a Functional Constituent of the Murine Leukemia Virus Pre-Integration Complex

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    The p12 protein is a cleavage product of the Gag precursor of the murine leukemia virus (MLV). Specific mutations in p12 have been described that affect early stages of infection, rendering the virus replication-defective. Such mutants showed normal generation of genomic DNA but no formation of circular forms, which are markers of nuclear entry by the viral DNA. This suggested that p12 may function in early stages of infection but the precise mechanism of p12 action is not known. To address the function and follow the intracellular localization of the wt p12 protein, we generated tagged p12 proteins in the context of a replication-competent virus, which allowed for the detection of p12 at early stages of infection by immunofluorescence. p12 was found to be distributed to discrete puncta, indicative of macromolecular complexes. These complexes were localized to the cytoplasm early after infection, and thereafter accumulated adjacent to mitotic chromosomes. This chromosomal accumulation was impaired for p12 proteins with a mutation that rendered the virus integration-defective. Immunofluorescence demonstrated that intracellular p12 complexes co-localized with capsid, a known constituent of the MLV pre-integration complex (PIC), and immunofluorescence combined with fluorescent in situ hybridization (FISH) revealed co-localization of the p12 proteins with the incoming reverse transcribed viral DNA. Interactions of p12 with the capsid and with the viral DNA were also demonstrated by co-immunoprecipitation. These results imply that p12 proteins are components of the MLV PIC. Furthermore, a large excess of wt PICs did not rescue the defect in integration of PICs derived from mutant p12 particles, demonstrating that p12 exerts its function as part of this complex. Altogether, these results imply that p12 proteins are constituent of the MLV PIC and function in directing the PIC from the cytoplasm towards integration
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