Supernova Ia: a Converging Delayed Detonation Wave

A model of a carbon-oxygen (C--O) presupernova core with an initial mass 1.33 M_\odot, an initial carbon mass fraction 0.27, and with an average mass growth-rate 5 x 10^{-7} M_\odot/yr due to accretion in a binary system was evolved from initial central density 10^9 g/cm^3, and temperature 2.05 x 10^8 K through convective core formation and its subsequent expansion to the carbon runaway at the center. The only thermonuclear reaction contained in the equations of evolution and runaway was the carbon burning reaction 12C + 12C with an energy release corresponding to the full transition of carbon and oxygen (with the same rate as carbon) into 56Ni. As a parameter we take \alpha_c - a ratio of a mixing length to the size of the convective zone. In spite of the crude assumptions, we obtained a pattern of the runaway acceptable for the supernova theory with the strong dependence of its duration on \alpha_c. In the variants with large enough values of \alpha_c=4.0 x 10^{-3} and 3.0 x 10^{-3} the fuel combustion occurred from the very beginning as a prompt detonation. In the range of 2.0 x 10^{-3} >= \alpha_c >= 3.0 x 10^{-4} the burning started as a deflagration with excitation of stellar pulsations with growing amplitude. Eventually, the detonation set in, which was activated near the surface layers of the presupernova (with m about 1.33 M_\odot) and penetrated into the star down to the deflagration front. Excitation of model pulsations and formation of a detonation front are described in detail for the variant with \alpha_c=1.0 x 10^{-3}.Comment: 13 pages, 11 figures, to appear in Astronomy Letter

The origin of intergalactic thermonuclear supernovae

The population synthesis method is used to study the possibility of explaining the appreciable fraction (20^+12_15%) of the intergalactic (no-host) type Ia supernovae observed in galaxy clusters (Gal-Yam ete al. 2003) by binary whote dwarf merginngs in the cores of globular clusters. In a typical globular cluster, the number of merging double white dwarfs is fount to be smaller than 10^{-13} per year per average cluster star during the entire evolution of the cluster, which is a factor of 3 higher than in a Milky-Way-type galaxy. From 5 to 30% of the merging white dwarfs are dynamically expelled from the cluster with barycenter velocities up to 150 km/s. SN Ia explosions during the mergers of binary white dwarfs in dense star clusters may account for \sim 1% of the total rate of SN Ia in the central parts of galaxy clusters if the baryon mass fraction in such star clusters is \sim 0.3%.Comment: 8 pages, 3 figs. Astronomy Letters (in press

Dynamics and Radiation of Young Type-Ia Supernova Remnants: Important Physical Processes

We examine and analyze the physical processes that should be taken into account when modeling young type-Ia SNRs, with ages of several hundred years. It is shown, that energy losses in the metal-rich ejecta can be essential for remnants already at this stage of evolution. The influence of electron thermal conduction and the rate of the energy exchange between electrons and ions on the temperature distribution and the X-radiation from such remnants is studied. The data for Tycho SNR from the XMM-Newton X-ray telescope have been employed for the comparison of calculations with observations.Comment: 19 pages, 8 figure

Neutron stars in globular clusters: formation and observational manifestations

Population synthesis is used to model the number of neutron stars in globular clusters that are observed as LMXBs and millisecond PSRs. The dynamical interaction between binary and single stars in a GC are assumed to take place with a permanently replenished "background" of single stars whose density distribution keeps track with the cluster evolution as a whole and evolution of single stars. We use the hypothesis (Podsiadlowski et al) that NS forming in binary systems from components with initial masses \sim 8-12 M_\odot during the electron-capture collapse of the degenerate O-Ne-Mg core do not acquire a high space velocities (kicks). The remaining NSs (i.e. from single stars with M>8 M_\odot or binary comonents with M>12 M_\odot) are assumed to be born with high kicks, as found from obsrevations of single pulsars (Hobbs et al. 2005). Under this assumption, a sizeable fraction of NSs remain in GCs (about 1000 NSs in a GC with a mass of 5\times 10^5 M_\odot). The number of ms PSRs formed in the cluster via accretion spin-up in binaries is then about 10, which is consistent with observations. Our modelling reproduces the observed shape of the X-ray luminosity function for accreting NSs in binaries with normal and degenerate components and the distribution of spin periods of ms PSRs in GCs under the assumption of accretion-driven magnetic field decay of NSs up to a bottom value of 10^8 G. The number of LMXBs and ms PSRs dynamically expelling from GCs is also calculated.Comment: LATEX, 21 pages, 8 gif figures, Astronomy Letters, in pres

Modulation of the Cholesterol-Dependent Activity of Macrophages IC-21 by CRAC Peptides with Substituted Motif-Forming Amino Acids

Abstract: The activity of many membrane proteins, such as receptors, ionic channels, transporters, and enzymes, is cholesterol dependent; however, mechanisms of the cholesterol-dependent regulation of protein functions remain obscure. Recent studies suggest that membrane proteins can directly interact with cholesterol owing to the presence of the cholesterol-recognizing amino-acid consensus (CRAC) motifs. One of the ways to verify and further develop this notion is a design of CRAC-containing peptides and investigation of their effects on cholesterol-dependent cell functions. Previously we showed that a newly constructed peptide RTKLWEMLVELGNMDKAVKLWRKLKR (peptide P4) containing two CRAC motifs modulates cholesterol-dependent interactions of cultured macrophages IC-21 with 2-μm particles. In this work, in order to clarify the role of CRAC-forming amino acids, we employed the same experimental system to test the activity of peptides closely related to P4 but with modified CRAC motifs. We found that peptide STKLSEMLSELGNMDKASKLSRKLSR (Mut2) analogous to P4, except that all CRAC-forming amino acids (V, W, K/R) were substituted by serine, did not produce any effect in the concentration range 0.5–50 μM corresponding to the range of the P4 activity. Neither was effective peptide RTKLSEMLVELGNMDKAVKLSRKLKR (Mut3), in which only aromatic amino acids (W) of the CRAC motifs were substituted. Peptide STKLWEMLVELGNMDKAVKLWRKLSR (Mut4), in which only cationic amino acids (R/K) in the CRAC motifs were changed, produced almost the same effect as that of peptide P4 with a bell-shape dose–response curve. At low concentrations (1–4 μM) Mut4 notably increased the number of beads per cell, at higher concentrations this parameter diminished, and at 50 μM Mut4 produced a robust toxic effect. Finally, peptide EWGMAVLWERNRKLKKDLKVLKMLRT (Mut1) composed of the same amino acid residues as P4 but in a random order (“scramble”) and possessing one CRAC motif, different from that in P4, produced a moderate stimulation at 4–10 μM but was not toxic at 50 μM. As in the case of peptide P4, the effects of Mut4 and Mut1 depended on the cholesterol content in the cell membrane: after the incubation of cells with cholesterol-extracting agent methyl-β-cyclodextrin stimulatory effects produced by Mut4 and Mut1 at low doses were suppressed. Our results indicate that CRAC motifs play an important role in the mechanisms of the peptide-induced modulations of cholesterol-dependent cell functions in the experimental system used and that of the three motif-forming amino acids, critical is the presence of the aromatic amino acid (W). Further research is required to comprehend the molecular mechanisms of interactions of CRAC-containing peptides with cell membrane components that lead to modulation of cell functions. We anticipate that CRAC-containing peptides may provide a basis for the development of new tools for directed regulation of the activity of target cholesterol-dependent membrane proteins and for the design of new antimicrobial and immunomodulating drugs in particular

Modulation of the cholesterol-dependent activity of macrophages IC-21 by CRAC peptides with substituted motive-forming amino acids

The activity of many membrane proteins, such as receptors, ionic channels, transporters, and enzymes, is cholesterol dependent; however, mechanisms of the cholesteroldependent regulation of protein functions remain obscure. Recent studies suggest that membrane proteins can directly interact with cholesterol owing to the presence of the cholesterolrecognizing aminoacid consensus (CRAC) motifs. One of the ways to verify and further develop this notion is a design of CRACcontaining peptides and investigation of their effects on cholesteroldependent cell functions. Previously we showed that a newly constructed peptide RTKL ÏÏEMJLVJELGNM DKAVKLWRKLKR (peptide P4) containing two CRAC motifs modulates cholesteroldependent interactions of cultured macrophages IC21 with 2u.m particles. In this work, in order to clarify the role of CRACforming amino acids, we employed the same experimental system to test the activity of peptides closely related to P4 but with modified CRAC motifs. We found that peptide STKLSEMLSEL GNMDKASKL SRKLS R (Mut2) analogous to P4, except that all CRACforming amino acids were substituted by serine (V»S,W»S,R>S), did not produce any effect in the concentration range 0.550 fiM corresponding to the range of the P4 activity. Neither was effective peptide RTKLSEMLVEL GNMDKAVKLSRKLKR (Mut3), in which only aromatic amino acids of the C R A C motifs were substituted (W » S). Peptide STKLWEMLVEL GNMDKAVKLWRKLSR (Mut4), in which only cationic amino acids in the CRAC motifs were changed (R / K » S), produced almost the same effect as that of peptide P4 with a bellshape dose—response curve. At low concentrations (1 —4 ]iM) Mut4 notably increased the number of beads per cell, at higher concentrations this parameter diminished, and at 50 Ц.М Mut4 produced a robust toxic effect. Finally, peptide EWGMAYLffiEßNRKLKKDLKVLKMLRT (Muti) composed of the same amino acid residues as P4 but in a random order ("scramble") and possessing one CRAC motif, different from that in P4, produced a moderate stimulation at 4—10 |J.M but was not toxic at 50 u.M. As in the case of peptide P4, the effects of Mut4 and Muti depended on the cholesterol content in the cell membrane: after the incubation of cells with cholesterolextracting agent methylßcyclodextrin stimulatory effects produced by Mut4 and Muti at low doses were suppressed. Our results indicate that CRAC motifs play an important role in the mechanisms of the peptide-induced modulations of cholesterol-dependent cell functions in the experimental system used and that of the three motif-forming amino acids, critical is the presence of aromatic amino acids (W). Further research is required to comprehend the molecular mechanisms of interactions of CRAC-containing peptides with cell membrane components that lead to modulation of cell functions. We anticipate that CRAC-containing peptides may provide a basis for the development of new tools for directed regulation of the activity of target cholesterol-dependent membrane proteins and for the design of new antimicrobial and immunomodulating drugs in particular

Membrane Permeability Changes at Early Stages of Influenza Hemagglutinin-Mediated Fusion

While biological membrane fusion is classically defined as the leak-free merger of membranes and contents, leakage is a finding in both experimental and theoretical studies. The fusion stages, if any, that allow membrane permeation are uncharted. In this study we monitored membrane ionic permeability at early stages of fusion mediated by the fusogenic protein influenza hemagglutinin (HA). HAb2 cells, expressing HA on their plasma membrane, fused with human red blood cells, cultured liver cells PLC/PRF/5, or planar phospholipid bilayer membranes. With a probability that depended upon the target membrane, an increase of the electrical conductance of the fusing membranes (leakage) by up to several nS was generally detected. This leakage was recorded at the initial stages of fusion, when fusion pores formed. This leakage usually accompanied the “flickering” stage of the early fusion pore development. As the pore widened, the leakage reduced; concomitantly, the lipid exchange between the fusing membranes accelerated. We conclude that during fusion pore formation, HA locally and temporarily increases the permeability of fusing membranes. Subsequent rearrangement in the fusion complex leads to the resealing of the leaky membranes and enlargement of the pore