125 research outputs found
Thermal Equilibria of Optically Thin, Magnetically Supported, Two-Temperature, Black Hole Accretion Disks
We obtained thermal equilibrium solutions for optically thin, two-temperature
black hole accretion disks incorporating magnetic fields. The main objective of
this study is to explain the bright/hard state observed during the bright/slow
transition of galactic black hole candidates. We assume that the energy
transfer from ions to electrons occurs via Coulomb collisions. Bremsstrahlung,
synchrotron, and inverse Compton scattering are considered as the radiative
cooling processes. In order to complete the set of basic equations, we specify
the magnetic flux advection rate. We find magnetically supported (low-beta),
thermally stable solutions. In these solutions, the total amount of the heating
via the dissipation of turbulent magnetic fields goes into electrons and
balances the radiative cooling. The low- solutions extend to high mass
accretion rates and the electron temperature is moderately cool. High
luminosities and moderately high energy cutoffs in the X-ray spectrum observed
in the bright/hard state can be explained by the low-beta solutions.Comment: 24 pages, 10 figures,accepted for publication in Astrophysical
Journa
Thermal Equilibria of Magnetically Supported, Black Hole Accretion Disks
We present new thermal equilibrium solutions for optically thin and thick
disks incorporating magnetic fields. The purpose of this paper is to explain
the bright hard state and the bright/slow transition observed in the rising
phases of outbursts in BHCs. On the basis of the results of 3D MHD simulations,
we assume that magnetic fields inside the disk are turbulent and dominated by
the azimuthal component and that the azimuthally averaged Maxwell stress is
proportional to the total pressure. We prescribe the magnetic flux advection
rate to determine the azimuthal magnetic flux at a given radius.
We find magnetically supported, thermally stable solutions for both optically
thin and thick disks, in which the heating enhanced by the strong magnetic
field balances the radiative cooling. The temperature in a low- disk is
lower than that in an ADAF/RIAF but higher than that in a standard disk. We
also study the radial dependence of the thermal equilibrium solutions.
The optically thin, low- branch extends to , in which the temperature anti-correlates with the mass accretion
rate. Thus optically thin low- disks can explain the bright hard state.
Optically thick, low- disks have the radial dependence of the effective
temperature . Such disks will be observed as
staying in a high/soft state. Furthermore, limit cycle oscillations between an
optically thick low- disk and a slim disk will occur because the
optically thick low- branch intersects with the radiation pressure
dominated standard disk branch. These limit cycle oscillations will show a
smaller luminosity variation than that between a standard disk and a slim disk.Comment: 23 pages, 9 figures, accepted for publication in Ap
P38 Mitogen-Activated Protein Kinase Inhibitor, FR167653, Inhibits Parathyroid Hormone Related Protein-Induced Osteoclastogenesis and Bone Resorption
p38 mitogen-activated protein kinase (MAPK) acts downstream in the signaling pathway that includes receptor activator of NF-κB (RANK), a powerful inducer of osteoclast formation and activation. We investigated the role of p38 MAPK in parathyroid hormone related protein (PTHrP)-induced osteoclastogenesis in vitro and PTHrP-induced bone resorption in vivo. The ability of FR167653 to inhibit osteoclast formation was evaluated by counting the number of tartrate-resistant acid phosphatase positive multinucleated cells (TRAP-positive MNCs) in in vitro osteoclastgenesis assays. Its mechanisms were evaluated by detecting the expression level of c-Fos and nuclear factor of activated T cells c1 (NFATc1) in bone marrow macrophages(BMMs) stimulated with sRANKL and M-CSF, and by detecting the expression level of osteoprotegerin (OPG) and RANKL in bone marrow stromal cells stimulated with PTHrP in the presence of FR167653. The function of FR167653 on bone resorption was assessed by measuring the bone resorption area radiographically and by counting osteoclast number per unit bone tissue area in calvaria in a mouse model of bone resorption by injecting PTHrP subcutaneously onto calvaria. Whole blood ionized calcium levels were also recorded. FR167653 inhibited PTHrP-induced osteoclast formation and PTHrP-induced c-Fos and NFATc1 expression in bone marrow macrophages, but not the expression levels of RANKL and OPG in primary bone marrow stromal cells treated by PTHrP. Furthermore, bone resorption area and osteoclast number in vivo were significantly decreased by the treatment of FR167653. Systemic hypercalcemia was also partially inhibited. Inhibition of p38 MAPK by FR167653 blocks PTHrP-induced osteoclastogenesis in vitro and PTHrP-induced bone resorption in vivo, suggesting that the p38 MAPK signaling pathway plays a fundamental role in PTHrP-induced osteoclastic bone resorption
Chiral vanadyl salen catalyst immobilized on mesoporous silica as support for asymmetric oxidation of sulfides to sulfoxides
The Mammalian Disaggregase Machinery: Hsp110 Synergizes with Hsp70 and Hsp40 to Catalyze Protein Disaggregation and Reactivation in a Cell-Free System
Bacteria, fungi, protozoa, chromista and plants all harbor homologues of Hsp104, a AAA+ ATPase that collaborates with Hsp70 and Hsp40 to promote protein disaggregation and reactivation. Curiously, however, metazoa do not possess an Hsp104 homologue. Thus, whether animal cells renature large protein aggregates has long remained unclear. Here, it is established that mammalian cytosol prepared from different sources possesses a potent, ATP-dependent protein disaggregase and reactivation activity, which can be accelerated and stimulated by Hsp104. This activity did not require the AAA+ ATPase, p97. Rather, mammalian Hsp110 (Apg-2), Hsp70 (Hsc70 or Hsp70) and Hsp40 (Hdj1) were necessary and sufficient to slowly dissolve large disordered aggregates and recover natively folded protein. This slow disaggregase activity was conserved to yeast Hsp110 (Sse1), Hsp70 (Ssa1) and Hsp40 (Sis1 or Ydj1). Hsp110 must engage substrate, engage Hsp70, promote nucleotide exchange on Hsp70, and hydrolyze ATP to promote disaggregation of disordered aggregates. Similarly, Hsp70 must engage substrate and Hsp110, and hydrolyze ATP for protein disaggregation. Hsp40 must harbor a functional J domain to promote protein disaggregation, but the J domain alone is insufficient. Optimal disaggregase activity is achieved when the Hsp40 can stimulate the ATPase activity of Hsp110 and Hsp70. Finally, Hsp110, Hsp70 and Hsp40 fail to rapidly remodel amyloid forms of the yeast prion protein, Sup35, or the Parkinson's disease protein, alpha-synuclein. However, Hsp110, Hsp70 and Hsp40 enhanced the activity of Hsp104 against these amyloid substrates. Taken together, these findings suggest that Hsp110 fulfils a subset of Hsp104 activities in mammals. Moreover, they suggest that Hsp104 can collaborate with the mammalian disaggregase machinery to rapidly remodel amyloid conformers
Social Transfer of Pathogenic Fungus Promotes Active Immunisation in Ant Colonies
Social contact with fungus-exposed ants leads to pathogen transfer to healthy nest-mates, causing low-level infections. These micro-infections promote pathogen-specific immune gene expression and protective immunization of nest-mates
Mathematical models for immunology:current state of the art and future research directions
The advances in genetics and biochemistry that have taken place over the last 10 years led to significant advances in experimental and clinical immunology. In turn, this has led to the development of new mathematical models to investigate qualitatively and quantitatively various open questions in immunology. In this study we present a review of some research areas in mathematical immunology that evolved over the last 10 years. To this end, we take a step-by-step approach in discussing a range of models derived to study the dynamics of both the innate and immune responses at the molecular, cellular and tissue scales. To emphasise the use of mathematics in modelling in this area, we also review some of the mathematical tools used to investigate these models. Finally, we discuss some future trends in both experimental immunology and mathematical immunology for the upcoming years
SIRT1 activator (SRT1720) improves the follicle reserve and prolongs the ovarian lifespan of diet-induced obesity in female mice via activating SIRT1 and suppressing mTOR signaling
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