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-$\beta$ 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-$\beta$ 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-$\beta$ branch extends to $\dot M \gtrsim 0.1 {\dot M}_{\rm Edd}$, in which the temperature anti-correlates with the mass accretion rate. Thus optically thin low-$\beta$ disks can explain the bright hard state. Optically thick, low-$\beta$ disks have the radial dependence of the effective temperature $T_{\rm eff} \propto \varpi^{-3/4}$. Such disks will be observed as staying in a high/soft state. Furthermore, limit cycle oscillations between an optically thick low-$\beta$ disk and a slim disk will occur because the optically thick low-$\beta$ 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

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

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