Detailed X-ray images and spectra of the galactic-center region up to 10 keV were obtained with ASCA. Diffuse thermal-emission with distinct Kα lines from highly ionized ions of various elements has confirmed the presence of an extended high-temperature plasma. The fluorescent X-ray emission from cold iron atoms in molecular clouds was also found, possibly due to irradiation by X-rays from the center, which was bright in the past, but is presently dim. The results suggest that the galactic center exhibited intermittent activities with a time-averaged energy generation rate comparable to Seyfert nuclei, a class of active galactic nuclei.

IL-6 is a multifunctional proinflammatory cytokine that is elevated in the serum of patients with pulmonary arterial hypertension (PAH) and can predict the survival of patients with idiopathic PAH (IPAH). Previous animal experiments and clinical human studies indicate that IL-6 is important in PAH; however, the molecular mechanisms of IL-6-mediated pathogenesis of PAH have been elusive. Here we identified IL-21 as a downstream target of IL-6 signaling in PAH. First, we found that IL-6 blockade by the monoclonal anti-IL-6 receptor antibody, MR16-1, ameliorated hypoxiainduced pulmonary hypertension (HPH) and prevented the hypoxia-induced accumulation of Th17 cells and M2 macrophages in the lungs. Consistently, the expression levels of IL-17 and IL-21 genes, one of the signature genes for Th17 cells, were significantly up-regulated after hypoxia exposure in the lungs of mice treated with control antibody but not in the lungs of mice treated with MR16-1. Although IL-17 blockade with an anti-IL-17A neutralizing antibody had no effect on HPH, IL-21 receptor-deficient mice were resistant to HPH and exhibited no significant accumulation of M2 macrophages in the lungs. In accordance with these findings, IL-21 promoted the polarization of primary alveolar macrophages toward the M2 phenotype. Of note, significantly enhanced expressions of IL-21 and M2 macrophage markers were detected in the lungs of IPAH patients who underwent lung transplantation. Collectively, these findings suggest that IL-21 promotes PAH in association with M2 macrophage polarization, downstream of IL-6-signaling. The IL-6/IL-21-signaling axis may be a potential target for treating PAH.pulmonary arterial hypertension | interleukin-21 | interleukin-6 | Th17 cells | M2 macrophage

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Hydrogen sulphide (H2S), a chemical hazard in oil and gas production, has recently become a dreadful method of suicide, posing specific risks and challenges for the first responders. Currently, there is no proven effective treatment against H2S poisoning and its severe neurological, respiratory or cardiac after-effects. We have recently described that H2S is present in various compartments, or pools, in the body during sulphide exposure, which have different levels of toxicity. The general goals of our study were to (1) determine the concentrations and kinetics of the various pools of hydrogen sulphide in the blood, i.e., gaseous (CgH2S) versus total sulphide, i.e., reacting with monobromobimane (CMBBH2S), during and following H2S exposure in a small and large mammal and (2) establish the interaction between the pools of H2S and a methemoglobin (MetHb) solution or a high dose of hydroxocobalamin (HyCo). We found that CgH2S during and following H2S infusion was similar in sedated sheep and rats at any given rate of infusion/kg and provoked symptoms, i.e., hyperpnea and apnea, at the same CgH2S. After H2S administration was stopped, CgH2S disappeared within 1 min. CMBBH2S also dropped to 2-3μM, but remained above baseline levels for at least 30 min. Infusion of a MetHb solution during H2S infusion produced an immediate reduction in the free/soluble pool of H2S only, whereas CMBBH2S increased by severalfold. HyCo (70 mg/kg) also decreased the concentrations of free/soluble H2S to almost zero; CgH2S returned to pre-HyCo levels within a maximum of 20 min, if H2S infusion is maintained. These results are discussed in the context of a relevant scenario, wherein antidotes can only be administered after H2S exposure.

The combustion wave structure and thermal decomposition process of azide polymer were studied to determine the parameters which control the burning rate. The azide polymer studied was glycidyl azide polymer (GAP) which contains energetic – N3 groups. GAP was cured with hexamethylene diisocyanate (HMDI) and crosslinked with trimethylolpropane (TMP) to formulate GAP propellant. From the experiments, it was found that the burning rate of GAP propellant is significantly high even though the adiabatic flame temperature of GAP propellant is lower than that of conventional solid propellants. The energy released at the burning surface of GAP propellant is caused by the scission of NN2 bond which produces gaseous N2. The heat flux transferred back from the gas phase to the burning surface is very small compared with the heat generated at the burning surface. The activation energy of the decomposition of the burning surface of GAP propellant, Es, is determined to be 87 kJ/mol. The burning rate is represented by r = 9.16 × 103 exp(–Es/RTs) where r (m/s) is burning rate, Ts (K) is the burning surface temperature, and R is the universal gas constant. The observed high temperature sensitivity of burning rate is correlated to the relationship of (∂Ts/∂T0)p = 0.481 at 5 MPa, where T0 is the initial propellant temperature.