We present a systematic spectral analysis of six ultraluminous X-ray sources (NGC 1313 X-1 and X-2, IC 342 X-1, Ho IX X-1, NGC 5408 X-1, and NGC 3628 X-1) observed with the XMM-Newton observatory. These extranuclear X-ray sources in nearby late-type galaxies have been considered as intermediate-mass black hole candidates. We have performed Monte Carlo simulations of Comptonized multicolor blackbody accretion disks. This unified and self-consistent spectral model assumes a spherically symmetric, thermal corona around each disk and accounts for the radiation transfer in the Comptonization. We find that the model provides satisfactory fits to the XMM-Newton spectra of the sources. The characteristic temperatures of the accretion disks (T in ), for example, are in the range of $0.05-0.3 keV, consistent with the intermediate-mass black hole interpretation. We find that the black hole mass is typically about a few times 10 3 M and has an accretion rate of $10 À6 to 10 À5 M yr À1 . For the spectra considered here, we find that the commonly used multicolor blackbody accretion disk model with an additive power-law component, although not physical, provides a good mathematical approximation to the Monte Carlo simulated model. However, the latter model provides additional constraints on the properties of the accretion systems, such as the disk inclination angles and corona optical depths.
COX plays an important role in inflammatory diseases such as rheumatoid arthritis. To determine the role of COX in Sjögren's syndrome (SS), we examined COX expression in the salivary glands of SS patients. We examined 15 patients with SS and two normal subjects. Labial salivary gland tissue samples were analysed immunohistochemically using anti‐COX‐1 and COX‐2 antibodies. All biopsy samples from 15 patients with SS were stained for COX‐1. In contrast, COX‐1 immunostaining was not detected in normal salivary gland tissues. Co‐expression of COX‐1 and CD68 was confirmed by mirror section technique and double antibody immunostaining. This finding indicated that COX‐1‐expressing cells in SS salivary glands were infiltrating macrophages. In contrast to COX‐1 staining, only a little COX‐2 immunostaining was observed in salivary gland tissues from SS patients. These data suggest that COX‐1 expression on infiltrating macrophages may contribute to the inflammatory process of salivary glands in SS.
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