18 research outputs found

    The HERA-B Ring Imaging Cherenkov Counter

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    The HERA-B RICH uses a radiation path length of 2.8 m in C_4F_10 gas and a large 24 square meters spherical mirror for imaging Cherenkov rings. The photon detector consists of 2240 Hamamatsu multi-anode photomultipliers with about 27000 channels. A 2:1 reducing two-lens telescope in front of each PMT increases the sensitive area at the expense of increased pixel size, resulting in a contribution to the resolution which roughly matches that of dispersion. The counter was completed in January of 1999, and its performance has been steady and reliable over the years it has been in operation. The design performance of the RICH was fully reached: the average number of detected photons in the RICH for a beta=1 particle was found to be 33 with a single hit resolution of 0.7 mrad and 1 mrad in the fine and coarse granularity regions, respectively.Comment: 29 pages, 23 figure

    Complex Formation among Murine Cytomegalovirus US22 Proteins Encoded by Genes M139, M140, and M141

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    The murine cytomegalovirus (MCMV) proteins encoded by US22 genes M139, M140, and M141 function, at least in part, to regulate replication of this virus in macrophages. Mutant MCMV having one or more of these genes deleted replicates poorly in macrophages in culture and in the macrophage-dense environment of the spleen. In this report, we demonstrate the existence of stable complexes formed by the products of all three of these US22 genes, as well as a complex composed of the products of M140 and M141. These complexes form in the absence of other viral proteins; however, the pM140/pM141 complex serves as a requisite binding partner for the M139 gene products. Products from all three genes colocalize to a perinuclear region of the cell juxtaposed to or within the cis-Golgi region but excluded from the trans-Golgi region. Interestingly, expression of pM141 redirects pM140 from its predominantly nuclear residence to the perinuclear, cytoplasmic locale where these US22 proteins apparently exist in complex. Thus, complexing of these nonessential, early MCMV proteins likely confers a function(s) independent of each individual protein and important for optimal replication of MCMV in its natural host

    Changes in microglia activity of rat brain induced by Macrovipera lebetina obtusa venom

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    Aim: The microglia activity of rat brain following exposure of the Macrovipera lebetina obtusa venom was investigated.Methods: Histochemical analysis of brain microcirculatory bed staining by Ca2+ ATPase method for variable doses after intraperitoneal injections given for different time periods was used. The hemorrhagic activity of snake venom metalloproteinases was tested. Toxicological data were calculated using Behrens and Miller-Tainter methods. Surface, size of brain microglial cells (MGCs) and staining intensity were quantified using ImageJ software.Results: The vasodestructive action of the venom resulted in changes in ATPase activity. The intensity of staining of rat brain microcirculatory bed was venom dose-, and time-dependent. Increased activity of MGCs in hemorrhagic loci of different regions of venom affected brain was also demonstrated.Conclusion: The activation of microglia and changes of its form, size, and position strongly correlates with hemorrhage-induced cerebrovascular damage

    A humanized model of experimental autoimmune uveitis in HLA class II transgenic mice

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    Experimental autoimmune uveitis (EAU) is a disease of the neural retina induced by immunization with retinal antigens, such as interphotoreceptor retinoid-binding protein (IRBP) and arrestin (retinal soluble antigen, S-Ag). EAU serves as a model for human autoimmune uveitic diseases associated with major histocompatibility complex (HLA) genes, in which patients exhibit immunological responses to retinal antigens. Here we report the development of a humanized EAU model in HLA transgenic (TG) mice. HLA-DR3, -DR4, -DQ6, and -DQ8 TG mice were susceptible to IRBP-induced EAU. Importantly, HLA-DR3 TG mice developed severe EAU with S-Ag, to which wild-type mice are highly resistant. Lymphocyte proliferation was blocked by anti-HLA antibodies, confirming that antigen is functionally presented by the human MHC molecules. Disease could be transferred by immune cells with a Th1-like cytokine profile. Antigen-specific T cell repertoire, as manifested by responses to overlapping peptides derived from S-Ag or IRBP, differed from that of wild-type mice. Interestingly, DR3 TG mice, but not wild-type mice, recognized an immunodominant S-Ag epitope between residues 291 and 310 that overlaps with a region of S-Ag recognized by uveitis patients. Thus, EAU in HLA TG mice offers a new model of uveitis that should represent human disease more faithfully than currently existing models
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