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    Inhibition of ShcA isoforms p46/p52Shc enhances HIV-1 replication in CD4+ T-lymphocytes

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    HIV-1 infection decreases the number of CD4(+) T-cells, and apoptosis has been suggested among the mechanisms. Proteins of the Shc family are involved in a complex network of signal transcluction, differentiation, and apoptotic response to stress in many different cell types. Out of three homologous gene products (ShcA, ShcB, and ShcC, only two splicing variants of ShA are expressed in T-lymphocytes, namely p46Shc and p52Shc. In the present study, we report that inhibition of p46Shc and p52Shc by a dominant negative mutant enhances the yield of HIV-1 particles production without affecting efficiency of viral gene expression in CD4(+)-infected cells. The increase in HIV-1 replication in cells expressing the dominant negative mutant isoform ultimately correlates with a decrease in the percentage of cells entering apoptosis. The data presented suggest that ShcA proteins can play a role in committing CID4(+) T-cells to apoptosis, as a response to HIV-1 infectio

    Anthrax toxins: a paradigm of bacterial immune suppression

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    Several species of microorganism have developed immune evasion and/or immunosuppression strategies. Bacillus anthracis secretes two toxins, edema toxin and lethal toxin, that enter the cytosol of almost every cell type, including the cells of the innate and adaptive immune systems, and subvert cell signaling. Edema toxin causes a consistent elevation of cyclic adenosine monophosphate, whereas lethal toxin cleaves most isoforms of mitogen-activated protein kinase kinases. In a concerted manner, these toxins alter major signaling pathways involved in the development of immune-cell effector functions, with the inhibition of bacterial clearance by phagocytes and of B. anthracis-specific responses. Thus, B. anthracis can invade the host, with ensuing massive bacteremia and toxemia. Here, we review the specific effects of B. anthracis on neutrophils, macrophages, dendritic cells, T- and B-lymphocytes

    Going Beyond Counting First Authors in Author Co-citation Analysis

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    The present study examines one of the fundamental aspects of author co-citation analysis (ACA) - the way co-citation counts are defined. Co-citation counting provides the data on which all subsequent statistical analyses and mappings are based, and we compare ACA results based on two different types of co-citation counting - the traditional type that only counts the first one among a cited work's authors on the one hand and a non-traditional type that takes into account the first 5 authors of a cited work on the other hand. Results indicate that the picture produced through this non-traditional author co-citation counting contains more coherent author groups and is therefore considerably clearer. However, this picture represents fewer specialties in the research field being studied than that produced through the traditional first-author co-citation counting when the same number of top-ranked authors is selected and analyzed. Reasons for these effects are discussed
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