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    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

    HIV-1 p17 binds heparan sulfate proteoglycans to activated CD4(+) T cells

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    We have previously shown that HIV-1 p17 binds to activated peripheral blood mononuclear cells and enhances secretion of pro-inflammatory cytokines, but we were unable to define a ligand on activated cells. In this work we evaluate the hypothesis that HIV-1 p17 may be a heparin/heparan sulfate-binding protein. HIV-1 p17 contains C- and N-terminal sequences with positively charged residues and a consensus cluster for heparin binding.We demonstrated by affinity chromatography that HIV-1 p17 binds strongly to heparin-agarose at physiological pH. Soluble heparins and heparan sulfate but not chondroitin 4-sulfate and dextran sulfate inhibit binding of HIV-1 p17 to heparin solid phase and to activated CD4+ T cells. Furthermore the inhibition of cell sulfatation by chlorate treatment completely counteracts HIV-1 p17 binding to activated cells. These results indicate for the first time that HIV-1 p17 can be ascribed to the heparin binding protein family and suggest that this interaction might play a key role in the ability of the protein to induce an inflammatory effect on activated cells

    RAC2 and primary human immune deficiencies

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    RAC2 is a GTPase that is exclusively expressed in hematopoietic cells. Animal models have suggested important roles for RAC2 in the biology of different cell types, such as neutrophils and lymphocytes. Primary immunodeficiencies represent “experimentum naturae” and offer priceless insight on the function of the human immune system. Mutations in RAC2 have been identified in a small number of patients giving rise to different forms of primary immunodeficiencies ranging from granulocyte defects caused by dominant negative mutations to combined immunodeficiency due to dominant activating mutations. This review will focus on the clinical and immunologic phenotype of patients with germline mutations in RAC2
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