1,721,036 research outputs found

    Immunopathogenesis of Psoriasis and Pharmacalogical Perspectives.

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    Psoriasis is a chronic inflammatory disorder resulting from a combination of genetic and environmental factors, although the precise causal agents have not yet been identified. The immune system has a major role in the development of psoriasis, and the possibility exists that self antigens, antigens from microbial agents, or microbial superantigens initiate a vigorous immune response. Different subsets of T lymphocytes and dendritic cells, mast cells, and granulocytes participate in the pathogenesis; and several cytokines and chemokines have been identified in tissue lesions. Tumor necrosis factor-alpha, interleukin 17 (IL-17), and IL-23 are key cytokines with important pathogenetic roles in psoriasis. Angiogenesis is a prominent early event in lesional psoriatic skin. Potential targets in the treatment of this disorder include biologic agents aimed at blockade of cytokines, chemokines, and angiogenic factors

    Modulation of mast cell and basophil functions by benzene metabolites

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    Benzene is a carcinogenic compound used in industrial manufacturing and a common environmental pollutant mostly derived from vehicle emissions and cigarette smoke. Benzene exposure is associated with a variety of clinical conditions ranging from hematologic diseases to chronic lung disorders. Beside its direct toxicity, benzene exerts multiple effects after being converted to reactive metabolites such as hydroquinone and benzoquinone. Mast cells and basophils are primary effector cells involved in the development of respiratory allergies such as rhinitis and bronchial asthma and they play an important role in innate immunity. Benzene and its metabolites can influence mast cell and basophil responses either directly or by interfering with other cells, such as T cells, macrophages and monocytes, which are functionally connected to mast cells and basophils. Hydroquinone and benzoquinone inhibit the release of preformed mediators, leukotriene synthesis and cytokine production in human basophils stimulated by IgE- and non IgE-mediated agonists. Furthermore, these metabolites reduce IgE-mediated degranulation of mast cells and the development of allergic lung inflammation in rats. Both in vitro and in vivo studies indicate that benzene metabolites alter biochemical and functional activities of other immunocompetent cells and may impair immune responses in the lung. These inhibitory effects of benzene metabolites are primarily mediated by interference with early transduction signals such as PI3 kinase. Together, currently available studies indicate that benzene metabolites interfere by multiple mechanisms with the role of basophils and mast cells in innate immunity and in chronic inflammation in the lung. © 2011 Bentham Science Publishers

    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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