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The accurate identification of risk factors is central to the development of effective efforts to prevent young people from using alcohol, tobacco and other substances. To date, a key limitation of the prevention literature has been the paucity of research that examines the extent to which substance use risk factors identified in studies of white adolescents generalize to African American (and other non-white) youth. In the absence of research on race differences in risk factor exposure and vulnerability, current preventive interventions are based on the implicit assumptions that 1) the risk factors for African American and white adolescents' substance use are identical; and 2) that African American and white adolescents are equally exposed and equally vulnerable to these risk factors. The purpose of the present study was to begin to examine empirically the equal exposure and vulnerability assumption. Specifically, the paper used Hawkins, Catalano and Millers' widely cited 1992 article on risk and protective factors for adolescent and young adult substance use as a framework within which to review past risk factor research and as a guide to identify risk factors to examine for race differences in exposure and/or vulnerability. Based upon our review of the existing literature and our analysis of data from the University of Michigan's Monitoring the Future study, we conclude that the simple assumption that African American and white youth are equally exposed and vulnerable to the same risk factors is not correct. In fact, we found that African American and white seniors' differed significantly in their exposure to more than half of the 55 risk factors examined. Similarly, nearly one third of the 165 tests for race differences in vulnerability were highly significant (i.e., p < .01). While it is possible that some of the differences we identified resulted from chance, their consistency across variables, within the same risk factor domain, and across drug categories, makes the likelihood that our findings are primarily statistical artifacts unlikely. Based upon the results of this study it is clear that additional theoretically and empirically rigorous race-specific research is needed to better understand the etiology of substance use among African American adolescents. Further research is also needed to identify those risk factors that are most salient for African American adolescents and most amenable to change through well designed, and perhaps, culturally tailored preventive interventions.  相似文献   
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Nasal polyps and allergic rhinitis are upper airway inflammatory conditions characterized by increased numbers of eosinophils and metachromatic cells in the epithelial layer of the nasal mucosa. The objective of the current studies was to investigate the potential contribution of epithelial cells to the accumulation of inflammatory cells in the tissue. We have established pure cultures of human upper airway epithelial cells from normal and inflamed nasal polyps and allergic rhinitis tissue and examined the ability of conditioned medium from these cells (EpCM) to induce differentiation of human hemopoietic progenitors in vitro. We show that, under appropriate culture conditions, EpCMs, particularly those from cells derived from inflamed tissues, induce histamine-containing cell differentiation of cells of the human HL-60 myeloid leukemia cell line. These EpCMs also induce the emergence of both eosinophil/basophil and granulocyte/macrophage colonies in methylcellulose cultures of human peripheral blood mononuclear cells. We also show that CMs from epithelial cells derived from inflamed tissues contain greater amounts of granulocyte-macrophage colony-stimulating factor (GM-CSF) compared to CMs from normal epithelial cells. Finally, we show that the histamine-containing cell differentiation of HL-60 cells as well as the colony growth induced by EpCM can be fully inhibited by preincubating this CM with a monoclonal neutralizing antibody to human GM-CSF. These studies: (a) illustrate the ability of human upper airway epithelial cells to secrete GM-CSF in vitro; (b) demonstrate differences between normal and inflamed tissue-derived epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   
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Costimulation through the inducible costimulator (ICOS) and its ligand (ICOSL) is essential for T cell-dependent B cell responses, but the cellular and temporal dynamics underlying its in vivo effects are poorly defined. Here we have shown that Icosl(-/-) and Icos(-/-) mice had similar phenotypes and that ICOS-ICOSL costimulation modulated the early but not late phases of IgG1 affinity maturation. Exploiting the adoptive transfer of T or B cells from primed Icosl(-/-) mice, we provided genetic evidence that costimulation through ICOSL was essential for primary but not secondary helper T cell responses and for the control of both T and B cell activities, resulting in T cell-dependent IgG1 production.  相似文献   
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Halpern MT  Cifaldi MA  Schmier JK 《COPD》2005,2(2):217-223
We used decision-analysis modeling to compare costs and outcomes of clarithromycin extended-release (Biaxin XL, Abbott Laboratories, Abbott Park, Illinois, USA) and clarithromycin immediate-release (Biaxin, Abbott Laboratories, Abbott Park, Illinois, USA) for outpatients with lower respiratory tract infections (LRTI). More patients achieved clinical cure with extended-release (83.9%) versus immediate-release (72.8%); fewer discontinued due to adverse events. Total costs with extended-release were $32 (16%) less; incorporating greater adherence for extended-release (once-daily) therapy resulted in greater savings. Results indicate that clarithromycin extended-release is cost-saving compared with immediate-release for LRTI.  相似文献   
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