Although incarceration rates have risen sharply since the 1970s, medical sociology has largely neglected the health effects of imprisonment. Incarceration might have powerful effects on health, especially if it instills stigma, and it could provide sociologists with another mechanism for understanding health disparities. This study identifies some of incarceration's direct and indirect effects and rigorously tests them using the National Longitudinal Survey of Youth. It finds that incarceration has powerful effects on health, but only after release. A history of incarceration strongly increases the likelihood of severe health limitations. Furthermore, any contact with prison is generally more important than the amount of contact, a finding consistent with a stigma-based interpretation. Although this relationship is partly attributable to diminished wage growth and marital instability, the bulk of the effect remains even under the most stringent of specifications, including controls for intelligence and the use of fixed effects, suggesting a far-reaching process with a proliferation of risk factors. The study also finds that incarceration contributes only modestly to racial disparities, that there are few synergistic interactions between incarceration and other features of inequality, including schooling, and that the evidence for a causal effect is much weaker among persistent recidivists and those serving exceptionally long sentences. These study findings are inconsistent with recent speculation; nevertheless, incarceration is an important addition to sociology's research agenda. Exploring incarceration could lead to, among other things, a fruitful synergy among studies on fundamental causes, stigma, and stress.

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A wide variety of contaminants are ingested through food, among them the pro-carcinogenic polycyclic aromatic hydrocarbon benzo[a]pyrene (BP) that is resorbed and partially metabolized in the enterocytes of the small intestine. Previous in vitro studies have revealed that BP phenols are excreted as Phase II metabolites including glucuronides and sulfates. This export is mediated by the breast cancer resistance protein (ABCG2). The ultimate carcinogenic Phase I BP metabolite anti-BP-7,8-dihydrodiol-9,10-epoxide (BPDE) can be detoxified by glutathione conjugate formation catalyzed by glutathione S-transferases. In the present study, differentiated human intestinal Caco-2 cells were used as a model for the human small intestine to investigate the detoxification of BPDE and excretion of stereoisomeric glutathione conjugates in the presence of an inhibitor of the glutathione-cleaving enzyme γ-glutamyl transpeptidase at the cell surface. The results indicate that the glutathione conjugates of BPDE are formed and excreted mainly to the apical and to a minor extent to the basolateral side of polarized Caco-2 monolayers. Inhibition studies revealed that the multidrug resistance-associated proteins (ABCCs) are involved in the transport of BPDE glutathione conjugates. Stable ABCC1, ABCC2 and ABCC3 knockdown cell lines were generated, thus making it possible to demonstrate that ABCC1 mediates the basolateral and ABCC2 the apical excretion of BPDE glutathione conjugates. In conclusion, the ultimate carcinogen BPDE is detoxified via glutathione conjugation and subsequently excreted by Caco-2 cells in both apical and basolateral directions. This finding is equivalent to a transport into feces as well as blood system in the in vivo situation.

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There is a remarkable clonality among invasive GBS isolates that are widely spread geographically and in time; however, no specific clonal lines could be correlated to disease severity and outcome.

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In this study we have examined the relationship of benzo[a]pyrene (B[a]P) exposure with B[a]P-7,8-diol-9,10-epoxide (BPDE) adduct formation in globin and serum albumin (SA). We also have evaluated the relationship of BPDE-globin and -SA adduct formation with urinary 1 -hydroxypyrene ( 1 -OH-pyrene), and bulky DNA adducts in peripheral blood lymphocytes. The study groups consist of male Hungarian garage mechanics (smokers and nonsmokers) exposed to diesel engine exhaust and matched control samples from a blood bank in Budapest. The mean level of BPDEglobin adducts in the garage mechanics (n=15) is 5.914.8 fmoVmg globin (ranging from 0.5 to 19.9 fmol/mg globin) and that in controls (n=15), is 2.4*2.5 fmol/mg globin (ranging from ND to 8.5 fmol BPDE/mg globin). The mean of BPDE-SA in garage mechanics is 0.3650.6 fmol/mg SA (ranging from ND to 2.6 fmol/mg SA) and, in controls it is 0.29i0.3 fmol/mg SA (ranging from ND to 1.3 fmol/mg SA). The results of this study indicate that levels of BPDE-SA adducts are about one order of magnitude lower than levels of globin adducts. The mean of BPDE-globin and -SA adducts in garage mechanics are 2.4-fold (p=0.02) and 1.2-fold @=0.7) higher than I15 I26 A. A. MELIKIAN e t a /those in controls, respectively. Similarly, levels of urinary 1 -0H-pyrene in the exposed group are 2.1 -fold higher than those in controls @=0.03). The correlation coefficients between estimated B[n]P exposure (both ingested and inhaled) and formation of globin adducts and urinary 1-OH-pyrene are ~0 . 4 9 (p=0.06), and r=0.3 1 (p=0.26), respectively. This study suggests that BPDE-globin adducts and urinary 1-OH-pyrene may be better biomarkers of exposure than BPDE-SA adducts.