38 and 2.45, respectively]. Using multiple SNPs in the logistic regression for covariates, wild-type AhR and mutant AhRR combination was significantly higher in patients (67.8%) than in controls (48.0%) (OR = 2.76). On the other hand, mutant AhRR in combination with GSTM1 null genotype was significantly higher in patients
(35.5%) than in controls (19.3%) (OR = 6.12). Conclusion Polymorphisms of dioxin receptor complex components and detoxification-related genes jointly confer susceptibility to advanced-stage endometriosis in the Taiwanese Han population. “
“Clostridium difficile is a pathogen responsible for diarrhoea and colitis, particularly after antibiotic treatment. Obeticholic Acid mouse We evaluated the C. difficile protease Cwp84, found to be associated with the S-layer proteins, as a vaccine antigen to limit the C. difficile intestinal colonization and therefore the development of the infection in a clindamycin-treated hamster model. First, we evaluated the immune response and the animal protection against death induced by several immunization routes: rectal, intragastric and subcutaneous. Antibody production was variable according to the immunization routes. In addition, serum Cwp84 antibody titres did not always correlate with animal protection after challenge with a toxigenic RO4929097 cost C. difficile strain. The best survival rate was observed with the rectal route of immunization. Then, in a second assay, we selected
this immunization route to perform a larger immunization assay including a Cwp84 immunized group and a control group. Clostridium difficile intestinal colonization and survival rate, as well as the immune response were examined. Clostridium difficile hamster challenge resulted in a 26% weaker and slower C. difficile intestinal
colonization in the immunized group. Furthermore, hamster survival in the Cwp84 immunized group was 33% greater than that of the control group, with a significant statistical difference. Following the disruption of the normal bowel microbiota by antibiotic therapy, Clostridium difficile colonizes the gut, resulting in a spectrum of diseases ranging 3-mercaptopyruvate sulfurtransferase from asymptomatic carriage to pseudomembranous colitis (PMC) (Kelly & LaMont, 1998; Wilcox, 2003). The disease symptoms are mediated by two secreted enterotoxins: TcdA and TcdB. Clostridium difficile is shed in the faeces as spores that persist in the environment and facilitate the colonization of new individuals. Clostridium difficile is thus a particular problem in health care facilities, where transmission easily occurs between patients and from carriers to patients (McFarland et al., 1989). Measures to prevent C. difficile infection (CDI) through patient isolation are costly and have had variable success. Although previously considered rare, the incidences of community-acquired CDI and colitis are on the increase. After the acquisition of C.