Application of Bayesian techniques to model the burden of human salmonellosis attributable to U.S. food commodities at the point of processing: adaptation of a Danish model.

Mathematical models that estimate the proportion of foodborne illnesses attributable to food commodities at specific points in the food chain may be useful to risk managers and policy makers to formulate public health goals, prioritize interventions, and document the effectiveness of mitigations aimed at reducing illness. Using human surveillance data on laboratory-confirmed Salmonella infections from the Centers for Disease Control and Prevention and Salmonella testing data from U.S. Department of Agriculture Food Safety and Inspection Service's regulatory programs, we developed a point-of-processing foodborne illness attribution model by adapting the Hald Salmonella Bayesian source attribution model. Key model outputs include estimates of the relative proportions of domestically acquired sporadic human Salmonella infections resulting from contamination of raw meat, poultry, and egg products processed in the United States from 1998 through 2003. The current model estimates the relative contribution of chicken (48%), ground beef (28%), turkey (17%), egg products (6%), intact beef (1%), and pork (<1%) across 109 Salmonella serotypes found in food commodities at point of processing. While interpretation of the attribution estimates is constrained by data inputs, the adapted model shows promise and may serve as a basis for a common approach to attribution of human salmonellosis and food safety decision-making in more than one country.

Effect of simvastatin administration on periodontitis-associated bone loss in ovariectomized rats.

BACKGROUND: Hydroxyl methylglutaryl-coenzyme A reductase inhibitors, so-called statins, have been widely used for hyperlipidemic patients. Recently, it has been reported that they promote bone formation. The purpose of this study was to evaluate the effect of simvastatin on ligature-induced bone resorption in the mandible of the ovariectomized rat. METHODS: Forty-nine rats were divided into seven groups; ligature was placed in all groups except group 7, which was considered the sham group: group 1 (N = 7), ovariectomy (OVX) plus simvastatin (10(-6) M); group 2 (N = 7), OVX plus simvastatin (3 x 10(-7) M); group 3 (N = 7), OVX plus simvastatin (10(-7) M); group 4 (N = 7), OVX plus normal saline; group 5 (N = 7), OVX group; group 6 (N = 7), ligature without OVX; and group 7 (N = 7), sham surgery without OVX and ligature. Simvastatin was administered subperiosteally in the buccal fold of the bottom right first molar twice a week during the study. Four weeks after insertion of the ligatures, the animals were sacrificed. Mandibles were removed for radiologic and histologic analysis. Bone density, bone loss (BL), and attachment loss were measured. Analysis of variance (ANOVA) was used to compare groups. RESULTS: Histologic analysis showed that the simvastatin groups developed significantly less periodontal breakdown (P <0.05). BL was less in the simvastatin experimental group, but there was not a significant statistical difference between the simvastatin groups (groups 1 through 3) and the experimental control groups (groups 5 and 6; P >0.05). CONCLUSION: Within the limits of this study, it can be concluded that simvastatin shows protective features against the impact of periodontitis on attachment apparatus and alveolar bone.