Polycyclic aromatic hydrocarbons (PAHS) (I): Measures of prevention and control

Measures of prevention and control against polycyclic aromatic hydrocarbons (PAHs) focus on an official food control, a code of best practice to reduce PAHs levels by controlling industry and in the development of a chemopreventive strategy. Regulation (EU) 835/2011 establishes maximum levels of PAHs for each food group. In addition, Regulations (EU) 333/2007 and 836/2011 set up the methods of sampling and analysis for its official control. Scientific studies prove that the chemopreventive strategy is effective against these genotoxic compounds effects. Most chemopreventive compounds studied with proven protective effects against PAHs are found in fruit and vegetables.

Treatment of effluents contaminated with prions. Chemical reactor design

The control and elimination of prionic infective agents that may be present in the effluents, turns out to be a complicated mechanism inside a High Containment bological Facility. There are two ways to carry out this neutralization: Installation of thermal systems to ensure achieve a minimum temperature of 134 ° C sterilization plateau for a residence time of 18 minutes, and the use of chemical reactors based on the addition of sodium hypochlorite so the mixture maintained 2% of free chlorine during the reaction period. This study presents the design phases, elements and benefits, of a chemical reactor that allows the treatment of prion effluents in order to serve as a model to biocontainment facilities with areas of animal experimentation, who want to develop their work with prions.

The Relationship between Hospital Infection Surveillance and Control Activities and Antibiotic Resistant Pathogen Rates

Objective: The purpose of the study was to examine the relationship of surveillance and control activities in Canadian hospitals with rates of nosocomial methicillin-resistant S. aureus (MRSA), C. difficile associated diarrhea (CDAD), and vancomycin-resistant Enterococcus (VRE). Methods: Surveys were sent to Infection Control programs in hospitals that participated in an earlier survey of infection control practices in Canadian acute care hospitals. Results: One hundred and twenty of 145 (82.8%) hospitals responded to the survey. The mean MRSA rate was 2.0 (SD 2.9) per 1,000 admissions, the mean CDAD rate was 3.8 (SD 4.3), and the mean VRE rate was 0.4 (SD 1.5). Multiple stepwise regression analysis found hospitals that reported infection rates by specific risk groups (r = - 0.27, p < 0.01) and that kept attendance records of infection control teaching activities (r = - 0.23, p < 0.01) were associated with lower MRSA rates. Multiple stepwise regression analysis found larger hospitals (r = 0.25, p < 0.01) and hospitals where infection control committees or staff had the direct authority to close a ward or unit to further admissions due to outbreaks (r = 0.22, p < 0.05) were associated with higher CDAD rates. Multiple logistic regression analysis found larger hospitals (OR = 1.6, CI 1.2 - 2.0, p = 0.003) and teaching hospitals (OR = 3.7, CI 1.2 - 11.8, p = 0.02) were associated with the presence of VRE. Hospitals were less likely to have VRE when infection control staff frequently contacted physicians and nurses for reports of new infections (OR = 0.5, CI 0.3 - 0.7, p = 0.02) and there were in-service programs for updating nursing and ancillary staff on current infection control practices (OR = 0.2, CI 0.1 - 0.7, p = 0.01). Conclusions: Surveillance and control activities were associated with MRSA and CDAD rates and the presence of VRE. Surveillance and control activities might be especially beneficial in large and teaching hospitals.

Investigation of the effect of intrauterine inflammation and infection on fetal brain injury using human and animal models

In recent years, increased focus has been placed on the role of intrauterine infection and inflammation in the pathogenesis of fetal brain injury leading to neurodevelopmental disorders such as cerebral palsy. At present, the mechanisms by which inflammatory processes during pregnancy cause this effect on the fetus are poorly understood. Our previous work has indicated an association between experimentally-induced intrauterine infection, increased proinflammatory cytokines, and increased white matter injury in the guinea pig fetus. In order to further elucidate the pathways by which inflammation in the maternal system or the fetal membranes leads to fetal impairment, a number of studies investigating aspects of the disease process have been performed. These studies represent a body of work encompassing novel research and results in a number of human and animal studies. Using a guinea pig model of inflammation, increased amniotic fluid proinflammatory cytokines and fetal brain injury were found after a maternal inflammatory response was initiated using endotoxin. In order to more closely monitor the fetal response to chorioamnionitis, a model using the chronically catheterized fetal ovine was carried out. This study demonstrated the adverse effects on fetal white matter after intrauterine exposure to bacterial inoculation, though the physiological parameters of the fetus were relatively stable throughout the experimental protocol, even when challenged with intermittent hypoxic episodes. The placenta is an important mediator between mother and fetus during gestation, though its role in the inflammatory process is largely undefined. Studies on the placental role in the inflammatory process were undertaken, and the limited ability of proinflammatory cytokines and endotoxin to cross the placenta are detailed herein. Neurodevelopmental disorders can be monitored in animal models in order to determine effective disease models for characterization of injury and use in therapeutic strategies. Our characterizations of postnatal behaviour in the guinea pig model using motility monitoring and spatial memory testing have shown small but significant differences in pups exposed to inflammatory processes in utero. The data presented herein contributes a breadth of knowledge to the ongoing elucidation of the pathways by which fetal brain injury occurs. Determining the pathway of damage will lead to discovery of diagnostic criteria, while determining the vulnerabilities of the developing fetus is essential in formulating therapeutic options.