Life and death: A systematic comparison of antemortem and postmortem gene expression.

Gene expression is the process by which DNA is decoded to produce a functional transcript. The collection of all transcripts is referred to as the transcriptome and has extensively been used to evaluate differentially expressed genes in a certain cell or tissue type. In response to internal or external stimuli, the transcriptome is greatly regulated by epigenetic changes. Many studies have elucidated that antemortem gene expression (transcriptome) may be linked to an array of disease etiologies as well as potential targets for drug discovery; on the other hand, a number of studies have utilized postmortem gene expression (thanatotranscriptome) patterns to determine cause and time of death. The "transcriptome after death" involves the study of mRNA transcripts occurring in human tissues after death (thanatos, Greek for death). While antemortem gene expression can provide a wide range of important information about the host, the determination of the communication of genes after a human dies has recently been explored. After death a plethora of genes are regulated via activation versus repression as well as diverse regulatory factors such as the absence or presence of stimulated feedback. Even postmortem transcriptional regulation contains many more cellular constituents and is massively more complicated. The rates of degradation of mRNA transcripts vary depending on the types of postmortem tissues and their combinatorial gene expression signatures. mRNA molecules have been shown to persist for extended time frames; nevertheless, they are highly susceptible to degradation, with half-lives of selected mRNAs varying between minutes to weeks for specifically induced genes. Furthermore, postmortem genetic studies may be used to improve organ transplantation techniques. This review is the first of its kind to fully explore both gene expression and mRNA stability after death and the trove of information that can be provided about phenotypical characteristics of specific genes postmortem.

Inactivation of human norovirus using chemical sanitizers.

The porcine gastric mucin binding magnetic bead (PGM-MB) assay was used to evaluate the ability of chlorine, chlorine dioxide, peroxyacetic acid, hydrogen peroxide, and trisodium phosphate to inactivate human norovirus within 10% stool filtrate. One-minute free chlorine treatments at concentrations of 33 and 189 ppm reduced virus binding in the PGM-MB assay by 1.48 and 4.14 log10, respectively, suggesting that chlorine is an efficient sanitizer for inactivation of human norovirus (HuNoV). Five minute treatments with 5% trisodium phosphate (pH~12) reduced HuNoV binding by 1.6 log10, suggesting that TSP, or some other high pH buffer, could be used to treat food and food contact surfaces to reduce HuNoV. One minute treatments with 350 ppm chlorine dioxide dissolved in water did not reduce PGM-MB binding, suggesting that the sanitizer may not be suitable for HuNoV inactivation in liquid form. However a 60-min treatment with 350 ppm chlorine dioxide did reduce human norovirus by 2.8 log10, indicating that chlorine dioxide had some, albeit limited, activity against HuNoV. Results also suggest that peroxyacetic acid has limited effectiveness against human norovirus, since 1-min treatments with up to 195 ppm reduced human norovirus binding by <1 log10. Hydrogen peroxide (4%) treatment of up to 60 min resulted in minimal binding reduction (~0.1 log10) suggesting that H2O2 is not a good liquid sanitizer for HuNoV. Overall this study suggests that HuNoV is remarkably resistant to several commonly used disinfectants and advocates for the use of chlorine (sodium hypochlorite) as a HuNoV disinfectant wherever possible.

Suppression of Listeria monocytogenes by the Native Micro-Flora in Teewurst Sausage.

Modern consumers are interested in the use of non-chemical methods to control pathogens when heat sterilization is not an option. Such is the case with teewurst sausage, a raw spreadable sausage and a popular German commodity. Although Listeria was not found in teewurst, the optimal microbial growing conditions of teewurst coupled with the ubiquity of L. monocytogenes in nature, makes the possibility of contamination of products very possible. This pilot study was conducted to examine teewurst's native micro-flora's ability to suppress the outgrowth of L. monocytogenes at 10 °C using standard plate counts and PCR-DGGE. Traditional plating methods showed L. monocytogenes growth significantly decreased when in competition with the teewurst's native micro-flora (p < 0.05). The native micro-flora of the teewurst suppressed the overall growth of L. monocytogenes by an average of two logs, under these conditions. Denaturing Gradient Gel Electrophoresis (DGGE) amplicons with unique banding patterns were extracted from DGGE gel for identification. Brochothrix thermosphacta and Lactobacillus curvatus were identified as a part of the teewurst's native micro-flora. Although the native micro-flora did not decrease L. monocytogenes to below limits of detection, it was enough of a decrease to warrant further investigation.