Use of yellow mombin (Spondias mombin L.) in marination: Effect on quality properties of Boston butt pork during refrigerated storage.

This research aimed to evaluate the effect of yellow mombin (Spondias mombin L.) juice as a marinade liquid on the quality properties of Boston butt pork during refrigerated storage. Yellow mombin juice was used as a marinade liquid at different concentrations: 0% (C0), 50% (C50), 75% (C75), and 100% (C100) in Boston butt pork samples which were analyzed for technological properties, proximate composition, and sensory characteristics on day 0 of storage. In addition, the pH, lipid oxidation, textural, and microbiological analyzes were carried out during refrigerated storage for 21 days. The results showed that the pH of the marinated samples was affected by yellow mombin juice (P < 0.05), with final values of 4.65 (C50), 4.56 (C75), and 4.39 (C100). Regarding the texture properties, C75 and C100 had the lowest values for hardness during storage. In addition, C100 had the lowest total aerobic mesophilic (5.69 log CFU g-1), total aerobic psychrophilic (7.10 log CFU g-1), and Enterobacteriaceae (5.30 log CFU g-1) counts at the end of storage. Regarding sensory properties, samples C50 and C75 were the best-rated marinated samples regarding overall acceptability and purchase intention. Therefore, the use of 75% yellow mombin juice (C75) as a marinade liquid could be a viable alternative for marinating Boston butt pork.

Everybody loves cheese: crosslink between persistence and virulence of Shiga-toxin Escherichia coli.

General cheese manufacturing involves high temperatures, fermentation and ripening steps that function as hurdles to microbial growth. On the other hand, the application of several different formulations and manufacturing techniques may create a bacterial protective environment. In cheese, the persistent behavior of Shiga toxin-producing Escherichia coli (STEC) relies on complex mechanisms that enable bacteria to respond to stressful conditions found in cheese matrix. In this review, we discuss how STEC manages to survive to high and low temperatures, hyperosmotic conditions, exposure to weak organic acids, and pH decreasing related to cheese manufacturing, the cheese matrix itself and storage. Moreover, we discuss how these stress responses interact with each other by enhancing adaptation and consequently, the persistence of STEC in cheese. Further, we show how virulence genes eae and tir are affected by stress response mechanisms, increasing either cell adherence or virulence factors production, which leads to a selection of more resistant and virulent pathogens in the cheese industry, leading to a public health issue.

Contribution of the platelet activating factor signaling pathway to cerebral microcirculatory dysfunction during experimental sepsis by ExoU producing Pseudomonas aeruginosa.

Intravital microscopy was used to assess the involvement of ExoU, a Pseudomonas aeruginosa cytotoxin with phospholipase A2 activity, in dysfunction of cerebral microcirculation during experimental pneumosepsis. Cortical vessels from mice intratracheally infected with low density of the ExoU-producing PA103 P. aeruginosa strain exhibited increased leukocyte rolling and adhesion to venule endothelium, decreased capillar density and impaired arteriolar response to vasoactive acetylcholine. These phenomena were mediated by the platelet activating factor receptor (PAFR) pathway because they were reversed in mice treated with a PAFR antagonist prior to infection. Brains from PA103-infected animals exhibited a perivascular inflammatory infiltration that was not detected in animals infected with an exoU deficient mutant or in mice treated with the PAFR antagonist and infected with the wild type bacteria. No effect on brain capillary density was detected in mice infected with the PAO1 P. aeruginosa strain, which do not produce ExoU. Finally, after PA103 infection, mice with a targeted deletion of the PAFR gene exhibited higher brain capillary density and lower leukocyte adhesion to venule endothelium, as well as lower increase of systemic inflammatory cytokines, when compared to wild-type mice. Altogether, our results establish a role for PAFR in mediating ExoU-induced cerebral microvascular failure in a murine model of sepsis.