Is the Salmonella contamination of swine carcasses at slaughter related to the Salmonella load in caecum?

The aim of this study was to examine the relationship between the load of Salmonella spp. in caeca and the carcass contamination in an Italian slaughterhouse. The sampling scheme was designed to be representative of the pigs slaughtered in a day and to estimate a 12% prevalence of pigs highly contaminated by Salmonella spp. (HCP, cecal load ≥3log). Environmental swabs were taken before slaughter. Cecal contents and carcass swabs were collected from the same pig. Salmonella MPN were estimated according to ISO6579- 2:2012/A1 and ISO7218:2007/E. The overall Salmonella prevalence were 34.64% and 7.19% for ceca and carcasses respectively, with S. Derby and S. 4,[5],12:i:- being the prevalent serotypes. The HCP prevalence was 11.44%. 7/59 environmental swabs tested positive; when the same serotype was isolated from the environment and from carcasses, the samples were excluded from further analysis. Statistical analysis was performed to investigate the relationship between Salmonella spp. loads in the cecum and contamination of the carcass of the same pig and the prevalence of HCP and the contamination of carcasses on the same day. For this purpose, the days were classified as “high prevalence days” depending on the proportion of caeca resulted positive (≥36%) and as “high load” days depending on the prevalence of HCP (≥10%). A correlation between the contamination of carcasses and the cecal Salmonella loads of the same animal was found (Spearman’s correlation coefficient: 0.2254; p-value=0.0001). No correlation was found between the contamination of carcasses and the categorization of the day of sampling as “high prevalence day”. Conversely, a correlation was found between the contamination of carcasses and the “high load” category of the sampling day (Wilcoxon test, p=0.0011). Notably, not the prevalence of pigs carrying Salmonella spp. but the prevalence of highly contaminated pigs was shown to be related to the contamination of carcasses

α-Tocopheryl succinate promotes selective cell death induced by vitamin K3 in combination with ascorbate

BACKGROUND: A strategy to reduce the secondary effects of anti-cancer agents is to potentiate the therapeutic effect by their combination. A combination of vitamin K3 (VK3) and ascorbic acid (AA) exhibited an anti-cancer synergistic effect, associated with extracellular production of H2O2 that promoted cell death. METHODS: The redox-silent vitamin E analogue a-tocopheryl succinate (a-TOS) was used in combination with VK3 and AA to evaluate their effect on prostate cancer cells. RESULTS: Prostate cancer cells were sensitive to a-TOS and VK3 treatment, but resistant to AA upto 3.2mM. When combined, a synergistic effect was found for VK3\u2013AA, whereas a-TOS\u2013VK3 and a-TOS\u2013AA combination showed an antagonist and additive effect, respectively. However, sub-lethal doses of AA\u2013VK3 combination combined with a sub-toxic dose of a-TOS showed to induce efficient cell death that resembles autoschizis. Associated with this cell demise, lipid peroxidation, DNA damage, cytoskeleton alteration, lysosomal\u2013mitochondrial perturbation, and release of cytochrome c without caspase activation were observed. Inhibition of lysosomal proteases did not attenuate cell death induced by the combined agents. Furthermore, cell deaths by apoptosis and autoschizis were detected. CONCLUSION: These finding support the emerging idea that synergistic combinations of some agents can overcome toxicity and other side-effects associated with high doses of single drugs creating the opportunity for therapeutically relevant selectivity

Serum Albumin Is Inversely Associated With Portal Vein Thrombosis in Cirrhosis

We analyzed whether serum albumin is independently associated with portal vein thrombosis (PVT) in liver cirrhosis (LC) and if a biologic plausibility exists. This study was divided into three parts. In part 1 (retrospective analysis), 753 consecutive patients with LC with ultrasound-detected PVT were retrospectively analyzed. In part 2, 112 patients with LC and 56 matched controls were entered in the cross-sectional study. In part 3, 5 patients with cirrhosis were entered in the in vivo study and 4 healthy subjects (HSs) were entered in the in vitro study to explore if albumin may affect platelet activation by modulating oxidative stress. In the 753 patients with LC, the prevalence of PVT was 16.7%; logistic analysis showed that only age (odds ratio [OR], 1.024; P = 0.012) and serum albumin (OR, -0.422; P = 0.0001) significantly predicted patients with PVT. Analyzing the 112 patients with LC and controls, soluble clusters of differentiation (CD)40-ligand (P = 0.0238), soluble Nox2-derived peptide (sNox2-dp; P < 0.0001), and urinary excretion of isoprostanes (P = 0.0078) were higher in patients with LC. In LC, albumin was correlated with sCD4OL (Spearman's rank correlation coefficient [r(s)], -0.33; P < 0.001), sNox2-dp (r(s), -0.57; P < 0.0001), and urinary excretion of isoprostanes (r(s), -0.48; P < 0.0001) levels. The in vivo study showed a progressive decrease in platelet aggregation, sNox2-dp, and urinary 8-iso prostaglandin F2 alpha-III formation 2 hours and 3 days after albumin infusion. Finally, platelet aggregation, sNox2-dp, and isoprostane formation significantly decreased in platelets from HSs incubated with scalar concentrations of albumin. Conclusion: Low serum albumin in LC is associated with PVT, suggesting that albumin could be a modulator of the hemostatic system through interference with mechanisms regulating platelet activation

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