Salmonella, Escherichia coli and Enterobacteriaceae in the peanut supply chain: From farm to table.

Due to recent foodborne outbreaks, peanuts have been considered a potential risk for Salmonella transmission. For this reason, the aim of this study was to determine the prevalence and contamination load of Salmonella, Escherichia coli and Enterobacteriaceae throughout the peanut supply chain in Brazil. Samples of peanuts and peanut-containing processed products from post-harvest (n=129), secondary processing (n=185) and retail market (n=100) were analyzed. The results showed high Enterobacteriaceae counts in the post-harvest samples. At the end of the secondary processing, 16% of the samples remained contaminated by this group of microorganisms. Six peanut samples from primary production and one sample of peanut butter were tested positive for E. coli while Salmonella was detected in nine samples (2.2%): six from post-harvest, two from the initial stage of the secondary processing and one from retail. The Salmonella counts ranged between 0.004 and 0.092MPN/g and five serotypes were identified (Muenster, Miami, Javiana, Oranienburg, Glostrup). The results demonstrated a high prevalence of Enterobacteriaceae and low prevalence of E. coli throughout the peanut supply chain. Furthermore, it was verified that peanuts may become contaminated by Salmonella during different stages of the supply chain, especially at post-harvest.

Comparison of stem cell properties of cells isolated from normal and inflamed dental pulps.

AIM: To compare cells from normal and inflamed human dental pulps regarding the presence of stem cells, their proliferation and differentiation potential. METHODOLOGY: Human dental pulp stem cells (hDPSCs) were isolated from normal (DPSC-N) and inflamed dental pulps (DPSC-I). They were compared in respect to proliferation (MTT assay), morphology and STRO-1 expression. STRO-1-positive cells were subject to proliferation (MTT and CFU counting) and morphological analyses and then submitted to odonto-osteogenic, adipogenic and condrogenic differentiation. Differentiated cells were evaluated concerning morphology and the expression, by qRT-PCR, of BSP, LPL and SOX-9 genes. The amount of mineralized matrix produced after odonto-osteogenic differentiation was compared with quantitative Alizarin Red staining. RESULTS: No difference was observed in the morphology and in the proliferation rate of DPSC-N and DPSC-I either before or after separation of STRO-1-positive cells. These cells represented 0.46% (±0.14) and 0.43% (±0.19) of the cell population from normal and inflamed dental pulps, respectively. Both DPSC-N and DPSC-I were capable of differentiating under the three assayed conditions and presented similar patterns for BSP, LPL and SOX-9 expression. Mineralized matrix production was also compatible. In all the quantitative experiments, differences were found between cells from each patient, either from normal or from inflamed pulps. Nonetheless, there was no statistical difference between these two groups. CONCLUSION: The morphology, proliferation rate and differentiation potential of DPSC-I were similar to the observed in DPSC-N, thus demonstrating that the inflammatory process did not affect the stem cell properties that were assessed.

Antioxidant effect of haptoglobin phenotypes against DNA damage induced by hydrogen peroxide in human leukocytes.

Human haptoglobin is classified into three major phenotypes: Hp1-1, Hp2-1 and Hp2-2; there are two autosomal alleles Hp*1 and Hp*2, and the Hp*1 allele has two subtypes, Hp*1F and Hp*1S. Haptoglobin acts as an antioxidant, preventing hemoglobin-driven oxidative damage. We used the comet assay to examine oxidative damage to DNA induced by hydrogen peroxide in human leukocytes; we also looked for differences in the antioxidant capacity of haptoglobin subtypes. Haptoglobin genotypes were determined through allele-specific polymerase chain reaction, visualized on a polyacrylamide gel. The Hp1-1 genotype had the least DNA damage; this indicates that Hp alleles differ in their protective effects against oxidative damage. Among Hp*1 alleles, Hp*1F was the most protective.