Effect of temperature on the growth of Staphylococcus aureus in ready-to-eat cooked rice with pork floss.

Cooked rice with pork floss (CRPF) wrapped in dried seaweed is one of the most popular ready-to-eat (RTE) foods in many Asian countries, particularly in Taiwan. The products are susceptible to Staphylococcus aureus contamination and temperature abuse during manufacturing, distribution, and storage. The objective of this study was to examine the effect of temperature on its growth in RTE CRPF for use in risk assessment and prevention of staphylococcal food poisoning (SFP). Inoculated CRPF samples were stored at 4, 12, 18, 25, and 35°C, and the change in the populations of S. aureus during storage were analyzed using three primary models to determine specific growth rate (µmax), lag-phase duration (λ), and maximum population density (ymax). The Ratkowsky square-root and Huang square-root (HSR) models were used as the secondary models to describe the effect of temperature on µmax, and a linear and an exponential regression models were used to describe the effect of temperature on λ and ymax, respectively. The model performance was evaluated by the root mean square error (RMSE), bias factor (Bf), and accuracy factor (Af) when appropriate. Results showed that three primary models were suitable for describing the growth curves, with RMSE ≤ 0.3 (log MPN/g). Using µmax obtained from the Huang model, the minimum growth temperature (Tmin) estimated by the HSR model was 7.0°C, well in agreement with the reported Tmin. The combination of primary and secondary models for predicting S. aureus growth was validated by additional growth curves at 30°C, which showed that the RMSE was 0.6 (log MPN/g). Therefore, the developed models were acceptable for predicting the growth of S. aureus in CRPF under likely temperature abuse conditions and can be applied to assess the risk of S. aureus in CRPF and design temperature controls to reduce the risk of SFP.

Beneficial effects of Camellia Oil (Camellia oleifera Abel.) on ketoprofen-induced gastrointestinal mucosal damage through upregulation of HO-1 and VEGF.

Nonsteroidal anti-inflammatory drugs, such as ketoprofen, are generally used to treat pain and inflammation and as pyretic agents in clinical medicine. However, the usage of these drugs may lead to oxidative injury to the gastrointestinal mucosa. Camellia oil ( Camellia oleifera Abel.) is commonly used in Taiwan and China as cooking oil. Traditional remedies containing this oil exert beneficial health effects on the bowel, stomach, liver, and lungs. However, the effects of camellia oil on ketoprofen-induced oxidative gastrointestinal mucosal lesions remain unknown. The objective of this study was to evaluate the effect of camellia oil on ketoprofen-induced acute gastrointestinal ulcers. The results showed that treatment of Int-407 cells with camellia oil (50-75 µg/mL) not only increased the levels of heme oxygenase-1 (HO-1), glutathione peroxidase (GPx), and superoxide dismutase (SOD) mRNA expression but also increased vascular endothelial growth factor (VEGF) and prostaglandin E2 (PGE2) protein secretion, which served as a mucosal barrier against gastrointestinal oxidative injury. Moreover, Sprague-Dawley (SD) rats treated with camellia oil (2 mL/kg/day) prior to the administration of ketoprofen (50 mg/kg/day) successfully inhibited COX-2 protein expression, inhibited the production of interleukin-6 (IL-6) and nitrite oxide (NO), reversed the impairment of the antioxidant system, and decreased oxidative damage in the gastrointestinal mucosa. More importantly, pretreatment of SD rats with camellia oil strongly inhibited gastrointestinal mucosal injury induced by ketoprofen, which was proved by the histopathological staining of gastrointestinal tissues. Our data suggest that camellia oil exerts potent antiulcer effects against oxidative damage in the stomach and intestine induced by ketoprofen.