Mitigating the adverse effects of Aflatoxin B1 in LMH, IPEC-J2 and 3D4/21 cells by a novel integrated agent.

This study was to evaluate the efficacy of TOXO-XL (XL), an integrated mycotoxin-mitigating agent, on aflatoxin B1 (AFB1)-induced damage in Leghorn male hepatoma (LMH), porcine jejunum epithelial cell line (IPEC-J2) and porcine alveolar macrophages (3D4/21) cells, and to explore its potential mechanisms. The results showed that 30% inhibition concentration (IC30) of AFB1 in LMH, IPEC-J2 and 3D4/21 cells was 0.5, 15.0, and 2.5 mg/L, respectively. Notably, cell viability, ROS, apoptosis and DNA lesion induced by AFB1 (IC30) could be ameliorated by the supplementation with XL at the dosage of 0.025, 0.025 and 0.005%, respectively. Additionally, the migration and phagocytosis abilities impaired by AFB1 were also restored by XL in 3D4/21. Further experiments revealed that XL supplementation markedly attenuated AFB1-induced inflammatory response by decreasing IL-1ß, IL-6 and IL-10 in LMH, IL-6 in IPEC-J2 and IL-1ß in 3D4/21 cells. Meanwhile, XL supplementation reversed the alterations of BAX, BCL-2 and caspase-3 induced by AFB1 in the three cells, suggesting that AFB1-induced apoptosis may be suppressed via the mitochondria-dependent pathway. Furthermore, XL may have a protective effect on the intestinal barrier through the restoration of occludin protein. Conclusively, these findings indicated that XL could alleviate AFB1-induced cytotoxicity in the three cells, potentially through the regulation of cytokines, ROS, apoptotic and DNA damage signaling.

[Temperature changes of patients with severe acute respiratory syndrome: a comparative study].

OBJECTIVE: To explore the patterns of temperature changes of patients with the severe acute respiratory syndrome (SARS) and the effect of glucocorticoid hormone on the temperature of these patients. METHODS: The clinical data of 94 SARS cases treated during the outbreak of SARS in South China in 2003 were collected for a retrospective review. According to different treatment regimens, the patients were divided into hormone group (n=35) and non-hormone group (n=59). The control groups consisted of 65 patients with interstitial pneumonia, 78 with bacterial pneumonia and 57 with upper respiratory tract infection. The changes in body temperature were compared between the SARS patients and those with other respiratory diseases and the effect of glucocorticoid hormone on controlling body temperature of the SARS patients was explored. RESULTS: The body temperature of patients with the 4 diseases all exhibited obvious reduction 7 days after hospitalization (P<0.001) with only subsequent mild fluctuation within the basically normal range. At each time point of measurement, the body temperature of SARS patients was significantly higher than that of patients with other diseases (P<0.03), with a fluctuation of 0.2 to 0.5 degrees C; and following a pattern of variation similar to those of the other diseases. Of the 4 time points of daily measurement, namely 6, 10, 14 and 18 o'clock, the temperature measured at 14 o'clock was significantly higher than those at the other 3 time points (P<0.001). Hormone therapy did not significantly affect the temperature of SARS patients (P=0.180), who had longer duration of high fever. CONCLUSION: SARS patients have higher body temperature and longer duration of high fever. Hormone therapy may not produce significant effect in controlling the temperature of SARS patients.

[Equivalence test and its performance with computer software].

Following brief introduction of the equivalence test, a sample is given to exemplify its performance with EquivTestTM 2.0 software and with the major results were interpreted.

[Probit analysis with SPSS 10.0 software].

The Probit analysis is illustrated with an example using Probit procedure of SPSS10.0 software, with interpretation of the major outputs.