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Epstein-Barr virus (EBV) latent infection is a critical event in nasopharyngeal carcinoma (NPC) tumorigenesis. EBV-encoded genes have been shown to be involved in immune evasion and in the regulation of various cellular signaling cascades. To elucidate the roles of EBV in NPC development, stable infection of EBV in nasopharyngeal epithelial cell lines was established. Similar to primary tumors of NPC, these infected cells exhibited a type II EBV latency expression pattern. In this study, multiple cellular signaling pathways in EBV-infected cells were investigated. We first demonstrated that in vitro EBV infection resulted in the activation of STAT3 and NFkappaB signal cascades in nasopharyngeal epithelial cells. Increased expression of their downstream targets (c-Myc, Bcl-xL, IL-6, LIF, SOCS-1, SOCS-3, VEGF, and COX-2) was also observed. Moreover, EBV latent infection induced the suppression of p38-MAPK activities, but did not activate PKR cascade. Our findings suggest that EBV latent infection is able to manipulate multiple cellular signal cascades to protect infected cells from immunologic attack and to facilitate cancer development.

A cephalosporin antibiotic and its primary degradation product can be separated by a mixed retention mechanism using an ion exchange column and a mobile phase containing acetonitrile and aqueous sodium phosphate. Assay ruggedness, specificity, linearity of response, and standard-sample stability are evaluated and found to be adequate for the desired application. Drug degradation at room temperature in formulations containing citrate and dextrose is found to be roughly first order; fit of the first order rate expression model is better when gain in degradate levels is used as opposed to the direct measurement of drug loss, especially when the magnitude of drug loss is small. The greater accuracy of projections based on the measurement of degradate gain is related to the effect of the imprecision of the analytical measurement on the accuracy of the model.