Mouse Anti-Human MYC Hybridoma [NZD DU 0-C8.4]

Infection of rainbow trout with the parasitic ciliate Ichthyophthirius multifiliis induces a stress response which can be monitored by serum cortisol measurements reflecting involvement of the pituitary-interrenal cell axis in parasite infected fish. Molecular mechanisms associated with the stress response have been less well elucidated especially with regard to stress effects on metabolism and growth in infected gills - which is the focus of the present study. A controlled experimental infection was performed followed by serum and gill sampling at day 8 post-infection. The stress reactions in the fish were elucidated by measurements of serum cortisol and lysozyme activity, and expression in gills of genes associated with stress, metabolism, and growth. Infection induced a marked elevation of serum cortisol and lysozyme levels, and major changes of metabolic processes in gills. A number of key genes involved in stress (hsps, foxo, saa) and energy metabolism (cyps, pfkfb3, rrm2, mthfd1l) were activated in response to infection whereas several central genes related to growth factors (wnt7a, igfbp7, insr, fgf7, tgfb3, tgfbr1, tgfbr3) were suppressed. A number of potential transcription factors including myc, e2f1, stat1, jun, e2f2, e2f3, and gli2 were found associated with regulation of genes in gills during infection. Mechanisms linking infection of mucosal surfaces and systemic responses are discussed.

Primary gastrointestinal diffuse large B-cell lymphoma (PGI-DLBCL) is a highly heterogeneous type of non-Hodgkin lymphoma. A number of studies have demonstrated that microRNA-130a (miR-130a) serves a role in the tumorigenesis and prognosis of numerous human tumors. However, to the best of our knowledge, the prognostic significance of miR-130a in PGI-DLBCL remains unknown. The present study explored the association between miR-130a and the clinical outcomes of PGI-DLBCL. Relative miR-130a expression was assessed by reverse transcription-quantitative PCR. Immunohistochemistry was used to detect expression levels of BCL-2, c-MYC, neprilysin, B-cell lymphoma 6 protein, PWWP domain-containing DNA repair factor 3A and proliferation marker protein Ki-67. A receiver operating characteristic curve was constructed to analyze the specificity and sensitivity of microRNA levels in the diagnosis of PGI-DLBCL. Survival curves were constructed using the Kaplan-Meier method. In the present study, miR-130a expression was notably higher in patients with PGI-DLBCL compared with in the controls (P<0.0001). miR-130a overexpression was closely associated with a high International Prognostic Index score (3-5) and drug resistance (P=0.017 and P=0.044, respectively). No significant difference in other clinical features was observed. Patients with increased expression levels of miR-130a had lower overall survival [hazard ratio (HR), 2.998; 95% CI, 1.347-6.673; P=0.007] and progression-free survival (HR, 3.325; 95% CI, 1.488-7.429; P=0.003) compared with patients who had lower expression levels of miR-130a. Furthermore, multivariate Cox regression analysis suggested that miR-130a was a negative prognostic parameter in PGI-DLBCL. Therefore, upregulation of miR-130a could become a potential prognostic marker for PGI-DLBCL. Additionally, further study of these results may have important guiding significance for the prognosis of patients with PGI-DLBCL in the clinical setting.