Deficiency tumor-induced

In five of six nondietary tumor-promotion experiments, sodium selenide significantly reduced the number of mice with tumors induced by 7,12-dimethyl-benzanthracene (DMBA)-croton oil (1). In these experiments, sodium selenide was applied concomitantly along with croton oil to female Swiss albino mice initiated with DMBA. Riley has also observed a reduction in DMBA-phorbol ester carcinogenesis by sodium selenide (2). The effect of selenium-deficient and selenium-adequate diets on DMBA-croton oil and benzopyrene skin carcinogenesis has also been studied. Supplemental dietary selenium inhibited both types of carcinogenesis. 

Chae, H.D., Choi, T-S., Kim, B.-M., Jimg, J.H., Bang, Y.-J., and Shin, DY. 2005. Oocyte-based screening of cytokinesis inhibitors and identification of pectenotoxin-2 fiiat induces Bim/Bax-mediated q)optosis in p53-deficient tumors. Oncogene 24,4813 819. 

Meyer, K., Lee, J. S., Dyck, P. A., Cao, W. Q., Rao, M. S., Thorgeirsson, S. S., and Reddy, J. K. (2003). Molecular profiling of hepatocellular carcinomas developing spontaneously in acyl-CoA oxidase deficient mice comparison with Uver tumors induced in wild-type mice by a peroxisome proliferator and a genotoxic carcinogen. Carcinogenesis 24, 975-984. 

Oncolytic viruses in IFN-deficient tumor cells. In the Type I IFN-deficient tumor cells innate immunity fights oncolytic vimses, but vaccination with viral oncoly-sates induced strong anti-tumor cell immune reactions. Hilary Koprowski presented a lecture at the young M.D. Anderson Hospital in 1957 on viral oncolysate therapy... 

Gradual diminution of 004 T-lymphocytes from the peripheral blood is the most consistent feature observed in HIV infection. Because the majority of 004 cells are T-helper lymphocytes, removal leads to deficiency of cellular immunity, which depends on T-helper cells to initiate cytotoxic T-ceU killing of vims-infected cells of cancer. The loss of immune surveillance leads to the appearance of viraHy induced tumors from unopposed clonal expansion of viraHy transformed cells. Furthermore, depletion of cellular immunity leads to exaggerated viral, fungal, and proto2oal infections. 

Nitro PAHs have been shown to exhibit a large variety of biological activities. Included in these are the induction of mutations in bacterial (Table I) and eukaryotic cells (9,17,54-57), the neoplastic transformation of cultured mammalian cells (58-59), and the induction of DNA strand breaks (60), DNA repair (61-62), sister chromatid exchanges (63-64), and chromosomal aberrations (65-66). Nitro PAHs have also been demonstrated to bind cellular DNA in bacteria (67-73) and mammalian cells (74-77), to inhibit preferentially the growth of repair-deficient bacteria (78), to have recombinogenic activity in yeast (66,79-80) and to induce tumors in experimental animals (Table II). 

To summarize, comorbidities on which a manic syndrome can be superimposed include ADHD, ODD, conduct or pervasive developmental disorders, Tour-ette s syndrome, or medical conditions such as brain tumors, multiple sclerosis, temporal lobe seizures, human immune-deficiency syndrome (HIV), and endocri-nopathies such as hyperthyroidism and Cushing s syndrome (James and Javaloyes, 2001). Organic affective syndrome, a condition given separate designation in DSM I-IIIR, is now subsumed under mood disorder due to a general medical condition in DSM IV. Substance induced mood disorder has a similar due to. . . designation. 

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