Correlation with tumor necrosis factor

Fig. 3. Detection of the collapse of mitochondrial electrochemical potential (A ) by LSC after cell staining with DiOC6 (3) and PI. Human histiomonocytic lymphoma U937 cells untreated (A) or to induce apoptosis by treatment treated with tumor necrosis factor-a (TNF-a) and cycloheximide (B refs. 26,28), were stained according to the protocol. The bivariate green vs red fluorescence distribution (scatterplot) represents A Pm vs uptake of PI, respectively. Nonapoptotic cells fluoresce only green, early apoptotic cells show decreased green fluorescence but no red fluorescence while late apoptotic cells stain cannot exclude PI and thus have red fluorescence. After relocation their stainability with DiOC6 (3) and PI can be correlated with morphology.

E10. Engel, A Kern, W. V., Miirdter, G., and Kern, P Kinetics and correlation with body temperature of circulating interleukin-6, interleukin-8, tumor necrosis factor alpha and interleukin-1 beta in patients with fever and neutropenia. Infection 22, 160-164 (1994). 

Robinson P, Okhuysen PC, Chappell CL, Lewis DE, Shahab I, Janecki A, White AC Jr Expression of tumor necrosis factor alpha and interleukin 1 beta in jejuna of volunteers after experimental challenge with Cryptosporidium parvum correlates with exposure but not with symptoms. Infect Immun 2001 69 1172-1174. 

Ad.TNF gene therapy is presently in clinical trials in patients receiving radiotherapy. An open-label, phase I, dose-escalation study of tumor necrosis factor-alpha (TNFerade) gene transfer with radiation therapy for locally advanced, recurrent, or metastatic solid tumors is currently accruing patients and has several endpoints (82), including toxicity and tolerable dose. Pharmacokinetics will be evaluated and biological correlates will determine the histologic response to therapy. 

Corticosteroids suppress both humoral and cellular immunity. Single doses produce a redistribution of lymphocytes with a concentration dependent decrease of CD4 and CDS positive cells. This in vivo lymphopenic effect correlates with the in vitro inhibition of stimulated T-cell proliferation. Furthermore, corticosteroids are able to inhibit the expression of genes coding for IL-1, IL-2, IL-6, interferon a, and tumor necrosis factor, TNE-a. Chronic administration decreases the size and also the cellu-larity of lymphoid tissues like lymph nodes, spleen, and thymus. Corticosteroids have more effect on the primary immune response and are less effective against previously sensitized immune responses. Their suppressive effects are more pronounced for T-cell immune responses than for the humoral immune response. 

Finally, in addition to the issues of costs and secondary events, treatment is also lacking for many more at-risk patients who cannot undergo successful angioplasty. These patients, who may have either diffuse, nonstentable, bifurcated lesions, or multivessel disease (i.e., diabetics), are not benefiting as much from DES, and improved treatments here also remain a clear clinical need. Often there is a systemic and local activation of the immune response, followed by a consequent local vascular incident. The role of the systemic immune response in these individuals, as well as in cardiovascular patients in general, is evidenced by the numerous reports of correlation of disease with increases in plasma markers such as CRB tumor necrosis factor, and even circulating white cell counts (87-89). 

Circulating tumor necrosis factor soluble receptors in systemic lupus erythematosus are significantly higher than in other rheumatic diseases and correlate with disease activity. J. Rheumatol, 24, 303-308. 

Meyers CA, Valentine AD, Wong FC, Leeds NE. Reversible neurotoxicity of interleukin-2 and tumor necrosis factor correlation of SPECT with neuropsychological testing. J Neuropsychiatry Clin Neurosci 1994 6(3) 285-8. 

Tanaka, A., Quaranta, S., MattaUa, A., Coppel, R., Rosina, F., Manns, M., Gershwin, M.E. The tumor necrosis factor-alpha promoter correlates with progression of primary biliary curhosis. X Hepatol. 1999 30 826-829... 

Janelsins MC, Mastrangelo MA, Oddo S, LaFerla EM, Federoff HJ, Bowers WJ (2005) Early correlation of microghal activation with enhanced tumor necrosis factor-alpha and monocyte chemoattractant protein-1 expression specifically within the entorhinal cortex of triple transgenic Alzheimer s disease mice. J Neuroinflammation 2 23. 

Oxaliplatin is generally well tolerated. Some patients develop fever, which appears to be related to a transient increase in cytokines, particnlarly interlenkin-6 and tnmor necrosis factor alfa. In one stndy the oxaliplatin-induced increase in body temperatnre correlated with a marked increase in interlenkin-6 sernm concentrations (peak 133 pg/ml) (251). Interlenkin-6 is a proinflamma-tory cytokine, which stimnlates acnte phase proteins and B lymphocytes. Premedication with metamizol, dexamethasone, and clarithromycin, which interferes with interleukin-6, did not prevent the fever. The roles of interleukin-6 and tumor necrosis factor alfa in the development of fever is strengthened by the observation that their serum concentrations fell during resolution of the fever (252). 

Gauchat, J.F., Aversa, G., Gascan, H. and De-Vries, J.E. (1992a). Modulation of IL-4 induced germline epsilon RNA synthesis in human B cells by tumor necrosis factor-alpha, anti-CD40 monoclonal antibodies or transforming growth factor-beta correlates with levels of IgE production. Int. Immunol. 4, 397-406. 

Current evidence suggests that accumulation of fat in NAFLD is a consequence of insulin resistance. A variety of mechanisms may lead to insulin resistance, including genetic predisposition, increased concentrations of free fatty acids, and presence of cytokines such as tumor necrosis factor alpha (TNF-a). Since TNF-a is produced by fat cells, correlates with body fat, and is critical to development of insulin resistance in obesity,it may be a key factor in development of NAFLD. The pathogenesis is likely to be more complicated, however, as a variety of other factors lead to increased fat accumulation in the liver, including increased carbohydrate intake, certain drugs, and mutations in lipid synthesis, but have not been associated with development of NASH. 

Powell, M. B., Mitchell, D., Lederman, J., Buckmeier, J., Zamvil, S. S., Graham, M., Ruddle, N. H., and Steinman, L., Lymphotoxin and tumor necrosis factor-a production by myelin basic protein-specific T cell clones correlates with encephalitogenicity, Int. Immunol., 2, 539, 1990. 

S., Manogue, K., Cerami, A., Shires, G. T., and Lowry, S. F. Serum cachectin/tumor necrosis factor in critically ill patients with bums correlates with infection and mortality. Surg., Gynecol. Obstet. 170, 32-38 (1990). 

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