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2. Fajardo LF et al. Dual role of tumor necrosis factor-alpha in angiogenesis. American Journal of Pathology 140(3): 539-42, 1992. TNF doses of 0.01-1 ng delivered either by osmotic minipump or by implanted pellet induced angiogenesis. The effect was maximum at 0.1 ng.
3. Aukrust P et al. Serum levels of tumor necrosis factor-alpha (TNF) and soluble TNF receptors in human immunodeficiency virus type 1 infection -- correlations to clinical, immunologic, and virologic parameters. Journal of Infectious Diseases. 169: 420-4, 1994. [published erratum appears in 169(5): 1186-7, 1994] "All clinical groups of HIV-infected patients, regardless of concurrent illness, had significantly elevated levels of both types of soluble TNF receptors (sTNFRs) and immuoreactive TNF-alpha (Medgenix EIA), with the highest concentrations among the AIDS patients." They concluded that levels increase with degree of immunodeficiency and progression of the disease and therefore "may give useful prognostic information."
4. Sunderkotter C et al. Macrophages and angiogenesis. Journal of Leukocyte Biology 55(3): 410-22, 1994. "By release of proteases, growth factors (bFGF, GM-CSF, TGF-a, TGF-1, PDGF, VEGF/VPF, TGF-b), and other monokines (IL-1, IL-6, IL-8, TNF-alpha, substance P, prostaglandins, interferons, thrombospondin 1), activated macrophages have the capability to influence each phase of the angiogenic processm such as alterations in the local extracellular matrix, induction of endothelial cells to migrate or proliferate..."
5. Barillari G et al. Effects of cytokines from activated immune cells on vascular cell growth and HIV-1 gene expression. Journal of Immunology. 149(11): 3727-34, 1992. KS may be one of the earliest signs of developing immunodeficiency. They suggest "products from activated immune cells may affect the development of AIDS-KS" and "conditioned media from activated or dysregulated T-cells contain a variety of cytokines that promote the growth of spindle cells derived from KS lesions of AIDS patients (AIDS-KS cells) and induce normal vascular cells, potential cell progenitors of the AIDS-KS cells, to acquire features of the KS cell phenotype (`spindle' cell morphology and growth responsiveness to the mitogenic effect of extracellular HIV-1 Tat protein). The same conditioned media or cytokines promote HIV-1 gene expression and rescue defective HIV-1 proviruses, interrupting HIV latency, and increasing Tat production. The cellular and viral effects of cytokines are increased in an additive or synergistic manner by picomolar concentration of extracellular Tat."
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