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Thymus hormones

Many attempts have been made to find immuno-stimulators among existing synthetic substances. Levamisole (5.5), one of the best of these, acts as a thymomimetic in mice. Thus, it can restore poorly functioning phagocytes and T-lymphocytes and induce T-cell differentiation, but it does not increase T-cell immune responses above their normal level. Moreover, it has no effect on B-lymphocytes. It readily breaks down in the body to 2-oxo-l-mercaptoethyl-4-phenylimidazole (5.7) which has all the properties of levamisole. Thus levamisole seems to be the pro-drug for OMPI (5.7) which acts directly on lymphocytes. OMPI also stimulates secretion of a factor, thought to be thymus hormone, which, too, stimulates lymphocytes (Symoens et al., 1979). [Pg.181]

Both levamisole and isoprinosine have received extensive in vivo immunopharmacologic testing in animals and man. Many of the immune functions that are affected by thymic hormones are shown also to be affected by levamisole, and isoprinosine in vitro and have been confirmed in vivo following administration to experimental animals or human subjects (Specter and Hadden 1985). Both have additional actions on macrophages which have not been tested extensively for the thymus hormones. Regarding their therapeutic usefulness, both have limitations as they are relatively mild in their actions. Levamisole treatment often takes weeks to months to achieve effects, and agranulocytosis as a side effect is significant. [Pg.376]

Reconstitution of T-ceU deficiencies with thymic hormones has not been successhil even though the various hormone preparations induce prothymocyte differentiation and functions of mature T-ceUs. They do not regulate the maturation of thymocytes in the thymus. In contrast, IL-2, endotoxin, thymic epithehal cell products, but not interleukin 1, were found to promote functional maturation of immature thymocytes. Two classes of dmgs show thymomimetic actions (Table 2). Levamisole [14769-73-4], sodium salt of diethyl dithiocarbamate (imuthiol) and certain... [Pg.431]

Atrophy of the thymus is a consistent finding in mammals poisoned by 2,3,7,8-TCDD, and suppression of thymus-dependent cellular immunity, particularly in young animals, may contribute to their death. Although the mechanisms of 2,3,7,8-TCDD toxicity are unclear, research areas include the role of thyroid hormones (Rozman et al. 1984) interference with plasma membrane functions (Matsumura 1983) alterations in ligand receptors (Vickers et al. 1985) the causes of hypophagia (reduced desire for food) and subsequent attempts to alter or reverse the pattern of weight loss (Courtney et al. 1978 Seefeld et al. 1984 Seefeld and Peterson 1984) and excretion kinetics of biotransformed metabolites (Koshakji et al. 1984). [Pg.1053]

The regulation of calcitonin synthesis and release from the parafollicular C cells of the thyroid gland is calcium dependent. Rising serum calcium is the principal stimulus responsible for calcitonin synthesis and release. Other hormones, such as glucagon, gastrin, and serotonin, also stimulate calcitonin release. Calcitonin has been isolated in tissues other than the parafollicular C cells (parathyroid, pancreas, thymus, adrenal), but it is not known whether this material is biologically active. [Pg.756]

Gland-derived extracts (thymus, adrenal, thyroid) Hormone replacement Risk of bacterial, viral, or prion transmission variable hormone content Avoid... [Pg.1354]

Oxytocin is a lessor known hormone produced in several areas of the body including the testes, pancreas, pineal gland, thymus, adrenal glands, and ovaries. So it would seem apparent that this is an important hormone. You don t know the half of it yet. [Pg.138]

The mechanism by which zinc mediates Immune function is not clear the depression of DNA synthesis during zinc deficiency is implicated (9. McCaffrey et al. (97) demonstrated that a zinc-containing DNA polymerase is present in the thymus but does not appear in the mature T cell. A reduction in thymus tissue caused by zinc deficiency would adversely affect the immunocompetence of thymocytes. This hypothesis has been confirmed in experiments where a sharp drop in the thymic hormone is induced by zinc deficiency. [Pg.101]

The nuclear vitamin D receptor was originally studied in intestinal mucosa, hut has subsequently been found in a variety of other tissues that have therefore been shown to be vitamin D-responsive, including kidneys, bone, parathyroid gland, -islet cells of the pancreas, pituitary, placenta, uterus, mammary glands, skin, thymus, monocytes, macrophages, and activated T lymphocytes. Like other steroid hormone receptors, it is a zinc finger protein it has the same high affinity (of the order of 10 " M) for both calcitriol and ercalcitriol. [Pg.91]

Crete hormones and include pituitary gland, pineal 7Z gland, hypothalamus, thyroid gland, parathyroid glands, c thymus, adrenal glands, pancreas, ovaries, and the testes. [Pg.680]


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