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Brust JCM: Drug dependence, in Joynt RJ ed ; : Clinical Neurology, vol 2. Hagerstown, MD, Harper & Row, 1992, chap. 21. Dreisbach RH, Robertson WO: Handbook of Poisoning: Prevention, Diagnosis and Treatment, 12th ed. Norwalk, CT, Appleton & Lange, 1987. Goldfrank LR, Flomenbaum NE, Lewin NA, et al eds ; : Goldfrank's Toxicologic Emergencies, 5th ed. Norwalk, CT, Appleton & Lange, 1994. Hardman JG, Limbrin LE, Molinoff PB, et al eds ; : Goodman and Gilman's The Pharmacological Basis of Therapeutics, 9th ed. New York, McGraw-Hill, 1996. Hollister LE: Clinical Pharmacology of Psychotherapeutic Drugs, 3rd ed. New York, Churchill Livingstone, 1990. Johnson MV, MacDonald RL, Young AB eds ; : Principles of Drug Therapy in Neurology. Philadelphia, Davis, 1992. Klaassen CD ed ; : Casarett and Doull's Toxicology: The Basic Science of Poisons, 5th ed. New York, McGraw-Hill, 1995. LeQuesne PM: Metal neurotoxicity, in Asbury AK, McKhann GM, McDonald WI eds ; : Diseases of the Nervous System, 2nd ed. Philadelphia, Saunders, 1992, pp 12501258. Levy BS, Wegman DH: Occupational Health: Recognizing and Preventing Work-Related Disease, 3rd ed. Boston, Little, Brown, 1995. Mahaffey KR: Exposure to lead in childhood. New Engl J Med 327: 1308, 1992. Pirodsky DM, Cohn JS: Clinical Primer of Psychopharmacology, 2nd ed. New York, McGraw-Hill, 1992. Rosenberg NL: Occupational and Environmental Neurology. Boston, Butterworth-Heinemann, 1995. Rottenberg DA ed ; : Neurological Complications of Cancer Therapy. Stoneham, MA, Butterworth-Heinemann, 1991. Spencer PS, Schaumburg HH eds ; : Experimental and Clinical Neurotoxicology. Baltimore, Williams & Wilkins, 1980. TNF and TNF can induce a wide variety of effects on a large number of cell types. Both proteins produce their biological responses by binding to specific receptors expressed on the plasma membrane of TNF responsive cells. TNF receptors TNF-R ; belong to the TNF receptors superfamily 8 ; and at least two distinct cell surface receptors exist on different cell types, TNF-R1 or p55 and TNF-R2 or p75. A conserved domain distinct from the ligand binding surface is present in the extracellular region of both proteins and mediates the assembly of receptor trimers required for signal transduction 9 ; . DEVELOPMENT OF ANTI-TNF THERAPY As already mentioned, blocking excess TNF can be therapeutically useful through its cascade effects on other pro-inflammatory cytokines. The first logical step in the development of protein drugs able to neutralize TNF emerged from basic preclinical research: hamster monoclonal antibodies Mabs ; directed at murine TNF were able to reduce inflammation as well as joint damage in animal models of arthritis 10 ; , definitively validating the antiTNF approach in autoimmune diseases. However, murine monoclonal antibodies suffer many limitations to their therapeutic exploitation due to their inherent immunogenicity, resulting in the early appearance in patients of human anti-mouse antibodies HAMA ; . Only chimeric or fully human antibodies in fact gained approval for the therapy of chronic autoimmune diseases: these drugs, respectively infliximab Remicade ; and adalimumab Humira ; represent an important line of well-known anti-TNF biologics with clinical applications. At the same time of development of monoclonal antibodies as therapeutics, soluble forms of TNF receptors TNF-Rs ; were isolated from human urine 11 ; : these truncated receptors are able to bind TNF and 11 ; and can regulate the biological activity of these cytokines 8 ; . The existence of soluble TNF-R in fluids of RA patients indicated an alternative way to exploit protein drugs as regulators of the activity of TNF in vivo: the design of dimeric soluble TNF receptors was another important line of development of biologics in the field, and represents a clever way to mimic a pathway of cytokine control. The final therapeutic product of this research is etanercept Enbrel ; , an engineered soluble receptor of TNF with clinical application in several autoimmune disorders, origi.

Calculated similarly to those in Section 3.3. No interference of potassium was verified. According to the above results, it was also predicted that other major cations coexisting in river waters such as sodium, magnesium, and calcium rarely interfered with ammonium determination. The following experiment was carried out to confirm the prediction. The concentrations of sodium, magnesium, and calcium in river waters are generally 9, 4, and 1.5 mg l [31]. Sample solutions containing 3.0 mg l ammonium and 090% volume of real river water were prepared and analyzed. Ammonium was not detected in this river water by the proposed method prior to this experiment. Similarly, the peak area, peak height, and migration time for ammonium were approximately constant, as expected from the lack of UV absorbance of alkali and alkaline earth metal ions. The respective RSDs of peak area, peak height, and migration time for ammonium were 3.2, 1.7, and 3.1%. The major cations such as sodium, magnesium, and calcium did not either interfere with ammonium determination by the proposed method.

Associated only to the acute episode or only to the disorder itself. According to Bhagwagar et al., 41 HPA-axis dysfunctions with high serum cortisol concentrations seem to be typical of acute cases of major depression. This is not clear, however, because alterations are present in patients with total remission of symptoms, once salivary cortisol is shown to have high concentrations in those patients. Psychiatric symptoms during treatment with glucocorticoids: Over the last 50 years, the corticoid therapy has been widely used and prescribed in a number of systemic diseases.42, 43 Different from alterations secondary to hypersecretion of endogenous corticosteroids, in which depression is more common, the administration of glucocorticoids to patients with normal adrenal function usually causes mild mood disturbances, and sometimes euphoria, irritability, motor activity increase, insomnia and even psychosis, in a lower percentage.17, 44 Brow et al., 37 Patten & Neutel, 42 Sirois43 and Wada et al.44 consider symptoms as mania, depression and psychosis hallucinations and deliriums ; are associated to corticoid therapy, while a prolonged administration of corticoids would be more associated to depressive symptoms, and the an acute administration to mania symptoms.45 Psychiatric symptoms usually occur within the first two weeks of corticosteroid therapy, and they include mania, depression, affective lability and psychosis. Yet, symptoms may arise up to the 20th week, and are rarely seen after this period.44, 46 The intensity of symptoms and their longitudinal course are directly proportional to dosage. Three studies have not found symptoms with low doses of corticosteroids.44, 46, 47 According to Rouchel et al., 48 less than 2% of patients receiving prednisone less than 40 mg day ; had psychiatric symptoms, as compared to the 4 to 6% who were receiving from 41 to 80 mg day, and the 18.4% who received more than 80 mg day. Potential individual risks such as presence of systemic diseases, previous history of psychiatric disease or previous use of corticosteroids still require further studies; therefore glucocorticoid drugs to patients with previous history of psychiatric diseases should be prescribed with caution.42, 46, 47.

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