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Having developed a pharmacokinetic method for studying the fate of orally administered arsenious anhydride by a radioactive tracer method, the influence of Hahnemannian dilutions of arsenicum album on the elimination and retention of this toxin in the rat was then investigated. The effects of centesimal (cH) and decimal (dH) dilutions were studied. All the dilutions studied were found to be active. The strongest effects were observed after the administration of dilutions corresponding to a concentration of 10-14 (14dH and 7cH). Overall, the decimal dilutions augmented the elimination of arsenic more than the centesimals. The observed results were submitted to mathematical analysis. A mathematical model, which confirms that Hahnemannian dilutions have biological effects which are a direct function of the degree of dilution, was developed.

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Gouty arthritis is the most frequent rheumatological complication among cyclosporine-treated organ transplant recipients. We report one case of pseudotumoral intramuscular tophaceous deposit of the forearm, in a heart transplant patient with a history of traumatic wound to the same area 17 years previously, and with no known arthritis.

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Age-related changes in plasma adrenocorticotropic hormone (ACTH), corticosterone, and aldosterone responses to exogenous corticotropin-releasing hormone (CRH) were studied concomitantly in both old and adult Long-Evans female rats. All animals were pretreated with dexamethasone and pento-barbital anesthetized. An acute intravenous injection of 1 µg rat CRH/100g body weight markedly increased the plasma concentrations of ACTH, corticosterone, and aldosterone – with similar temporal kinetics in the two groups of rats. However, the incremental CRH responses were significantly lower in old (approximately –70,–45–60, and –30–50%, respectively, for ACTH, corticosterone, and aldosterone) as compared with adult rats. Together with our recent findings, the present results suggest that the previously reported reduced secretion of corticosteroids in aged rats is due to both an impaired steroidogenetic capacity of adrenocortical cells to respond to ACTH and to a decreased ability of corticotropes to produce ACTH in response to CRH.