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The X-ray crystal structure of the complex of the extracellular domain of the human 55 kd tumor necrosis factor (TNF) receptor with human TNF beta has been determined at 2.85 A resolution. The complex has three receptor molecules bound symmetrically to one TNF beta trimer. The receptor fragment, a very elongated end to end assembly of four similar folding domains, binds in the groove between two adjacent TNF beta subunits. The structure of the complex defines the orientation of the ligand with respect to the cell membrane and provides a model for TNF receptor activation. The novel fold of the TNF receptor structure is likely to be representative of the nerve growth factor (NGF)/TNF receptor family as a whole.

A brief review of the limited sources in the literature on secondary amenorrhea indicates that this symptom may, in many cases, be psychogenic in origin. The disorder in such instances is often short term, spontaneously reversible, and occurs as a reaction to stress or a traumatic event. Most of these women are basically healthy, psychologically speaking. In some cases, however, this menstrual disturbance may continue for months or longer. In such instances, one may expect to find a neurotic conflict related to feminine identity as the cause. The therapeutic approach in these two alternative forms of secondary psychogenic amenorrhea (SPA) will differ; hence, it is essential that the gynecologist and psychiatrist distinguish between them. A case illustration is presented, describing in detail the treatment of a women with longstanding SPA which resolved with dynamically-oriented psychotherapy.

This article presents a case of self-induced diseases (Munchausen syndrome), among them a very dangerous cardiac condition. The psychotherapeutic process is described, through which the Munchausen behavior was effectively abolished. It is suggested that Munchausen syndrome may be a suicidal equivalent.

Administration of epinephrine in man has been shown previously to lead to a rise in plasma cyclic AMP levels by activation of the beta-adrenergic-stimulated adenylate cyclase. Therapeutic doses of lithium in humans block the epinephrine-induced rise in plasma cyclic AMP levels, suggesting that lithium inhibits beta-adrenergic adenylate cyclase. In contrast, ten subjects receiving haloperidol, a druh also effective in the treatment of mania, show a mean rise in plasma cyclic AMP levels after epinephrine administration and the magnitude of the response is the same as for non-drug treated individuals. These findings are discussed in relation to the possible pharmacological mechanisms of action of lithium and haloperidol in the control of mania.