Many reports of the efficacy of light therapy are not based on rigorous study designs. This analysis of randomized, controlled trials suggests that bright light treatment and dawn simulation for seasonal affective disorder and bright light for nonseasonal depression are efficacious, with effect sizes equivalent to those in most antidepressant pharmacotherapy trials. Adopting standard approaches to light therapy's specific issues (e.g., defining parameters of active versus placebo conditions) and incorporating rigorous designs (e.g., adequate group sizes, randomized assignment) are necessary to evaluate light therapy for mood disorders.

No abstract

No abstract

Controversy remains regarding the role of noradrenergic systems in determining clinical response to antidepressant pharmacotherapy. Pineal gland production of melatonin can serve as a physiologic index of noradrenergic function. The aim of this study was to examine the effects of antidepressant treatment on 24-hour urinary excretion of the principle metabolite of melatonin, 6-sulfatoxymelatonin in treatment responders and nonresponders. Twenty-four outpatients meeting DSM-III-R criteria for MajorThe introduction of effective antidepressant pharmacotherapies in the 1950s revolutionized the treatment of mood disorders. However, despite several decades of research, the mechanisms of action of antidepressants remain unclear. Elucidation of these mechanisms is of considerable clinical, as well as scientific, importance. Although the majority of patients respond to treatment, a substantial minority do not, and insights regarding the necessary psychobiologic components of treatment response could help predict, and perhaps prevent, some cases of treatment failure.Early observations focused attention on the role of norepinephrine (NE) in determining antidepressant response. All of the original antidepressants, including the tricyclic antidepressants (TCAs) and monoamine oxidase inhibitors (MAOIs), enhance noradrenergic neurotransmission, either directly or via active metabolites. Based on these observations, early theories of antidepressant action proposed that clinical response is related to increased noradrenergic activity in the brain (Schildkraut 1969). Later studies found that most antidepressants, including those with minimal direct biochemical effects on NE, can influence noradrenergic systems. For example, lithium, electroconvulsive therapy, the dopamine reuptake inhibitor bupropion, and the serotonin (5-HT) reuptake inhibitor zimelidine all decrease "whole-body norepinephrine turnover"; that 24 , NO . 6 is, the 24-hour excretion of NE and its major metabolites (Linnoila et al. 1983;Rudorfer et al. 1984;. Central NE turnover, as measured by cerebrospinal fluid concentrations of the NE metabolite 3-methoxy-4-hydroxy-phenylglycol (MHPG), is also reduced by a variety of antidepressants, including the 5-HT specific reuptake inhibitor zimelidine (Potter et al. 1985). Based on these observations, it seems that increased noradrenergic function is an integral component of antidepressant treatments.On the other hand, a wide variety of antidepressants, including tricyclic NE and 5-HT reuptake inhibitors, monoamine oxidase inhibitors, and repeated electroconvulsive shock, down-regulate the density of ␤ -adrenergic receptor ( ␤ AR) ligand-binding sites in limbic brain regions, including the cerebral cortex and the hippocampus (Vetulani and Sulser 1975;Banerjee et al. 1977;Sugrue 1983). Furthermore, nearly all antidepressants diminish the ability of ␤ ARs to stimulate adenylate cyclase-mediated cAMP production in these regions (Vetulani and Sulser 1975;Charney et al. 1981), and the time course for these receptor changes ...

Biochemical markers of stress failed to support a deleterious effect of stress on pregnancy outcome in women who underwent ART procedures. Subjective measurement of stress levels did not differ between women who became pregnant and those who did not.

No abstract

The cell-free protein synthetic activity of the postmitochondrial supernatant isolated from whole brain of 6- to 32-month-old male Fischer F344 rats was compared. Protein synthesis decreased 56% from 6 to 32 months of age. The decrease in cell-free protein synthesis was not due to an age-related increase in RNase activity. Although monomeric ribosomes (ribosomes stripped of mRNA) isolated from the brains of older rats were less active in polyuridylic acid directed polyphenylalanine synthesis, the fidelity of polyuridylic acid translation by monomeric ribosomes did not decrease with increasing age.

The overall results of this study of four cohorts of residents indicate only a small, nonsignificant association between pre- and postresidency evaluations. Further efforts to predict residency performance in applicants may help identify those trainees who might benefit from additional monitoring and supervision.