Recurrent priapism during treatment with clozapine and olanzapine.
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Biomedical subjects
Publications and source records attributed to M T Compton.
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BACKGROUND: The treatment of bipolar depression represents a relatively understudied area in clinical psychiatry. The depressive phases of bipolar disorder can be very disabling, with significant associated comorbidity and suicide risk, impairment in functioning, and infringement on quality of life. We review the current evidence for the management of bipolar depression. METHOD: References for this review were obtained through MEDLINE searches of the medical literature on subjects pertaining to the treatment of bipolar depression. Search terms included bipolar depression, antidepressants, and bipolar disorder. Only publications in English are reviewed here. RESULTS: Lithium is currently the gold standard and most appropriate initial treatment for the depressive phase of bipolar disorder. Other mood stabilizers have demonstrated preliminary efficacy. Of the antidepressants, bupropion and the selective serotonin reuptake inhibitors may be associated with less risk of inducing hypomania, mania, and rapid cycling compared with tricyclic antidepressants. Monoamine oxidase inhibitors should be considered for patients with anergic bipolar depression. Electroconvulsive therapy has been shown to be highly efficacious. Other treatment modalities, including psychotherapy, sleep deprivation, phototherapy, and newer medications, require further research. CONCLUSIONS: Although the treatment of bipolar depression can be a complicated clinical task, the treatment armamentarium is expanding. Further research, especially in the form of randomized controlled trials, is warranted. Clinicians should be familiar with general guidelines for the use of psychopharmacologic agents for treating bipolar depression.
The tyrosine kinase called pp125FAK is believed to play an important role in integrin-mediated signal transduction. pp125FAK is associated both functionally and spatially with integrins, which are the cell surface receptors for extracellular matrix components. Although the precise function of pp125FAK is not known, two possibilities have been proposed: pp125FAK may regulate the assembly of focal adhesions in spreading or migrating cells, or pp125FAK may participate in a signal transduction cascade to inform the nucleus that the cell is anchored. To test these models in living cells, a peptide representing the focal adhesion kinase (FAK)-binding site of the beta 1 tail was coupled to carrier protein and injected into cultured cells to competitively inhibit the binding of pp125FAK to endogenous integrin, thus inhibiting activation of pp125FAK on a cell-by-cell basis. In addition, an antibody directed against an epitope adjacent to the focal adhesion targeting sequence on pp125FAK was microinjected, as an alternative means of inhibiting pp125FAK activation. It was observed that when rounded cells were injected with either the integrin peptide or the anti-FAK antibody, the cells rapidly began to apoptose, within 4 h after injection. These results indicate that pp125FAK may play a critical role in suppressing apoptosis in fibroblasts.