Journal of affective disorders
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Randomized Controlled Trial
Repeat-dose ketamine augmentation for treatment-resistant depression with chronic suicidal ideation: A randomized, double blind, placebo controlled trial.
Several studies indicate that ketamine has rapid antidepressant effects in patients with treatment-resistant depression (TRD). The extent to which repeated doses of ketamine (versus placebo) reduce depression in the short and long term among outpatients with TRD and chronic, current suicidal ideation remains unknown. ⋯ Repeated, non-escalating doses of ketamine did not outperform placebo in this double-blind, placebo controlled study of patients with severe TRD and current, chronic suicidal ideation. This result may support our previously published open-label data that, in this severely and chronically ill outpatient population, the commonly used dose of 0.5 mg/kg is not sufficient.
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While suicide bereavement has been assumed to be different from bereavement following death by other modes, a number of studies have reported that there are several similarities, particularly for violent deaths. The aims of the current study are to test, using confirmatory factor analysis, the factor structure of Grief Experience Questionnaire (GEQ) that has been proposed in other studies; and to compare short term grief reactions, mental health, and suicidality six-months after bereavement in close family members bereaved by suicide versus sudden death. ⋯ The new knowledge of bereaved experiences specific to suicide loss at six-months post death, should be channelled into determining the most practical and satisfactory ways to alleviate the impacts of these potentially changeable states of experience.
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Inhibition of activated astrocyte ameliorates lipopolysaccharide- induced depressive-like behaviors.
Numerous studies indicate that inflammation plays important roles in the development of depression. Astrocytes are crucial regulators of immune response in the central nervous system, and strongly activated by pro-inflammatory cytokines. We hypothesized that inhibition of activated astrocytes contributed to ameliorate depressive-like symptoms. ⋯ Taken together, the results suggest that inhibition of activated astrocytes ameliorates LPS-induced depressive-like behavior, providing the first evidence that inhibition of activated astrocytes might represent a novel therapeutic target for depression.