App-based interventions for the prevention of postpartum depression: a systematic review and meta-analysis.

BACKGROUND: This study explored whether psychosocial intervention applications (apps) are effective in preventing postpartum depression. METHODS: We conducted an initial article search on 26 March 2020, and the updated search on 17 March 2023 on the electronic databases of the Cochrane Central Register of Controlled Trials (CENTRAL), MEDLINE via Ovid, Scopus, PsycINFO, CINAHL, and ProQuest Dissertations & Theses A&I. Furthermore, we searched the International Clinical Trials Platform Search Portal (ICTRP), and Clinical Trials. RESULTS: We identified 2515 references, and sixteen studies were ultimately included in this review. We conducted a meta-analysis of two studies on the onset of postpartum depression. There were no significant differences between the intervention and control groups (RR 0.80; 95% CI 0.62 to 1.04; P = 0.570). We performed a meta-analysis of the Edinburgh Postnatal Depression Scale (EPDS). The intervention group had significantly lower EPDS scores than the control group (mean difference -0.96; 95% CI -1.44 to -0.48; P < 0.001, I2 = 82%, Chi2 = 62.75, P < 0.001; high heterogeneity). CONCLUSION: This study presents the results of current RCTs on interventions with apps, including an app with an automated psychosocial component for preventing postpartum depression that has been conducted. These apps improved the EPDS score; furthermore, they may prevent postpartum depression.

Blockade of multiple monoamines receptors reduce insulin secretion from pancreatic ß-cells.

Clinical use of olanzapine frequently causes severe hyperglycemia as an adverse effect. In this study, we elucidated mechanisms by which olanzapine reduced insulin secretion using the hamster pancreatic ß-cell line HIT-T15. Reverse transcriptional-PCR analysis revealed expression of dopamine (D2, D3 and D4), serotonin (5-HT2A, 5-HT2B, 5-HT2C, and 5-HT6), and histamine (H1 and H2) receptors in HIT-T15 cells. Olanzapine decreased insulin secretion from HIT-T15 cells at clinically relevant concentrations (64-160 nM). A dopamine D2 agonist, D3 antagonist, and D4 antagonist suppressed insulin secretion, whereas a D2 antagonist and D3 agonist increased it. A serotonin 5-HT2B agonist slightly increased insulin secretion, while a 5-HT2C antagonist slightly decreased it. Other agonists and antagonists for serotonin receptors did not affect insulin secretion. A histamine H1 agonist increased insulin secretion, whereas an H1 antagonist and H2 agonist suppressed it. Our results suggest that dopamine (D2, D3 and D4), serotonin (5-HT2B and 5-HT2C), and histamine (H1 and H2) receptors, which are expressed on pancreatic ß-cells, directly modulate insulin secretion from pancreatic ß-cells. Thus, olanzapine may induce hyperglycemia in clinical settings by suppressing insulin secretion from pancreatic ß-cells through inhibition of dopamine D3, serotonin 5-HT2B and 5-HT2C, and histamine H1 receptors.