Effects of Mindfulness-Based Cognitive Therapy on Major Depressive Disorder with Multiple Episodes: A Systematic Review and Meta-Analysis.

This study synthesizes the effect of mindfulness-based cognitive therapy (MBCT) on depression and suicidal ideation among patients with major depressive disorder (MDD). During treatment, patients with MDD may experience repeated episodes, negative counseling, and suicidal ideation, which can lead to further depression and ultimately affect quality of life. Recent studies have shown that MBCT can improve the level of depression and suicidal ideation in patients with MDD. A systematic review and meta-analysis of randomized controlled trials was conducted. The literature search for articles up to December 2021 was performed in the following electronic databases: Airiti Library, PsycINFO, CINAHL, Cochrane Library, PubMed/MEDLINE, ProQuest, and the Index of the Taiwan Periodical Literature System. Records were independently evaluated by two reviewers. Disagreements were resolved through consensus. The quality of study was evaluated using the Modified Jadad Scale score. A meta-analysis was performed using Review Manager Version 5.3.5 software with a random-effects model. Thirteen studies (1159 participants) investigating MBCT for patients with MDD were included. The MBCT sessions lasted 1.5-2.5 h and were delivered by therapists five times per week for 8 weeks. The meta-effects of MBCT among patients with MDD showed significant improvement in depression and suicidal ideation. Future research should evaluate the long-term effects of MBCT. MBCT is relatively convenient and effective for preventing and alleviating depression and suicidal ideation. Further research can provide detailed suggestions for effective MBCT implementation.

Effect of NPC-14686 (Fmoc-l-Homophenylalanine) on Ca²âº Homeostasis and Viability in OC2 Human Oral Cancer Cells.

The effect of the anti-inflammatory compound NPC-14686 on intracellular Ca²âº concentration ([Ca²âº](i)) and viability in OC2 human oral cancer cells was investigated. The Ca²âº-sensitive fluorescent probe fura-2 was used to examine [Ca²âº](i). NPC-14686 induced [Ca²âº](i) rises in a concentration-dependent fashion. The effect was reduced approximately by 10% by removing extracellular Ca²âº. NPC-14686- elicited Ca²âº signal was decreased by nifedipine, econazole, SKF96365, and GF109203X. In Ca²âº-free medium, incubation with the endoplasmic reticulum Ca²âº pump inhibitor thapsigargin or 2,5-di-tert-butylhydroquinone (BHQ) abolished NPC-14686-induced [Ca²âº](i) rises. Conversely, pretreatment with NPC-14686 abolished thapsigargin or BHQ-induced [Ca²âº](i) rises. Inhibition of phospholipase C with U73122 abolished NPC-14686-induced [Ca²âº](i) rises. At 20-100 µM, NPC-14686 inhibited cell viability, which was not reversed by chelating cytosolic Ca²âº with 1,2-bis(2-aminophenoxy)ethane-N,N,N',N'- tetraacetic acid-acetoxymethyl ester (BAPTA/AM). NPC-14686 between 20 µM and 40 µM also induced apoptosis. Collectively, in OC2 cells, NPC-14686 induced [Ca²âº](i) rises by evoking phospholipase C-dependent Ca²âº release from the endoplasmic reticulum and Ca²âº entry via protein kinase C-regulated store-operated Ca²âº channels. NPC-14686 also caused Ca²âº-independent apoptosis.