Neurobiological mechanisms of dialectical behavior therapy and Morita therapy, two psychotherapies inspired by Zen.

Psychotherapy is a learning process. Updating the prediction models of the brain may be the mechanism underlying psychotherapeutic changes. Although developed in different eras and cultures, dialectical behavior therapy (DBT) and Morita therapy are influenced by Zen principles, and both emphasize the acceptance of reality and suffering. This article reviews these two treatments, their common and distinct therapeutic factors, and their neuroscientific implications. Additionally, it proposes a framework that includes the predictive function of the mind, constructed emotions, mindfulness, therapeutic relationship, and changes enabled via reward predictions. Brain networks, including the Default Mode Network (DMN), amygdala, fear circuitry, and reward pathways, contribute to the constructive process of brain predictions. Both treatments target the assimilation of prediction errors, gradual reorganization of predictive models, and creation of a life with step-by-step constructive rewards. By elucidating the possible neurobiological mechanisms of these psychotherapeutic techniques, this article is expected to serve as the first step towards filling the cultural gap and creating more teaching methods based on these concepts.

Hypoxia-mediated down-regulation of OCTN2 and PPARα expression in human placentas and in BeWo cells.

The objective of the present study was to investigate the effects of hypoxia on placental expression of OCTN2 and PPARα. OCTN2 and PPARα expression in the human placenta in the presence or absence of preeclampsia was examined by immunohistochemical (IHC) analysis, Western blotting, and quantitative polymerase chain reaction (qPCR). Effects of hypoxia on the expression of OCTN2 and PPARα in human placental explants and human choriocarcinoma BeWo cells were examined by Western blotting and qPCR analyses. IHC, Western blot, and qPCR studies showed that OCTN2 and PPARα protein and mRNA levels were lower in syncytiotrophoblasts from preeclamptic human placentas than in those from normal placentas. Hypoxic treatment caused a decrease in OCTN2 and PPARα expression in human placental explants and in BeWo cells. WY14643, a PPARα agonist, caused an increase in OCTN2 expression in BeWo cells under hypoxic conditions. In conclusion, under hypoxic conditions, placental OCTN2 is down-regulated through PPARα-mediated pathways.