The self-pattern and Buddhist psychology

In this paper, we address core insights from Buddhist psychology about mind-body phenomena and the self, and we relate such insights to the notion of the self-pattern developed in the pattern theory of self. We emphasize the dynamic, temporal and enactive characteristics of the self-pattern, consistent with the core Buddhist notion of non-self. Although there is no one-to-one mapping of Buddhist psychological concepts onto the pattern theory of self, there are important similarities among such concepts and the various processes and dynamical relations that constitute a pragmatic self-pattern that can explain both experiences of self and non-self. Buddhist psychology and the notion of the self-pattern offer mutual insight into the processes, the dynamics, and the implications for questions about well-being and a flexibility that avoids anxiety and reduces attachment, craving, and suffering

MTCH2/MIMP is a major facilitator of tBID recruitment to mitochondria

The BH3-only BID protein (BH3-interacting domain death agonist) has a critical function in the death-receptor pathway in the liver by triggering mitochondrial outer membrane permeabilization (MOMP). Here we show that MTCH2/MIMP (mitochondrial carrier homologue 2/Met-induced mitochondrial protein), a novel truncated BID (tBID)-interacting protein, is a surface-exposed outer mitochondrial membrane protein that facilitates the recruitment of tBID to mitochondria. Knockout of MTCH2/MIMP in embryonic stem cells and in mouse embryonic fibroblasts hinders the recruitment of tBID to mitochondria, the activation of Bax/Bak, MOMP, and apoptosis. Moreover, conditional knockout of MTCH2/MIMP in the liver decreases the sensitivity of mice to Fas-induced hepatocellular apoptosis and prevents the recruitment of tBID to liver mitochondria both in vivo and in vitro. In contrast, MTCH2/MIMP deletion had no effect on apoptosis induced by other pro-apoptotic Bcl-2 family members and no detectable effect on the outer membrane lipid composition. These loss-of-function models indicate that MTCH2/MIMP has a critical function in liver apoptosis by regulating the recruitment of tBID to mitochondria