Oxygen Consumption and Respiration During and After two Yoga Relaxation Techniques

Cyclic meditation (CM) is a technique which combines ‘stimulating’ and ‘calming’ practices, based on a statement in ancient yoga texts suggesting that such a combination may be especially helpful to reach a state of mental equilibrium. The oxygen consumption, breath rate and breath volume of 50 male volunteers (group mean age±SD, 27±6.3 years) were assessed before, during, and after sessions of CM and sessions of supine rest in the corpse posture (shavasana, SH). The sessions were one day apart and the order was alternated. The oxygen consumption, breath rate and breath volume increased during the ‘stimulating’ practices of CM, returned to the baseline during the ‘calming’ practices, and the oxygen consumption decreased by 19.3 percent below baseline values after CM. During the SH session the oxygen consumption, breath rate and breath volume reduced; however the decrease in oxygen consumption after SH was less than after CM (i.e., 4.8 percent). The results support the idea that a combination of yoga postures with supine rest (in CM) reduces the oxygen consumption more than resting supine alone does.     

Some lessons from the tissue transglutaminase knockout mouse

Transglutaminase 2 (TG2) is an inducible transamidating acyltransferase that catalyzes Ca²⁺-dependent protein modifications. It acts as a G protein in transmembrane signaling and as a cell surface adhesion mediator, this distinguishes it from other members of the transglutaminase family. The sequence motifs and domains revealed in the TG2 structure, can each be assigned distinct cellular functions, including the regulation of cytoskeleton, cell adhesion, and cell death. Though many biological functions of the enzyme have already been described or proposed previously, studies of TG2 null mice by our laboratory during the past years revealed several novel in vivo roles of the protein. In this review we will discuss these novel roles in their biological context.     

TAM kinase signaling is indispensable for proper skeletal muscle regeneration in mice

Skeletal muscle regeneration following injury results from the proliferation and differentiation of myogenic stem cells, called satellite cells, located beneath the basal lamina of the muscle fibers. Infiltrating macrophages play an essential role in the process partly by clearing the necrotic cell debris, partly by producing cytokines that guide myogenesis. Infiltrating macrophages are at the beginning pro-inflammatory, but phagocytosis of dead cells induces a phenotypic change to become healing macrophages that regulate inflammation, myoblast fusion and growth, fibrosis, vascularization and return to homeostasis. The TAM receptor kinases Mer and Axl are known efferocytosis receptors in macrophages functioning in tolerogenic or inflammatory conditions, respectively. Here we investigated their involvement in the muscle regeneration process by studying the muscle repair following cardiotoxin-induced injury in Mer^−/− mice. We found that Axl was the only TAM kinase receptor expressed on the protein level by skeletal muscle and C2C12 myoblast cells, while Mer was the dominant TAM kinase receptor in the CD45⁺ cells, and its expression significantly increased during repair. Mer ablation did not affect the skeletal muscle weight or structure, but following injury it resulted in a delay in the clearance of necrotic muscle cell debris, in the healing phenotype conversion of macrophages and consequently in a significant delay in the full muscle regeneration. Administration of the TAM kinase inhibitor BMS-777607 to wild type mice mimicked the effect of Mer ablation on the muscle regeneration process, but in addition, it resulted in a long-persisting necrotic area. Finally, in vitro inhibition of TAM kinase signaling in C2C12 myoblasts resulted in decreased viability and in impaired myotube growth. Our work identifies Axl as a survival and growth receptor in the mouse myoblasts, and reveals the contribution of TAM kinase-mediated signaling to the skeletal muscle regeneration both in macrophages and in myoblasts.Subject terms: Mechanisms of disease, Immunological disorders