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The mass mμ− of the negative muon is one of the parameters of the elementary particle Standard Model and it allows us to verify the CPT (charge–parity–time) symmetry theorem by comparing mμ− value with the mass mμ+ of the positive muon. However, the experimental determination precision of mμ− is 3.1ppm, which is an order of magnitude lower than the determination precision of mμ+ at 120ppb. The authors aim to determine mμ− and the magnetic moment μμ− with a precision of O(10ppb) through spectroscopy of the hyperfine structure (HFS) of muonic helium-4 atom (4Heμ−e−) under high magnetic fields. He4μ−e− is an exotic atom where one of the two electrons of the He4 atom is replaced by a negative muon. To achieve the goal, it is necessary to determine the HFS of He4μ−e− with a precision of O(1ppb). This paper describes the determination procedure of the HFS of He4μ−e− in weak magnetic fields reported recently, and the work towards achieving the goal of higher precision measurement.

Calorie restriction (CR) is a widely recognized dietary approac h with beneficial impacts on the entire body, including enhancements in oxidative metabolism and life span extension, while maintaining nutritional balance and calorie intake. However, CR leads to reductions in skeletal muscle and fat mass due to decreased food intake. Consequently, CR significantly modifies the metabolic profile of the entire body and its tissues. The observed benefits in skeletal muscle during CR may be attributed to CR-induced signaling mediators or significant changes in blood profiles asso ciated with CR that regulate homeostasis maintenance. This study aimed to examine the mammalian target of rapamycin signaling and mitochondrial function of skeletal muscle from mice that undergone 8 weeks of CR and cells cultured in their serum to determine whether changes in blood secreted factors during CR affect skeletal musc le cells. C57BL6/J male mice were used. For 8 weeks, these were subjected to ad libitum (AL) or 40% CR. C2C12 myotubes were subsequently treated with media containing 10% mo use serum from AL or CR for 24 h. The results indicated that 8 weeks of CR dec reased muscle mass and protein synthesis response compared with the AL group. Inte restingly, myotubes conditioned with CR serum exhibited an elevation in the protein synthesis response compared with those treated with AL serum. Furthermore, mitocho ndrial function was enhanced in both CR mice and cells treated with CR serum. These findings suggest that while CR decreases the protein synthesis response, secretory factors present in the blood during CR can activate protein synthesis and promote mitochondrial function. [ABSTRACT FROM AUTHOR]

Purpose: The purpose of this study was to investigate the effects of proteasome activity inhibition on muscle protein synthesis and degradation-related signaling proteins in cultured skeletal muscle cells. Methods: Six days after induction of differentiation, 0.05% DMSO / PBS or MG 132 (10 µM), an inhibitor of proteasome activity dissolved in this solvent, was mixed in the medium of C2C12 myotubes, and after 3 hours of incubation, cells were collected and proteins related to muscle protein synthesis and degradation were quantified. Results and Discussion: The amount of puromycin- labeled protein, a measure of protein synthesis, was significantly lower with the addition of MG132. However, the expression levels of phosphorylated Akt and rpS6, those are signals related to muscle protein synthesis, showed no significant change. The expression level of MAFbx, an ubiquitin E3 ligase, also showed no significant change. These results suggest that addition of MG132 to cultured skeletal muscle cells decreases protein synthesis without affecting protein synthesis- and degradation-related signals, eximined. [ABSTRACT FROM AUTHOR]

Purpose: The role of the mechanistic target of rapamycin complex 1 (mTORC1), a regulator of muscle protein synthesis, on mitochondrial adaptation during mechanical overload-induced skeletal muscle hypertrophy is unclear. The purpose of this study was to examine whether rapamycin-induced mTORC1 inhibition suppresses skeletal muscle mitochondrial adaptation during mechanical overload. Methods: Seven-week-old male ICR (Institute of Cancer Research) mice were subjected to 4 days of myotenectomy (MTE) combined with the i.p. administration of the mTORC1 inhibitor, rapamycin. Results and Conclusion: Our data showed that rapamycin-sensitive mTORC1 inhibition unaffected the decrease in OXPHOS protein levels and increase in mitochondrial dynamics (fusion and fission) related protein levels after 4 days following MTE. In contrast, morphological analysis through transmission electron microscopy imaging showed an inhibitory effect on MTE-induced increase in mitochondrial area by rapamycin-sensitive mTORC1 inhibition. In conclusion, rapamycin-sensitive mTORC1 may regulate mitochondrial morphological adaptation, but its molecular mechanisms are independent of the signal expression responses involved in mitochondrial content, fusion, and fission evaluated in this study. [ABSTRACT FROM AUTHOR]