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In object reallocation problems, if preferences are strict but otherwise unrestricted, TTC is the leading rule: It is the only rule satisfying efficiency, the endowment lower bound, and strategy-proofness. However, on the subdomain of single-peaked preferences, Bade (J Econ Theory 180:81–99, 2019) defines a new rule, the “crawler”, which also satisfies these properties, and in fact enjoys a stronger strategic property. We identify additional interesting properties that the crawler satisfies, and provide two characterizations of this rule. The first characterization is based on the endowment lower bound and two invariance properties, “adjacent-endowment-swapping invariance” and “separability”. The second characterization is based on the endowment lower bound, strategy-proofness, adjacent-endowment-swapping invariance, and another invariance property, “non-bossiness”.

Previous studies have demonstrated the beneficial effects of apple polyphenol (AP) intake on muscle endurance. Since mitochondria are critical for muscle endurance, we investigated mitochondrial enzyme activity, biogenesis, degradation and protein quality control. Twenty‐four Wistar rats were randomly fed a 5% AP diet (5% AP group, n = 8), a 0.5% AP diet (0.5% AP group, n = 8), or a control diet (control group, n = 8). After a 4‐week feeding period, the expression level of peroxisome proliferator‐activated receptor γ coactivator‐1α, a mitochondrial biosynthetic factor, did not increase, whereas that of transcription factor EB, another regulator of mitochondrial synthesis, significantly increased. Moreover, the mitochondrial count did not differ significantly between the groups. In contrast, mitophagy‐related protein levels were significantly increased. The enzymatic activities of mitochondrial respiratory chain complexes II, III and IV were significantly higher in the AP intake group than in the control group. We conclude that AP feeding increases the activity of respiratory chain complex enzymes in rat skeletal muscles. Moreover, mitochondrial biosynthesis and degradation may have increased in AP‐treated rats. What is the central question of this study? Does the administration of apple polyphenols (AP) affect mitochondrial respiratory chain complex enzyme activity, biogenesis, degradation and protein quality control in rat skeletal muscles? What is the main finding and its importance? AP feeding increases respiratory chain complex enzyme activity in rat skeletal muscle. Moreover, AP administration increases transcription factor EB activation, and mitophagy may be enhanced to promote degradation of dysfunctional mitochondria, but mitochondrial protein quality control was not affected.

The relationship between mechanistic target of rapamycin complex 1 (mTORC1) activation after resistance exercise and acetylcholine receptor (AChR) subunit gene expression remains largely unknown. Therefore, we aimed to investigate the effect of electrical stimulation‐induced intense muscle contraction, which mimics acute resistance exercise, on the mRNA expression of AChR genes and the signalling pathways involved in neuromuscular junction (NMJ) maintenance, such as mTORC1 and muscle‐specific kinase (MuSK). The gastrocnemius muscle of male adult Sprague–Dawley rats was isometrically exercised. Upon completion of muscle contraction, the rats were euthanized in the early (after 0, 1, 3, 6 or 24 h) and late (after 48 or 72 h) recovery phases and the gastrocnemius muscles were removed. Non‐exercised control animals were euthanized in the basal state (control group). In the early recovery phase, Agrn gene expression increased whereas LRP4 decreased without any change in the protein and gene expression of AChR gene subunits. In the late recovery phase, Agrn, Musk, Chrnb1, Chrnd and Chrne gene expression were altered and agrin and MuSK protein expression increased. Moreover, mTORC1 and protein kinase B/Akt‐histone deacetylase 4 (HDAC) were activated in the early phase but not in the late recovery phase. Furthermore, rapamycin, an inhibitor of mTORC1, did not disturb changes in AChR subunit gene expression after muscle contraction. However, rapamycin addition slightly increased AChR gene expression, while insulin did not impact it in rat L6 myotube. These results suggest that changes in the AChR subunits after muscle contraction are independent of the rapamycin‐sensitive mTORC1 pathway. What is the central question of this study? Can muscle contraction‐induced activation of mechanistic target of rapamycin complex 1 (mTORC1) be linked to changes in acetylcholine receptor (AChR) gene expression and molecular signalling for maintaining neuromuscular junctions (NMJs)? What is the main finding and its importance? An acute high‐intensity muscle contraction dynamically changes AChR gene expression and muscle‐specific kinase (MuSK) signalling proteins at the late recovery phase of the contraction. Additionally, pharmacological inhibition of mTORC1 via rapamycin does not affect muscle contraction‐induced alterations in AChR genes. Our findings indicate that an acute high‐intensity muscle contraction induces changes in MuSK signalling and mTORC1‐independent changes in expression of AChR genes.

Cancer cachexia causes severe muscle wasting, and current treatments remain limited. Belt-type electrical muscle stimulation (bEMS) has emerged as a passive rehabilitation tool capable of activating multiple lower limb muscles simultaneously. We investigated whether bEMS prevents muscle wasting and improves functional outcomes in rats with cancer cachexia. Cancer cachexia was induced in male Sprague-Dawley rats by intraperitoneal injection of AH130 Yoshida hepatoma cells. Acute and chronic effects of bEMS were tested. Muscle protein synthesis was evaluated using the SUnSET method, and muscle fiber cross-sectional area (CSA) and ankle torque were measured after chronic stimulation. bEMS increased puromycin-labeled protein levels on day 3 post-injection (~1.5–2.0 fold; p < 0.05). After 10 days, bEMS mitigated reductions in muscle CSA in the gastrocnemius and tibialis anterior compared to the cachexia group. However, muscle strength (ankle torque) was not significantly improved. bEMS preserved muscle fiber size in cancer cachexia but failed to restore muscle function. These findings suggest bEMS may serve as a supportive strategy against muscle atrophy in cachectic conditions.

Belt electrode skeletal muscle stimulation (B-SES) is a method of applying electricity to contract muscles using belt-shaped electrodes. We previously reported that twitch contractions increase mitochondrial synthesis and suppress muscle proteolysis. In contrast, tetanus contraction increases muscle protein synthesis and suppresses muscle proteolysis. This study aimed to determine whether combining twitch- and tetanus-mode stimulations, which are known to differentially regulate mitochondrial and protein synthesis pathways, can more effectively attenuate muscle atrophy induced by denervation. Male Sprague-Dawley rats were subjected to acute or chronic B-SES. In the acute study, animals were assigned to control (CONT), tetanus (60 Hz), or Combined Stimulation (CS: 7–8 Hz for 15 min to 60 Hz for 3 min) groups. Four groups were tested in the chronic study: CONT, denervation (DEN), DEN + 60 Hz, and DEN + CS groups. Acute stimulation resulted in significantly lower muscle glycogen level, increased phosphorylated AMPK and p70S6K in the gastrocnemius muscle (GAS、n = 4) at 60 and CS compared to CONT, with no difference between 60 and CONT. After seven days, both muscle wet weight and cross-sectional area (CSA) were significantly reduced in the DEN group. Although both 60 Hz and CS attenuated atrophy, CS resulted in greater preservation (GAS CSA: DEN + CS, 71% CONT; DEN + 60, 61% CONT). In conclusion, the combination of different stimulation modalities (frequencies) was more effective than continuous tetanus stimulation in preventing denervation-induced muscle atrophy owing to an increase in muscle protein synthesis and inhibition of mitochondrial reduction.

White adipose tissue (WAT) in mice undergoes browning in response to cold exposure. Brown and beige adipocytes contain multilocular lipid droplets and abundant iron-containing mitochondria expressing uncoupling protein 1 (UCP-1). Cold exposure-induced browning WAT is accompanied by increased density of blood vessels and sympathetic nerve fibres. A previous study reported a more than threefold increase in sympathetic nerve dendritic tone in inguinal white adipose tissue (iWAT) after cold exposure. Therefore, we hypothesized that water molecule diffusion would be more restricted in brown and beige adipocytes compared to white adipocytes. The characteristics of T2* values and anisotropy parameters by diffusion tensor imaging (DTI) in browning WAT are unclear. The aim of the present study was to investigate the effect of cold exposure on T2* values and anisotropy parameters (fractional anisotropy [FA], apparent diffusion coefficient [ADC], radial diffusivity [RD] and eigenvalues λ1, λ2, λ3) in brown adipose tissue (BAT), iWAT and epididymal white adipose tissue (epiWAT). Furthermore, these parameters were investigated in vivo through additional validation experiments in three control mice. Mice in the cold exposure (CE) group were exposed to a cold environment at 4 °C for 10 days, while these in the control (C) group were maintained at 22 °C throughout the experiment. T2* values, FA, ADC, RD and eigenvalues (λ1, λ2, λ3) were measured in BAT, iWAT and epiWAT using a 9.4T magnetic resonance scanner (Bruker Biospin AG). T2* values of epiWAT in the C group were significantly higher than these of BAT in the C group and iWAT in the CE group. No significant differences were observed between groups for FA, ADC, RD, λ1 and λ2 of iWAT and epiWAT. However, the λ3 values of iWAT and epiWAT in the CE group were significantly higher than these of iWAT, epiWAT and BAT in the C group. Compared to ex vivo measurements, in vivo measurements in control mice showed higher T2* values with reduced intertissue variability while maintaining tissue-specific patterns. These results suggest that T2* values and anisotropy parameters might serve as potential markers for the assessment of adipose tissue plasticity. Further studies are required to investigate their utility as non-invasive indicators of browning WAT.

Endothelial cells acquire different phenotypes to establish functional vascular networks. Vascular endothelial growth factor (VEGF) signaling induces endothelial proliferation, migration, and survival to regulate vascular development, which leads to the construction of a vascular plexuses with a regular morphology. The spatiotemporal localization of angiogenic factors and the extracellular matrix play fundamental roles in ensuring the proper regulation of angiogenesis. This review article highlights how and what kinds of extracellular environmental molecules regulate angiogenesis. Close interactions between the vascular and neural systems involve shared molecular mechanisms to coordinate developmental and regenerative processes. This review article focuses on current knowledge about the roles of angiogenesis in peripheral nerve regeneration and the latest therapeutic strategies for the treatment of peripheral nerve injury.

Belt electrode skeletal muscle electrical stimulation (B-SES) can simultaneously contract multiple muscle groups. Although the beneficial effects of B-SES in clinical situations have been elucidated, its molecular mechanism remains unknown. In this study, we developed a novel rodent B-SES ankle stimulation system to test whether low-frequency stimulation prevents denervation-induced muscle atrophy. Electrical stimulations (7‒8 Hz, 30 min) with ankle belt electrodes were applied to Sprague–Dawley rats daily for one week. All animals were assigned to the control (CONT), denervation-induced atrophy (DEN), and DEN + electrical stimulation (ES) groups. The tibialis anterior (TA) and gastrocnemius (GAS) muscles were used to examine the effect of ES treatment. After seven daily sessions of continuous stimulation, muscle wet weight (n = 8–11), and muscle fiber cross-sectional area (CSA, n = 4–6) of TA and GAS muscles were lower in DEN and DEN + ES than in CON. However, it was significantly higher in DEN than DEN + ES, showing that ES partially prevented muscle atrophy. PGC-1α, COX-IV, and citrate synthase activities (n = 6) were significantly higher in DEN + ES than in DEN. The mRNA levels of muscle proteolytic molecules, Atrogin-1 and Murf1, were significantly higher in DEN than in CONT, while B-SES significantly suppressed their expression (p < 0.05). In conclusion, low-frequency electrical stimulation of the bilateral ankles using belt electrodes (but not the pad electrodes) is effective in preventing denervation-induced atrophy in multiple muscles, which has not been observed with pad electrodes. Maintaining the mitochondrial quantity and enzyme activity by low-frequency electrical stimulation is key to suppressing muscle protein degradation.

Oxidative stress and mitochondrial dysfunction are associated with the aging process. However, the role of nuclear factor erythroid 2 ‐related factor 2 (Nrf2) in skeletal muscle during aging remains to be clarified. In the current study, we assessed whether the lack of Nrf2, which is known as a master regulator of redox homeostasis, promotes age‐related mitochondrial dysfunction and muscle atrophy in skeletal muscle. Here, we demonstrated that mitochondrial 4‐hydroxynonenal and protein carbonyls, markers of oxidative stress, were robustly elevated in aged Nrf2 knockout (KO) mice because of the decreased expression of Nrf2‐target antioxidant genes. Mitochondrial respiration declined with aging; however, there was no difference between Nrf2 KO and age‐matched WT mice. Similarly, cytochrome c oxidase activity was lower in aged WT and Nrf2 KO mice compared with young WT mice. The expression of Mfn1 and Mfn2 mRNA was lower in aged Nrf2 KO muscle. Mitochondrial reactive oxygen species production per oxygen consumed was elevated in aged Nrf2 KO mice. There was no effect of Nrf2 KO on muscle mass normalized to body weight. These results suggest that Nrf2 deficiency exacerbates age‐related mitochondrial oxidative stress but does not affect the decline of respiratory function in skeletal muscle. We demonstrated that mitochondrial 4‐hydroxynonenal and protein carbonyls, markers of oxidative stress, were robustly elevated in aged Nrf2 knockout mice, due to the decreased expression of Nrf2‐target antioxidant genes. However, Nrf2 deficiency did not affect the decline of mitochondrial respiratory function in aged skeletal muscle.

Osteosarcopenia, the coexistence of osteoporosis and sarcopenia, is linked to adverse clinical outcomes, emphasizing the need for routine assessment of this comorbidity. Phase angle (PhA), measured by bioelectrical impedance analysis (BIA), reflects cellular health (vitality and integrity) and nutritional status. This study investigated the relationship between PhA and osteosarcopenia or mortality and its predictive potential for both clinical events in patients with chronic liver disease (CLD). A retrospective study included 316 patients with CLD, 161 with cirrhosis. PhA was measured using direct segmental multi-frequency BIA. Osteoporosis and sarcopenia were diagnosed according to the World Health Organization and Japan Society of Hepatology criteria, respectively. Osteosarcopenia was present in 57 patients (18.0%). Over a median follow-up of 63.3 months, 47 liver-related deaths (29.2%) occurred among cirrhotic patients. Multivariate analysis identified low PhA as an independent risk factor for osteosarcopenia (odds ratio, 0.147; p  < 0.001). The optimal PhA cutoff for predicting osteosarcopenia was 4.3° (sensitivity/specificity, 0.737/0.811). In patients with cirrhosis, survival rates were significantly lower in those with PhA < 4.3° compared to PhA ≥ 4.3° ( p  < 0.001). Multivariate analysis identified PhA < 4.3° as an independent predictor of mortality (hazard ratio, 2.588; p  = 0.008). PhA, derived from BIA, was strongly associated with osteosarcopenia and mortality, making it a valuable indicator for simultaneously predicting these adverse outcomes in patients with CLD.