Control Of Muscle Research Articles

An exercise stress test for contrast-enhanced duplex ultrasound assessment of lower limb muscle perfusion in patients with peripheral arterial disease

ObjectiveThe aim of the present study was to develop a standardized contrast-enhanced duplex ultrasound (CE-DUS) protocol to assess lower-extremity muscle perfusion before and after exercise and determine relationships of perfusion with clinical and functional measures. MethodsCE-DUS (EPIQ 5G, Philips) was used before and immediately after a 10-minute, standardized bout of treadmill walking to compare microvascular perfusion of the gastrocnemius muscle in older (55-82 years) patients with peripheral arterial disease (PAD) (n = 15, mean ankle-brachial index, 0.78 ± 0.04) and controls (n = 13). Microvascular blood volume (MBV) and microvascular flow velocity (MFV) were measured at rest and immediately following treadmill exercise, and the Modified Physical Performance Test (MPPT) was used to assess mobility function. ResultsIn the resting state (pre-exercise), MBV in patients with PAD was not significantly different than normal controls (5.17 ± 0.71 vs 6.20 ± 0.83 arbitrary units (AU) respectively; P = .36); however, after exercise, MBV was ∼40% lower in patients with PAD compared with normal controls (5.85 ± 1.13 vs 9.53 ± 1.31 AU, respectively; P = .04). Conversely, MFV was ∼60% higher in patients with PAD compared with normal controls after exercise (0.180 ± 0.016 vs 0.113 ± 0.018 AU, respectively; P = .01). There was a significant between-group difference in the exercise-induced changes in both MBV and MFV (P ≤ .05). Both basal and exercise MBV directly correlated with MPPT score in the patients with PAD (r = 0.56-0.62; P < .05). ConclusionsThis standardized protocol for exercise stress testing of the lower extremities quantifies calf muscle perfusion and elicits perfusion deficits in patients with PAD. This technique objectively quantifies microvascular perfusion deficits that are related to reduced mobility function and could be used to assess therapeutic efficacy in patients with PAD.

Aloe Inspired Special Structure Hydrogel Pressure Sensor for Real‐Time Human‐Computer Interaction and Muscle Rehabilitation System

AbstractIn recent years, significant progress has been made in the research and development of conventional hydrogel sensors. However, the development of hydrogels with special structures, achieved through specific designs or fabrication strategies, remains relatively scarce. Inspired by aloe, a specially structured hydrogel (named Skin‐Polyvinyl alcohol‐Polyaniline‐AgNWs, S‐PPA) is successfully prepared with skin. Innovatively utilizing the hydrogen bonding interaction between ions and water molecules, the surface of the hydrogel is treated to create a protective skin. The S‐PPA hydrogel with a protective skin demonstrates strong resistance to damage (with a tensile strength of 5 MPa, &gt;11 times higher compared to hydrogel without skin) and exhibits dual conductivity (0.8 S m−1 for the inner skin and 0.33 S m−1 for the outer skin). In addition, the S‐PPA hydrogel also possesses water retention capabilities, antibacterial properties (89.4% inhibition rate against Staphylococcus aureus (S. aureus)), and minimal corrosion to metal electrodes. Based on the S‐PPA hydrogel and combined with wireless Bluetooth technology and Python programming, intelligent applications are developed such as multi‐gradient intelligent control and finger muscle condition evaluation, achieving real‐time human‐ computer interaction (HCI). The intelligent pressure‐sensitive hydrogel proposed by this study shows great potential in the fields of medical rehabilitation, artificial intelligence, and the Internet of Things.

Jakyak-gamcho-tang, a decoction of Paeoniae Radix and Glycyrrhizae Radix et Rhizoma, ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

BackgroundAlthough chronic treatment with glucocorticoids, such as dexamethasone, is frequently associated with muscle atrophy, effective and safe therapeutics for treating muscle atrophy remain elusive. Jakyak-gamcho-tang (JGT), a decoction of Paeoniae Radix and Glycyrrhizae Radix et Rhizoma, has long been used to relieve muscle tension and control muscle cramp-related pain. However, the effects of JGT on glucocorticoid-induced muscle atrophy are yet to be comprehensively clarified. PurposeThe objective of the current study was to validate the protective effect of JGT in dexamethasone-induced muscle atrophy models and elucidate its underlying mechanism through integrated in silico – in vitro – in vivo studies. Study design and MethodsDifferential gene expression was preliminarily analyzed using the RNA-seq data to determine the effects of JGT on C2C12 myotubes. The protective effects of JGT were further validated in dexamethasone-treated C2C12 myotubes by assessing cell viability, myotube integrity, and mitochondrial function or in C57BL/6 N male mice with dexamethasone-induced muscle atrophy by evaluating muscle mass and physical performance. Transcriptomic pathway analysis was also performed to elucidate the underlying mechanism. ResultsBased on preliminary gene set enrichment analysis using the RNA-seq data, JGT regulated various pathways related to muscle differentiation and regeneration. Dexamethasone-treated C2C12 myotubes and muscle tissues of atrophic mice displayed substantial muscle protein degradation and muscle loss, respectively, which was efficiently alleviated by JGT treatment. Importantly, JGT-mediated protective effects were associated with observations such as preservation of mitochondrial function, upregulation of myogenic signaling pathways, including protein kinase B/mammalian target of rapamycin/forkhead box O3, inhibition of ubiquitin-mediated muscle protein breakdown, and downregulation of inflammatory and apoptotic pathways induced by dexamethasone. ConclusionTo the best of our knowledge, this is the first report to demonstrate that JGT could be a potential pharmaceutical candidate to prevent muscle atrophy induced by chronic glucocorticoid treatment, highlighting its known effects for relieving muscle spasms and pain. Moreover, transcriptomic pathway analysis can be employed as an efficient in silico tool to predict novel pharmacological candidates and elucidate molecular mechanisms underlying the effects of herbal medications comprising diverse biologically active ingredients.

Refractory myasthenia gravis: the more we learn, the less we know.

Refractory myasthenia gravis identifies the group of patients that have inadequate symptom control and persistent muscle weakness and fatigability despite the use of multiple immune modulatory therapies. This manuscript highlights what is currently known about refractory myasthenia gravis and underlines major knowledge gaps, drawing attention to the unmet needs in our understanding of this disease subset. This review raises questions about our current understanding of refractory disease and how emerging data as well as therapies may alter our thinking and patients’ disease course.

The FSHD muscle-blood biomarker: a circulating transcriptomic biomarker for clinical severity in facioscapulohumeral muscular dystrophy.

Facioscapulohumeral muscular dystrophy (FSHD) is a prevalent, incurable skeletal myopathy. Clinical trials for FSHD are hindered by heterogeneous biomarkers poorly associated with clinical severity, requiring invasive muscle biopsy. Macroscopically, FSHD presents with slow fatty replacement of muscle, rapidly accelerated by inflammation. Mis-expression of the transcription factor DUX4 is currently accepted to underlie pathogenesis, and mechanisms including PAX7 target gene repression have been proposed. Here, we performed RNA-sequencing on MRI-guided inflamed and isogenic non-inflamed muscle biopsies from the same clinically characterized FSHD patients (n = 24), alongside isogenic peripheral blood mononucleated cells from a subset of patients (n = 13) and unaffected controls (n = 11). Multivariate models were employed to evaluate the clinical associations of five published FSHD transcriptomic biomarkers. We demonstrated that PAX7 target gene repression can discriminate control, inflamed and non-inflamed FSHD muscle independently of age and sex (P < 0.013), while the discriminatory power of DUX4 target genes was limited to distinguishing FSHD muscle from control. Importantly, the level of PAX7 target gene repression in non-inflamed muscle associated with clinical assessments of FSHD severity (P = 0.04). DUX4 target gene biomarkers in FSHD muscle showed associations with lower limb fat fraction and D4Z4 array length but not clinical assessment. Lastly, PAX7 target gene repression in FSHD muscle correlated with the level in isogenic peripheral blood mononucleated cells (P = 0.002). A refined PAX7 target gene biomarker comprising 143/601 PAX7 target genes computed in peripheral blood (the FSHD muscle-blood biomarker) associated with clinical severity in FSHD patients (P < 0.036). Our new circulating biomarker validates as a classifier of clinical severity in an independent data set of 54 FSHD patient and 29 matched control blood samples, with improved power in older patients (P = 0.03). In summary, we present the minimally invasive FSHD muscle-blood biomarker of FSHD clinical severity valid in patient muscle and blood, of potential use in routine disease monitoring and clinical trials.

Inactivation influences the extent of inhibition of voltage-gated Ca+2 channels by Gem-implications for channelopathies.

Voltage-gated Ca2+ channels (VGCC) directly control muscle contraction and neurotransmitter release, and slower processes such as cell differentiation, migration, and death. They are potently inhibited by RGK GTP-ases (Rem, Rem2, Rad, and Gem/Kir), which decrease Ca2+ channel membrane expression, as well as directly inhibit membrane-resident channels. The mechanisms of membrane-resident channel inhibition are difficult to study because RGK-overexpression causes complete or near complete channel inhibition. Using titrated levels of Gem expression in Xenopus oocytes to inhibit WT P/Q-type calcium channels by ∼50%, we show that inhibition is dependent on channel inactivation. Interestingly, fast-inactivating channels, including Familial Hemiplegic Migraine mutants, are more potently inhibited than WT channels, while slow-inactivating channels, such as those expressed with the Cavβ2a auxiliary subunit, are spared. We found similar results in L-type channels, and, remarkably, Timothy Syndrome mutant channels were insensitive to Gem inhibition. Further results suggest that RGKs slow channel recovery from inactivation and further implicate RGKs as likely modulating factors in channelopathies.

Skeletal muscle-enriched miRNAs are highly unstable in vivo and may be regulated in a Dicer-independent manner.

MicroRNAs (miRNAs) are small noncoding RNAs that control essential cellular processes. For several decades, the molecular mechanisms underlying the functions and biogenesis of miRNAs have been clarified, whereas the molecular dynamics of miRNAs are poorly understood. We recently found that muscle-enriched miRNAs were reduced by only 20 ~ 50% in the skeletal muscles even 4 weeks after the suppression of miRNA processing through an inducible depletion of Dicer1 gene. These data suggest that miRNAs are stably expressed in skeletal muscle. In this study, we investigated the half-lives of those miRNAs in adult skeletal muscle with an in vivo metabolic labeling strategy and a genetic mouse model. In contrast to the hypothesis, in vivo metabolic labeling revealed that the half-lives of skeletal-muscle-enriched miRNAs were approximately 11-20 h. Furthermore, the levels of mature miR-23a decreased rapidly in the skeletal muscle of mice lacking miR-23 clusters in a tamoxifen-inducible manner. These data suggest that skeletal-muscle-enriched miRNAs are not highly stable in vivo. We also observed that the transfer of miR-150 into Dicer1-deficient muscle increased the miR-150 level to the same as that in control muscle. Taken together, our data demonstrate that miRNAs are degraded within a few days in adult skeletal muscle and that a Dicer-independent biogenetic pathway may produce mature miRNAs.

Diabetes diminishes muscle precursor cell-mediated microvascular angiogenesis.

The skeletal muscles of Type II diabetic (T2D) patients can be characterized by a reduced vessel density, corresponding to deficiencies in microvascular angiogenesis. Interestingly, T2D also inhibits the function of many myogenic cells resident within skeletal muscle, including satellite cells, which are well-known for the role they play in maintaining homeostasis. The current study was undertaken to gain a better understanding of the mechanisms whereby satellite cell progeny, muscle precursor cells (MPCs), influence microvascular angiogenesis. Network growth and the expression of genes associated with angiogenesis were reduced when microvessels were treated with conditioned media generated by proliferating MPCs isolated from diabetic, as compared to control rat skeletal muscle, a phenomenon that was also observed when myoblasts from control or diabetic human skeletal muscle were used. When only exosomes derived from diabetic or control MPCs were used to treat microvessels, no differences in microvascular growth were observed. An evaluation of the angiogenesis factors in control and diabetic MPCs revealed differences in Leptin, vascular endothelial growth factor (VEGF), IL1-β, interleukin 10, and IP-10, and an evaluation of the MPC secretome revealed differences in interleukin 6, MCP-1, VEGF, and interleukin 4 exist. Angiogenesis was also reduced in tissue-engineered skeletal muscles (TE-SkM) containing microvessels when they were generated from MPCs isolated from diabetic as compared to control skeletal muscle. Lastly, the secretome of injured control, but not diabetic, TE-SkM was able to increase VEGF and increase microvascular angiogenesis. This comprehensive analysis of the interaction between MPCs and microvessels in the context of diabetes points to an area for alleviating the deleterious effects of diabetes on skeletal muscle.

AMPKγ3 Controls Muscle Glucose Uptake in Recovery From Exercise to Recapture Energy Stores.

Exercise-induced activation of AMPK in skeletal muscle has been proposed to regulate muscle glucose uptake in recovery from exercise. This study investigated whether the muscle-specific AMPKγ3-associated heterotrimeric complex was involved in regulating muscle glucose metabolism in recovery from exercise. The findings support that exercise-induced activation of the AMPKγ3 complex in human and mouse skeletal muscle enhances glucose uptake in recovery from exercise via increased translocation of GLUT4 to the plasma membrane. This work uncovers the physiological role of the AMPKγ3 complex in regulating muscle glucose uptake that favors replenishment of the muscle cellular energy stores.

Autophagy signaling in hypertrophied muscles of diabetic and control rats.

Autophagy plays a vital role in cell homeostasis by eliminating nonfunctional components and promoting cell survival. Here, we examined the levels of autophagy signaling proteins after 7 days of overload hypertrophy in the extensor digitorum longus (EDL) and soleus muscles of control and diabetic rats. We compared control and 3-day streptozotocin-induced diabetic rats, an experimental model for type 1 diabetes mellitus (T1DM). EDL muscles showed increased levels of basal autophagy signaling proteins. The diabetic state did not affect the extent of overload-induced hypertrophy or the levels of autophagy signaling proteins (p-ULK1, Beclin-1, Atg5, Atg12-5, Atg7, Atg3, LC3-I and II, and p62) in either muscle. The p-ULK-1, Beclin-1, and p62 protein expression levels were higher in the EDL muscle than in the soleus before the hypertrophic stimulus. On the contrary, the soleus muscle exhibited increased autophagic signaling after overload-induced hypertrophy, with increases in Beclin-1, Atg5, Atg12-5, Atg7, Atg3, and LC3-I expression in the control and diabetic groups, in addition to p-ULK-1 in the control groups. After hypertrophy, Beclin-1 and Atg5 levels increased in the EDL muscle of both groups, while p-ULK1 and LC3-I increased in the control group. In conclusion, the baseline EDL muscle exhibited higher autophagy than the soleus muscle. Although TDM1 promotes skeletal muscle mass loss and strength reduction, it did not significantly alter the extent of overload-induced hypertrophy and autophagy signaling proteins in EDL and soleus muscles, with the two groups exhibiting different patterns of autophagy activation.

Metabolic Pathway Modeling in Muscle of Male Marathon Mice (DUhTP) and Controls (DUC)-A Possible Role of Lactate Dehydrogenase in Metabolic Flexibility.

In contracting muscles, carbohydrates and fatty acids serve as energy substrates; the predominant utilization depends on the workload. Here, we investigated the contribution of non-mitochondrial and mitochondrial metabolic pathways in response to repeated training in a polygenic, paternally selected marathon mouse model (DUhTP), characterized by exceptional running performance and an unselected control (DUC), with both lines descended from the same genetic background. Both lines underwent three weeks of high-speed treadmill training or were sedentary. Both lines' muscles and plasma were analyzed. Muscle RNA was sequenced, and KEGG pathway analysis was performed. Analyses of muscle revealed no significant selection-related differences in muscle structure. However, in response to physical exercise, glucose and fatty acid oxidation were stimulated, lactate dehydrogenase activity was reduced, and lactate formation was inhibited in the marathon mice compared with trained control mice. The lack of lactate formation in response to exercise appears to be associated with increased lipid mobilization from peripheral adipose tissue in DUhTP mice, suggesting a specific benefit of lactate avoidance. Thus, results from the analysis of muscle metabolism in born marathon mice, shaped by 35 years (140 generations) of phenotype selection for superior running performance, suggest increased metabolic flexibility in male marathon mice toward lipid catabolism regulated by lactate dehydrogenase.

ACE Inhibitors Improve Skeletal Muscle by Preserving Neuromuscular Junctions in Patients with Alzheimer's Disease.

Hypertension and skeletal muscle decline are common findings in patients with Alzheimer's disease (AD). Angiotensin-converting enzyme (ACE) inhibitors preserve skeletal muscle and physical capacity; however, the driving mechanisms are poorly understood. We investigated the effects of ACE inhibitors on the neuromuscular junction (NMJ) with relevance to skeletal muscle and physical capacity in AD patients and age-matched controls. We evaluated controls (n = 59) and three groups of AD patients, including normotensive (n = 51) and patients with hypertension taking ACE inhibitors (n = 53) or other anti-hypertensive medications (n = 49) at baseline and one year later. We measure plasma c-terminal agrin fragment-22 (CAF22) as a marker of NMJ degradation, handgrip strength (HGS), and Short Physical Performance Battery (SPPB) as markers of physical capacity. At baseline AD patients demonstrated lower HGS and SPPB scores and higher CAF22 levels than controls, irrespective of the hypertension status (all p < 0.05). The use of ACE inhibitors was associated with higher HGS and relative maintenance of SPPB scores, gait speed, and plasma CAF22 levels. Conversely, other anti-hypertensive medications were associated with an unaltered HGS, reduced SPPB scores and elevated plasma CAF22 levels (both p < 0.05). We also found dynamic associations of CAF22 with HGS, gait speed, and SPPB in AD patients taking ACE inhibitors (all p < 0.05). These changes were associated with reduced oxidative stress in AD patients taking ACE inhibitors (p < 0.05). Altogether, ACE inhibitors are associated with higher HGS, preserved physical capacity, and the prevention of NMJ degradation in hypertensive AD patients.

Effects of Acupotomy on Immobilization-Induced Gastrocnemius Contracture and Fibrosis in Rats via Wnt/β-Catenin Signaling.

To determine whether acupotomy ameliorates immobilization-induced muscle contracture and fibrosis via Wnt/β-catenin signaling pathway. Thirty Wistar rats were randomly divided into 5 groups (n=6) by a random number table, including control, immobilization, passive stretching, acupotomy, and acupotomy 3 weeks (3-w) groups. The rat model of gastrocnemius contracture was established by immobilizing the right hind limb in plantar flexion for 4 weeks. Rats in the passive stretching group received passive stretching at gastrocnemius, a daily series of 10 repetitions for 30 s each at 30-s intervals for 10 consecutive days. Rats in the acupotomy and acupotomy 3-w groups received acupotomy once and combined with passive stretching at gastrocnemius a daily series of 10 repetitions for 30 s each at 30-s intervals for 10 consecutive days. Additionally, rats in the acupotomy 3-w group were allowed to walk freely for 3 weeks after 10-day therapy. After treatment, range of motion (ROM), gait analysis [i.e., paw area, stance/swing and maximum ratio of paw area to paw area duration (Max dA/dT)], gastrocnemius wet weight and the ratio of muscle wet weight to body weight (MWW/BW) were tested. Gastrocnemius morphometric and muscle fiber cross-sectional area (CSA) were assessed by hematoxylin-eosin staining. Fibrosis-related mRNA expressions (i.e., Wnt 1, β-catenin, axin-2, α-smooth muscle actin, fibronectin, and types I and III collagen) were measured using real-time quantitative polymerase chain reactions. Wnt 1, β-catenin and fibronectin concentrations were measured by enzyme-linked immunosorbent assay. Types I and III collagen in the perimysium and endomysium were analyzed using immunofluorescence. Compared with the control group, ROM, gait function, muscle weight, MWW/BW and CSA were significantly decreased in the immobilization group (all P<0.01), while protein levels of types I and III collagen, Wnt 1, β-catenin, fibronectin and mRNA levels of fibrosis-related genes were obviously increased (all P<0.01). Treatment with passive stretching or acupotomy restored ROM and gait function and increased muscle wet weight, MWW/BW and CSA (all P<0.05), while protein expression levels of Wnt 1, β-catenin, fibronectin, types I and III collagen and mRNA levels of fibrosis-related genes were remarkably declined compared with the immobilization group (all P<0.05). Compared with passive stretching group, ROM, gait function, MWW was remarkably restored (all P<0.05), and mRNA levels of fibrosis-related genes as well as protein expression levels of Wnt 1, β-catenin, fibronectin, types I and III collagen in the acupotomy group were obviously decreased (all P<0.05). Compared with the acupotomy group, ROM, paw area, Max dA/dT, and MWW were restored (all P<0.05), and mRNA levels of fibrosis-related genes along with protein levels of Wnt 1, β-catenin, fibronectin, types I and III collagen in the acupotomy 3-w group were decreased (P<0.05). Improvements in motor function, muscle contractures, and muscle fibrosis induced by acupotomy correlates with the inhibition of Wnt/β-catenin signaling pathway.

The relationship between bone parameters, body composition, and lower extremity strength in road cyclists.

This study aimed to compare the relationships between bone and body composition parameters, and isometric maximal voluntary contraction (MVC) force of knee extensor (KE) muscles in road cyclists and untrained controls. Twelve male road cyclists and 12 controls aged 20-34 years participated. The isometric MVC force of the KE muscles was assessed by a custom-made dynamometer. Bone mineral content (BMC), bone mineral density (BMD), and body composition were assessed using Dual-Energy X-ray Absorptiometry. No differences were found in body mass, lean body mass, leg lean mass, MVC, whole body, and leg BMD and BMC between cyclists and controls. Controls had a significantly greater (P<0.001) body mass index (BMI), whole body (P<0.01), and leg fat (P<0.001) mass than athletes. In road cyclists, BMC correlated positively with body mass (r=0.73; P<0.01) and BMI (r=0.65; P<0.05), body (r=0.85; P<0.001) and leg lean mass (r=0.81; P<0.001); BMD correlated positively with lean body mass (r=0.60; P<0.05), leg lean mass (r=0.65 and r=0.60; P<0.05). MVC of KE muscles correlated positively with bone parameters (P<0.01) and lean mass (P<0.05) only in controls. Regular cycling training was associated with lower BMI, and body and leg fat mass. There were no significant differences in bone parameters, body and leg lean mass, and isometric MVC force of KE muscle variables between road cyclists and controls. In road cyclists, bone parameters are associated with body mass, and body and leg lean mass, but not with the isometric strength of KE muscles.

SIRT3 overexpression in rat muscle does not ameliorate peripheral insulin resistance.

Reduced expression of the NAD+-dependent deacetylase, SIRT3, has been associated with insulin resistance and metabolic dysfunction in humans and rodents. In this study, we investigated whether specific overexpression of SIRT3 in vivo in skeletal muscle could prevent high-fat diet (HFD)-induced muscle insulin resistance. To address this, we used a muscle-specific adeno-associated virus (AAV) to overexpress SIRT3 in rat tibialis and extensor digitorum longus (EDL) muscles. Mitochondrial substrate oxidation, substrate switching and oxidative enzyme activity were assessed in skeletal muscles with and without SIRT3 overexpression. Muscle-specific insulin action was also assessed by hyperinsulinaemic-euglycaemic clamps in rats that underwent a 4-week HFD-feeding protocol. Ex vivo functional assays revealed elevated activity of selected SIRT3-target enzymes including hexokinase, isocitrate dehydrogenase and pyruvate dehydrogenase that was associated with an increase in the ability to switch between fatty acid- and glucose-derived substrates in muscles with SIRT3 overexpression. However, during the clamp, muscles from rats fed an HFD with increased SIRT3 expression displayed equally impaired glucose uptake and insulin-stimulated glycogen synthesis as the contralateral control muscle. Intramuscular triglyceride content was similarly increased in the muscle of high-fat-fed rats, regardless of SIRT3 status. Thus, despite SIRT3 knockout (KO) mouse models indicating many beneficial metabolic roles for SIRT3, our findings show that muscle-specific overexpression of SIRT3 has only minor effects on the acute development of skeletal muscle insulin resistance in high-fat-fed rats.

The Chronic Effect of Stair Climbing–Descending Exercises after Meals on Glycemic Control in Individuals with Type 2 Diabetes: A Randomized Controlled Trial

This study aimed to examine the chronic effect of a stair climbing–descending exercise (ST-EX) program on glycemic control in individuals with type 2 diabetes (T2D). Sixteen T2D participants were randomly divided into two groups and followed up over 12 weeks: they either performed regular ST-EX after meals at home (n = 8) or maintained their daily routine (CON; no training) (n = 8). The participants in the ST-EX group were instructed to perform a minimum of 12 sessions/week of ST-EX for more than three days/week. One session of ST-EX consisted of two repetitions of 3 min bouts of climbing to the second floor, followed by walking down to the first floor. Fourteen participants completed the study (seven for each group). The decrease in glycoalbumin levels was significantly greater in the ST-EX group (mean value: −1.0%) than in the CON group (+0.4%). Moreover, the knee extension force increased greatly in the ST-EX group (+0.2 Nm/kg) compared with that in the CON group (−0.1 Nm/kg), with no significant change in the skeletal muscle mass. Performing regular ST-EX after meals may be an effective strategy to improve glycemic control and lower-extremity muscle strength in individuals with T2D.

Temperature-Dependent Shape-Memory Textiles: Physical Principles and Applications

Textiles have been pivotal to economies and social relationships throughout history. In today’s world, there is an unprecedented demand for smart materials. The advent of smart textile fabrics, crafted from high-quality, high-performance fibers, has enabled the incorporation of specific functions into clothing and apparel brands. Notably, the rise of smart fabrics is evident in astronaut suits designed to regulate temperature and control muscle vibrations. Moreover, the scope of these products has expanded beyond everyday wear, encompassing fields such as medicine and healthcare, ecology/environmental protection, and military and aerospace. This review explores the recent advancements and challenges associated with intelligent fabrics, particularly temperature-dependent shape-memory metamaterials. The potential for innovative smart textile materials to enhance traditional fabrics’ overall functionality and utility is immense, especially in domains such as medical devices, fashion, entertainment, and defense. Crucially, ensuring user comfort is a primary consideration in these applications for promoting the widespread adoption of wearable devices. Developing smart textile devices necessitates a multidisciplinary approach that combines circuit design expertise, knowledge of smart materials, proficiency in microelectronics, and a deep understanding of chemistry and textile production. The synergy across these diverse fields is vital to unlocking the full potential of smart fabrics and enabling their broad implementation. By embracing this comprehensive approach, we can pave the way for groundbreaking advances in smart textile technology, driving innovation and progress in the field.

Myofiber Baf60c controls muscle regeneration by modulating Dkk3-mediated paracrine signaling.

Obesity and type 2 diabetes (T2D) are the leading causes of the progressive decline in muscle regeneration and fitness in adults. The muscle microenvironment is known to play a key role in controlling muscle stem cell regenerative capacity, yet the underlying mechanism remains elusive. Here, we found that Baf60c expression in skeletal muscle is significantly downregulated in obese and T2D mice and humans. Myofiber-specific ablation of Baf60c in mice impairs muscle regeneration and contraction, accompanied by a robust upregulation of Dkk3, a muscle-enriched secreted protein. Dkk3 inhibits muscle stem cell differentiation and attenuates muscle regeneration in vivo. Conversely, Dkk3 blockade by myofiber-specific Baf60c transgene promotes muscle regeneration and contraction. Baf60c interacts with Six4 to synergistically suppress myocyte Dkk3 expression. While muscle expression and circulation levels of Dkk3 are markedly elevated in obese mice and humans, Dkk3 knockdown improves muscle regeneration in obese mice. This work defines Baf60c in myofiber as a critical regulator of muscle regeneration through Dkk3-mediated paracrine signaling.

A Digital Twin-based Framework of Motion Control and State Monitoring for Pneumatic Muscle

Introduction: The current digital twin systems usually have the drawback of high cost and complex technology, and it is necessary to develop a simple solution to reduce the cost and cycle for the development of digital twin systems, especially for small projects or systems with simple structures. Objective: A low-cost patent technology of digital twin system was proposed by taking the motion control and state monitoring system (MCSMS) of pneumatic muscle as an example. Methods: The MCSMS is developed based on the browser/server architecture. The software of 3ds Max and SolidWorks are used to make the virtual model, Three.js and JavaScript are applied to build the browser side. Data of the physical world is collected and processed on the server side firstly, and then is sent to the browser side through HTTP communication protocol to realize data interchange between the browser and server. Results: In the roaming experiment and the experiment of motion control and state monitoring of pneumatic muscle, the MCSMS can work smoothly without obvious delay and has good real-time performance, which can realize the 3D visual monitoring of the pneumatic muscle very well. Conclusion: The experimental results indicate that the proposed method possesses the ability of good feasibility and effectiveness.

Automatic detection of Parkinson's disease from power spectral density of electroencephalography (EEG) signals using deep learning model.

Parkinson's disease (PD) is characterized by slowed movements, speech disorders, an inability to control muscle movements, and tremors in the hands and feet. In the early stages of PD, the changes in these motor signs are very vague, so an objective and accurate diagnosis is difficult. The disease is complex, progressive, and very common. There are more than 10 million people worldwide suffering from PD. In this study, an EEG-based deep learning model was proposed for the automatic detection of PD to support experts. The EEG dataset comprises signals recorded by the University of Iowa from 14 PD patients and 14 healthy controls. First of all, the power spectral density values (PSDs) ​​of the frequencies between 1 and 49Hz of the EEG signals were calculated separately using periodogram, welch, and multitaper spectral analysis methods. 49 feature vectors were extracted for each of the three different experiments. Then, the performances of support vector machine, random forest, k-nearest neighbor, and bidirectional long-short-term memory (BiLSTM) algorithms were compared using the PSDs feature vectors. After the comparison, the model integrating welch spectral analysis and the BiLSTM algorithm showed the highest performance as a result of the experiments. The deep learning model achieved satisfactory performance with 0.965 specificity, 0.994 sensitivity, 0.964 precision, 0.978 f1-score, 0.958 Matthews correlation coefficient, and 97.92% accuracy. The study is a promising attempt to detect PD from EEG signals and it also provides evidence that deep learning algorithms are more effective than machine learning algorithms for EEG signal analysis.