Altered Muscle Research Articles

Paleopathology, Entheseal Changes, and Cross-Sectional Geometry: The Zooarchaeology of Working Animals

Morphological changes in the skeletons of working animals such as reindeer, horse, and cattle have long been observed and documented in the archaeological record. Activities such as riding, carrying cargo on their backs, and pulling vehicles like sleds and ploughs throughout an animal’s life history cause alterations and variations to skeletal tissue. Such alterations include paleopatho­logical lesions, entheseal changes (EC)—alterations in muscle, tendon, and ligament attachment sites on bone—and variations in cross-sectional bone geometry (CSBG). These clues are helpful for reconstructing human-animal relationships in faunal remains of our archaeological past. However, other factors influence the morphological appearance of skeletal tissue besides working activities, such as age, sex, body size, nutrition, genetics, environmental factors, and management by human caretakers. This article explores how paleopathological lesions, EC, and CSBG in faunal skeletal remains are examined to reconstruct working activity and changes to human-animal rela­tionships in the archaeological record. In particular, we discuss two primary topics of inquiry: (1) a review of paleopathological identifiers in working animals such as cattle, horse, camel, and rein­deer; and (2) how EC and CSBG are understood in terms of bone functional adaptation, and their application in working and non-working animals such as reindeer and horse. Next, we analyze each topic highlighting their benefits and limitations, including how they contribute to archeolog­ical understandings of human-animal relationships in the past, as well as their implications for future research.

Understanding altered contractile properties in advanced age: insights from a systematic muscle modelling approach

Age-related alterations of skeletal muscle are numerous and present inconsistently, and the effect of their interaction on contractile performance can be nonintuitive. Hill-type muscle models predict muscle force according to well-characterised contractile phenomena. Coupled with simple, yet reasonably realistic activation dynamics, such models consist of parameters that are meaningfully linked to fundamental aspects of muscle excitation and contraction. We aimed to illustrate the utility of a muscle model for elucidating relevant mechanisms and predicting changes in output by simulating the individual and combined effects on isometric force of several known ageing-related adaptations. Simulating literature-informed reductions in free Ca2+ concentration and Ca2+ sensitivity generated predictions at odds qualitatively with the characteristic slowing of contraction speed. Conversely, incorporating slower Ca2+ removal or a fractional increase in type I fibre area emulated expected changes; the former was required to simulate slowing of the twitch measured experimentally. Slower Ca2+ removal more than compensated for force loss arising from a large reduction in Ca2+ sensitivity or moderate reduction in Ca2+ release, producing realistic age-related shifts in the force-frequency relationship. Consistent with empirical data, reductions in free Ca2+ concentration and Ca2+ sensitivity reduced maximum tetanic force only slightly, even when acting in concert, suggesting a modest contribution to lower specific force. Lower tendon stiffness and slower intrinsic shortening speed slowed and prolonged force development in a compliance-dependent manner without affecting force decay. This work demonstrates the advantages of muscle modelling for exploring sources of variation and identifying mechanisms underpinning the altered contractile properties of aged muscle.

Using a multiomics approach to unravel a septic shock specific signature in skeletal muscle

Sepsis is defined as a dysregulated host response to infection leading to organs failure. Among them, sepsis induces skeletal muscle (SM) alterations that contribute to acquired-weakness in critically ill patients. Proteomics and metabolomics could unravel biological mechanisms in sepsis-related organ dysfunction. Our objective was to characterize a distinctive signature of septic shock in human SM by using an integrative multi-omics approach. Muscle biopsies were obtained as part of a multicenter non-interventional prospective study. Study population included patients in septic shock (S group, with intra-abdominal source of sepsis) and two critically ill control populations: cardiogenic shock (C group) and brain dead (BD group). The proteins and metabolites were extracted and analyzed by High-Performance Liquid Chromatography-coupled to tandem Mass Spectrometry, respectively. Fifty patients were included, 19 for the S group (53% male, 64 ± 17 years, SAPS II 45 ± 14), 12 for the C group (75% male, 63 ± 4 years, SAPS II 43 ± 15), 19 for the BD group (63% male, 58 ± 10 years, SAPS II 58 ± 9). Biopsies were performed in median 3 days [interquartile range 1–4]) after intensive care unit admission. Respectively 31 patients and 40 patients were included in the proteomics and metabolomics analyses of 2264 proteins and 259 annotated metabolites. Enrichment analysis revealed that mitochondrial pathways were significantly decreased in the S group at protein level: oxidative phosphorylation (adjusted p = 0.008); branched chained amino acids degradation (adjusted p = 0.005); citrate cycle (adjusted p = 0.005); ketone body metabolism (adjusted p = 0.003) or fatty acid degradation (adjusted p = 0.008). Metabolic reprogramming was also suggested (i) by the differential abundance of the peroxisome proliferator-activated receptors signaling pathway (adjusted p = 0.007), and (ii) by the accumulation of fatty acids like octanedioic acid dimethyl or hydroxydecanoic. Increased polyamines and depletion of mitochondrial thioredoxin or mitochondrial peroxiredoxin indicated a high level of oxidative stress in the S group. Coordinated alterations in the proteomic and metabolomic profiles reveal a septic shock signature in SM, highlighting a global impairment of mitochondria-related metabolic pathways, the depletion of antioxidant capacities, and a metabolic shift towards lipid accumulation.ClinicalTrial registration: NCT02789995. Date of first registration 03/06/2016.

Muscle fatigue response of rotator cuff muscles in different postures

IntroductionMuscle fatigue is a leading cause of rotator cuff (RC) pathologies. Scapular orientation affected by changes in the thoracic spine account for differences in body postures leading to altered RC muscle activation. This posture-related alteration in RC muscle activation and its fatigue response needs to be analyzed.Materials and methodsThis study included 50 healthy shoulders with no coexisting spine pathologies. Raw data were recorded using electromyography sensors for RC muscles during two isometric maneuvers of abduction and external rotation, performed at 30% maximum voluntary contraction at 30°, 45°, and 90° arm elevation in sitting and standing. The raw data were analyzed in DataLITE® software, and the mean power frequency (MPF) was extracted to analyze the fatigue response of RC muscles. The Wilcoxon signed-rank test and Kruskal–Wallis test with Bonferroni corrections analyzed fatigue differences between postures and various activities. P < 0.05 was considered significant for the results.ResultsSupraspinatus muscle demonstrated significant fatigue at 90° of arm elevation in standing as compared to sitting (MPF −5.40: −5.41; P = 0.03) posture. Between the three elevation angles, all the RC muscles showed increased fatigue at 90° (MPF range −5.22 to −6.64). When compared between abduction and external rotation, only infraspinatus showed fatigue in external rotation (MPF range −5.42 to −6.08). Among all the three RC muscles, infraspinatus showed the maximum fatigue of MPF −6.64 when compared to supraspinatus −5.22 and teres minor −5.36.ConclusionThe findings indicate that alterations in the body postures and different elevation angles affect the RC muscles’ fatigue response.

UBR2 targets myosin heavy chain IIb and IIx for degradation: Molecular mechanism essential for cancer-induced muscle wasting

Cancer cachexia is a lethal metabolic syndrome featuring muscle wasting with preferential loss of fast-twitching muscle mass through an undefined mechanism. Here, we show that cancer induces muscle wasting by selectively degrading myosin heavy chain (MHC) subtypes IIb and IIx through E3 ligase UBR2-mediated ubiquitylation. Induction of MHC loss and atrophy in C2C12 myotubes and mouse tibialis anterior (TA) by murine cancer cells required UBR2 up-regulation by cancer. Genetic gain or loss of UBR2 function inversely altered MHC level and muscle mass in TA of tumor-free mice. UBR2 selectively interacted with and ubiquitylated MHC-IIb and MHC-IIx through its substrate recognition and catalytic domain, respectively, in C2C12 myotubes. Elevation of UBR2 in muscle of tumor-bearing or free mice caused loss of MHC-IIb and MHC-IIx but not MHC-I and MHC-IIa or other myofibrillar proteins, including α-actin, troponin, tropomyosin, and tropomodulin. Muscle-specific knockout of UBR2 spared KPC tumor-bearing mice from losing MHC-IIb and MHC-IIx, fast-twitching muscle mass, cross-sectional area, and contractile force. The rectus abdominis (RA) muscle of patients with cachexia-prone cancers displayed a selective reduction of MHC-IIx in correlation with higher UBR2 levels. These data suggest that UBR2 is a regulator of MHC-IIb/IIx essential for cancer-induced muscle wasting, and that therapeutic interventions can be designed by blocking UBR2 up-regulation by cancer.

Metabolic alterations of skeletal muscle and exercise intolerance in a mouse model of Fabry

Metabolic alterations of skeletal muscle and exercise intolerance in a mouse model of Fabry

Essential amino acid enriched meal replacement improves body composition and physical function in obese older adults: A randomized controlled trial.

Older adults are threatened by the risk of muscle atrophy and excess accumulation of adipose tissue. The objective of this study was to determine whether an essential amino acid enriched meal replacement would reduce excess fat and foster skeletal muscle retention, potentially improving physical function in this cohort. Using a double blind, randomized controlled trial, we compared the influence of an experimental meal replacement enriched with essential amino acids (EMR) to a commercially available, widely used meal replacement (Optifast®) provided once/day (q.d.) for four weeks on body composition, skeletal muscle and physical function in obese older participants. Twenty-eight individuals completed either EMR (n=13) or Optifast® (n=15) supplementation protocols. Measurements of body composition, thigh skeletal muscle cross-sectional area (CSA), blood panels, intrahepatic lipid, and physical function were completed pre- and post-supplementation. Body fat mass, visceral fat mass and volume, and intrahepatic lipid were reduced with EMR but not with Optifast®. Thigh muscle CSA increased (Δ 2.4±3.0cm2) with EMR but not Optifast® (Δ-1.8±6.0cm2). There was a significant increase in the distance covered during the 6-min walk test with EMR (Δ 23±27m) but no change in Optifast® (Δ 11±37m). Beneficial alterations in fat and muscle support the use of EMR-based meal replacements in obese older adults. ISRCTN registry under Reference Number ISRCTN15814848.

EMG-based co-contraction indexes for the assessment of motor impairments in persons post-stroke

Neuromuscular coordination can be described by activations of agonist–antagonist (AA) muscle pairs and plays an important role in the performing of daily activities. It is an important mechanism used by the central nervous system to regulate joint stability and provide movement accuracy [1]. As a result of a stroke there is an alteration in these coordination patterns that results in motor deficits of the arm function [2]. In fact, persons post-stroke have an exaggerated AA muscle co-contraction [2] associated to a higher joint stiffness [1]. The amount of co-contraction can be quantified through the use of EMG- based co-contraction indexes (CCIs) [1,2]. Therefore, the purpose of the study was to evaluate whether such EMG-based CCIs are able to assess impairment in the motor control of the upper limb in persons post-stroke. Thirty-five persons post-stroke, in chronic or sub-acute stages, were recruited in this study. Both paretic and non-paretic arms were evaluated during the execution of functional tasks related to activities of daily living (i.e., reaching, object placing and forearm pronation). The upper limb kinematics and EMG data of three AA muscle pairs (anterior/posterior deltoids, triceps/biceps and pronator/supinator) were recorded through a movement analysis system. Ten healthy subjects (HS) provided the normative data. The Rudolph’s CCI [1] was computed as proposed by Don (range 0-100%, higher values indicate a greater AA muscle co-contraction) [3]. All participants post-stroke were clinically assessed through the Fugl-Meyer Motor Assessment of Upper Extremity (FM-UE). The differences of Rudolph’s CCI between HS and subjects post-stroke, considering both the more affected (MA) and the less affected (LA) arm, were tested by ANOVA. Bonferroni post-hoc analysis was also used to establish if there were statistically significant differences among the three groups. A deviation from normative data for the MA CCIs was found in almost all functional tasks and antagonist muscle pairs. The LA CCIs also showed a significant deviation from HS. Such pattern is reported in Fig. 1 for Rudolph’s CCI during the forearm pronation task. Higher values of the EMG-based CCI were found both in LA and MA arms in persons post-stroke, indicating alterations in the neuromotor coordination for both sides. The altered AA muscle activation of the LA arm (non-paretic, ipsilateral to the brain lesion) in persons post-stroke, despite its kinematics not being compromised, could be a consequence of the over-use of the non-paretic limb in performing functional tasks. Therefore, also the non-paretic upper limb may benefit from rehabilitation, as recently suggested [4]. Our results show that EMG-based CCI is a quantitative and objective measure able to detect motor control impairment, not detectable by clinical scales.

Немалиновая миопатия редкой формы (случай из практики)

Introduction Nemaline myopathies (NM) are a group of neuromuscular diseases, the distinctive histological feature of which are nemaline rods in myosymplasts. The purpose of this work is to describe the morphology of a rare form of primary nemaline myopathy that progresses in adulthood. Material and methods The surgical material of the paravertebral muscles of a 51-year-old patient with scoliotic deformity at the level of L4-S1, who was repeatedly operated on to correct spinal deformity due to neurological disorders, was studied. Paraffin sections were stained with hematoxylineosin, according to Masson, using the Ptah method, studied using a 3DHISTECH Pannoramic MIDI II BF scanning microscope to digitize preparations using Whole slide imaging technology in two modes: Single layer mode and Extended focus (3DHISTECH, Hungary). Results In the fragments of the altered muscle tissue, filamentous structures of nemaline bodies in myosymplasts were identified, which were located diffusely-dotted throughout the sarcoplasm or formed clusters of various configurations. There was an increased variability in the diameters of muscle fibers, internal nuclei, myosymplasts altered by contraction and with signs of myophagy, patterns of gradual replacement of muscle fibers by adipocytes, massive fatty degeneration of fibers, and fibrosis of the interstitial space. Intramuscular nerve trunks showed signs of complete involution; fibrous perineurium was preserved, and there were single nerve fibers; neuromuscular spindles were distinguished by an enlarged connective tissue capsule. The vessels of the arterial flow had signs of fibrosis and obliteration of the lumen; the vessels of the venous bed were tortuous. Discussion Due to a large number of genes responsible for NM, genetic search can be difficult and is effective only in 50 % of cases. It has been established that nemaline bodies can be distributed diffusely or form clusters of irregular shape, more often subsarcolemmal and characteristic of small fibers. In the presented clinical case, nemaline bodies were observed over the entire area of the fibers and were characteristic of myosymplasts of various sizes. Conclusion The histopathological study of the paravertebral muscles established the neuromuscular nature of the disease, being nemaline myopathy that progressed in adulthood and had not been diagnosed at previous stages of treatment.

Evaluation of Muscle Synergy During Exoskeleton-Assisted Walking in Persons With Multiple Sclerosis.

Gait deficit after multiple sclerosis (MS) can be characterized by altered muscle activation patterns. There is preliminary evidence of improved walking with a lower limb exoskeleton in persons with MS. However, the effects of exoskeleton-assisted walking on neuromuscular modifications are relatively unclear. The objective of this study was to investigate the muscle synergies, their activation patterns and the differences in neural strategies during walking with (EXO) and without (No-EXO) an exoskeleton. Ten subjects with MS performed walking during EXO and No-EXO conditions. Electromyography signals from seven leg muscles were recorded. Muscle synergies and the activation profiles were extracted using non-negative matrix factorization. The stance phase duration was significantly shorter during EXO compared to the No-EXO condition (p<0.05). Moreover, typically 3-5 modules were extracted in each condition. The module-1 (comprising Vastus Medialis and Rectus Femoris muscles), module-2 (comprising Soleus and Medial Gastrocnemius muscles), module-3 (Tibialis Anterior muscle) and module-4 (comprising Biceps Femoris and Semitendinosus muscles) were comparable between conditions. During EXO condition, Semitendinosus and Vastus Medialis emerged in module-5 in 7/10 subjects. Compared to No-EXO, average activation amplitude was significantly reduced corresponding to module-2 during the stance phase and module-3 during the swing phase during EXO. Exoskeleton-assistance does not alter the existing synergy modules, but could induce a new module to emerge, and alters the control of these modules, i.e., modifies the neural commands indicated by the reduced amplitude of the activation profiles. The work provides insights on the potential underlying mechanism of improving gait functions after exoskeleton-assisted locomotor training.

To Determine Frequency of Anxiety and Depression in Temporo-mandibular Joint Disorders

Background: Temporomandibular disorder (TMD) is a general term that refers to disorders associated with the temporomandibular joint (TMJ) and the masticatory muscles. Due to the complexity of the masticatory system, TMD symptoms may be caused by different physiological and/or psychosocial factors, such as malocclusion and occlusal interferences, alterations in the masticatory muscles, direct trauma to the jaw or TMJ, micro trauma caused by continuous parafunctional habits Aim: To determine frequency of anxiety and depression in temporomandibular joint disorders. Methods: Cross sectional study design was conducted in the Department of Oral and Maxillofacial surgery, Mayo Hospital Lahore for a period 6 months. a total 365 cases fulfilling inclusion criteria was enrolled in study from Oral and Maxillofacial surgery Mayo Hospital Lahore. Informed written consent was taken from patients and then their data according to variables in proforma was recorded. Anxiety and depression was measured by researcher himself according to operational definition. Results: The mean age of cases was 28.95 ± 6.71 years with minimum and maximum age of 18 and 40 years. In this study there were 185(50.68%) male and 180(49.32%) female cases. The mean Hospital Anxiety and Depression (HAD) score was 12.15±11.75 with minimum and maximum score as 0 and 42. Anxiety and depression was seen in 180(49.32%) of the cases while 185(50.68%) of the cases did not has anxiety and depression. Conclusion Through the findings of this study it is found that the frequency of Anxiety and depression is very much high. So we should formulate proper treatment strategy with the help of psychiatry department to cope this issue. No doubt it will help to improve their prognosis and better quality of life. Keywords: Physical therapy specialty, Electromyography, Facial pain, Temporomandibular joint, Anxiety, Depression

Oxidative stress causes muscle structural alterations via p38 MAPK signaling in COPD mouse model.

Sarcopenia is a complication of Chronic Obstructive Pulmonary Disease (COPD) that negatively affects physical activity and quality of life. However, the underlying mechanism by which COPD affects skeletal muscles remains to be elucidated. Therefore, we investigated the association between oxidative stress and structural alterations in muscles in elastase-induced emphysema mouse models. Twelve-week-old male C57BL/6J mice were treated with either intratracheal porcine pancreatic elastase (PPE) dissolved in saline, or saline alone. The mice were euthanized 12weeks after treatment, and the lungs and limb muscles were used for protein analysis of oxidative stress, p38 mitogen-activated protein kinase (p38 MAPK) signaling pathway and muscle atrophy signaling pathway related with oxidative stress. Furthermore, C57BL/6J mice treated with PPE or saline were analyzed for the effects of oral administration of astaxanthin or p38 inhibitor. The weight of the soleus muscle, proportion of type I muscle fibers, and cross-sectional areas of muscle fibers in the PPE group were lower than those in the control group. Oxidative stress marker levels in the PPE group were elevated in skeletal muscles. The p38 MAPK signaling pathway was activated in the soleus muscles, leading to the activation of the ubiquitin-proteasome system and autophagy. Astaxanthin and p38 inhibitors attenuated alterations in muscle structure through the deactivation of the p38 MAPK signaling pathway. This study provides first evidence in COPD mouse model that oxidative stress trigger a series of muscle structural changes. Our findings suggest a novel target for sarcopenia in COPD.

Empagliflozin Preserves Skeletal Muscle Function in a HFpEF Rat Model.

Besides structural alterations in the myocardium, heart failure with preserved ejection fraction (HFpEF) is also associated with molecular and physiological alterations of the peripheral skeletal muscles (SKM) contributing to exercise intolerance often seen in HFpEF patients. Recently, the use of Sodium-Glucose-Transporter 2 inhibitors (SGLT2i) in clinical studies provided evidence for a significant reduction in the combined risk of cardiovascular death or hospitalization for HFpEF. The present study aimed to further elucidate the impact of Empagliflozin (Empa) on: (1) SKM function and metabolism and (2) mitochondrial function in an established HFpEF rat model. At the age of 24 weeks, obese ZSF1 rats were randomized either receiving standard care or Empa in the drinking water. ZSF1 lean animals served as healthy controls. After 8 weeks of treatment, echocardiography and SKM contractility were performed. Mitochondrial function was assessed in saponin skinned fibers and SKM tissue was snap frozen for molecular analyses. HFpEF was evident in the obese animals when compared to lean—increased E/é and preserved left ventricular ejection fraction. Empa treatment significantly improved E/é and resulted in improved SKM contractility with reduced intramuscular lipid content. Better mitochondrial function (mainly in complex IV) with only minor modulation of atrophy-related proteins was seen after Empa treatment. The results clearly documented a beneficial effect of Empa on SKM function in the present HFpEF model. These effects were accompanied by positive effects on mitochondrial function possibly modulating SKM function.

Altered skeletal muscle sarco-endoplasmic reticulum Ca2+-ATPase calcium transport efficiency after a thermogenic stimulus.

Exposure to predator threat induces a rapid and robust increase in skeletal muscle thermogenesis in rats. The central nervous system relays threat information to skeletal muscle through activation of the sympathetic nervous system, but muscle mechanisms mediating this thermogenesis remain unidentified. Given the relevance of sarcolipin-mediated futile calcium cycling through the sarco-endoplasmic reticulum Ca2+-ATPase (SERCA) pump to mammalian muscle nonshivering thermogenesis, we hypothesized that this plays a role in contextually induced muscle thermogenesis as well. This was assessed by measuring enzymatic activity of SERCA and sarcoplasmic reticulum Ca2+ transport, where the apparent coupling ratio (Ca2+ uptake rate divided by ATPase activity rate at a standard Ca2+ concentration) was predicted to decrease in association with muscle thermogenesis. Sprague-Dawley rats exposed to predator (ferret) odor (PO) showed a rapid decrease in the apparent coupling ratio in the soleus muscle, indicating SERCA uncoupling compared with control-odor-exposed rats. A rat model of high aerobic fitness and elevated muscle thermogenesis also demonstrated soleus muscle SERCA uncoupling relative to their obesity-prone, low-fitness counterparts. Both the high- and low-aerobic fitness rats showed soleus SERCA uncoupling with exposure to PO. Finally, no increase in sarcolipin expression in soleus muscle was detected with PO exposure. This dataset implicates muscle uncoupling of SERCA Ca2+ transport and ATP hydrolysis, likely through altered SERCA or sarcolipin function outside of translational regulation, as one contributor to the muscle thermogenesis provoked by exposure to predator threat. These data support the involvement of SERCA uncoupling in both muscle thermogenic induction and enhanced aerobic capacity.

Worksite-based intensive lifestyle therapy has profound cardiometabolic benefits in people with obesity and type 2 diabetes

Lifestyle therapy (energy restriction and exercise) is the cornerstone of therapy for people with type 2 diabetes (T2D) but is difficult to implement. We conducted an 8-month randomized controlled trial in persons with obesity and T2D (17 women and 1 man) to determine the therapeutic effects and potential mechanisms of intensive lifestyle therapy on cardiometabolic function. Intensive lifestyle therapy was conducted at the worksite to enhance compliance and resulted in marked (17%) weight loss and beneficial changes in body fat mass, intrahepatic triglyceride content, cardiorespiratory fitness, muscle strength, glycemic control, βcell function, and multi-organ insulin sensitivity, which were associated with changes in muscle NAD+ biosynthesis, sirtuin signaling, and mitochondrial function and in adipose tissue remodeling. These findings demonstrate that intensive lifestyle therapy provided at the worksite has profound therapeutic clinical and physiological effects in people with T2D, which are likely mediated by specific alterations in skeletal muscle and adipose tissue biology.

Altered Muscle Activation Patterns During Unexpected Single-leg Landing In Chronic Ankle Instability Patients

Chronic ankle instability (CAI) patients display altered motor controls during inversion perturbation. Although these alterations may be vulnerable motor controls compared to controls, inversion perturbation under anticipatory conditions makes a less realistic simulation of lateral ankle sprains. PURPOSE: To examine differences in muscle activation during an unexpected inversion perturbation among CAI, coper, and control groups. METHODS: Twenty-two CAI patients (M = 11, F = 11; 22 ± 3 yr, 174 ± 8 cm, 71 ± 10 kg), 22 controls (M = 11, F = 11; 21 ± 2 yr, 173 ± 7 cm, 71 ± 10 kg), and 22 copers (M = 11, F = 11; 21 ± 2 yr, 174 ± 8 cm, 70 ± 13 kg) participated. Participants completed 5 trials of unexpected ankle inversion perturbation during single-leg landing onto a tilted force platform (25º) from a height of 30 cm. EMG data of tibialis anterior (TA), peroneus longus (PL), medial gastrocnemius (MG), and gluteus maximus (GX) were collected from 200 ms before and after initial contact (IC). Functional linear models were used to detect between-group differences. If 95% CIs did not cross zero, differences were significant. RESULTS: Figure 1 shows that CAI patients displayed greater TA and MG activation before IC relative to copers and/or controls. In addition, CAI patients showed greater TA and PL activation after IC relative to copers and/or controls. Copers and controls had similar muscle activation patterns. CONCLUSION: While copers and controls showed similar muscle activation during unexpected ankle perturbation, increased TA and MG activation prior to IC in CAI patients may indicate a neuromuscular effort to stabilize the ankle to prevent further sprains. Increased TA and PL activation after IC in CAI patients may also represent a protective motor control to prevent excessive displacement of the rear foot from the inversion perturbation. However, similar patterns in copers and controls seem to elicit coping mechanisms in an attempt to prevent further injuries after their initial injuries.

Sarkopenie, myosteatóza a syndrom křehkosti u pacientů s cirhózou jater

Skeletal muscles are the biggest tissue in healthy people (30–40% of total body mass) and they comprise three quarters of total body proteins. Muscle alterations, especially muscle wasting and loss of muscle function, have an indisputable prognostic value in the outcome of chronic diseases, including chronic liver diseases. Muscle wasting is associated with higher morbidity, mortality and poor quality of life. The terms sarcopenia and myosteatosis are used to describe specific muscle alterations, both forming substantial components of multidimensional construct “frailty syndrome”. Sarcopenia is defined as loss of muscle mass and/or loss of muscle function. It is usually dia­gnosed using the skeletal muscle index from computed tomography (CT) image analysis at the L3 vertebra. Myosteatosis is defined as an excess intramyocelullar and intermyocellular fat deposition. Dia­gnosis of myosteatosis is based on a measurement of skeletal muscle density by CT imaging at the L3 vertebra (skeletal muscle radiation attenuation – SM-RA). Besides muscle alterations and decreased physical performance, frailty syndrome also comprises changes of other organ systems, leading to the loss of functional reserves and higher vulnerability. Different scoring systems, such as Fried Frailty Index (FFI) or modified Liver Frailty Index (LFI) for patients with liver cirrhosis, are used to dia­gnose patients with frail phenotype. The principle of the treatment of patients with muscle alterations is therapy of liver disease (including liver transplant in advanced cirrhosis), improvement of the nutritional status, adequate physical activity and supplementation of vitamin D deficiency, if necessary. In this review, we summarize up-to-date knowledge about pathophysiology, dia­gnostic tools and treatment options of sarcopenia, myosteatosis and frailty syndrome in patients with liver cirrhosis. Key words: sarcopenia – myosteatosis – frailty syndrome – liver cirrhosis

Polg mtDNA mutator mice reveal limited involvement of vertebral bone loss in premature aging-related thoracolumbar hyperkyphosis

BackgroundAge-related hyperkyphosis is multifactorial and involves alterations of vertebral bone, intervertebral discs (IVD) and paraspinal muscles. The relative contribution of these tissues remains unclear. Here, we compared differences in vertebral bone microarchitecture and IVD thickness between prematurely aging mice with spinal hyperkyphosis and wild type littermates. MethodsThoracolumbar vertebral columns were dissected from homozygous PolgD257A and age-matched wild type littermates. Micro-computed tomography was performed to quantify cortical and trabecular bone parameters at anterior and posterior portions of T8-L4 vertebrae. In addition, vertebral shape, transaxial facet joint orientation and IVD thickness were quantified. Differences in anterior/posterior ratios between genotypes were compared by Student's t-test and association between vertebral bone and IVD parameters was investigated using Pearson correlation analysis. ResultsHyperkyphotic homozygous mice displayed generalized osteopenia that was more pronounced at the posterior compared with anterior portion of thoracolumbar vertebrae. An increase in the anterior/posterior ratio of trabecular bone parameters was revealed at the thoracolumbar junction (T13-L1). PolgD257A displayed diffuse loss of cortical bone thickness, yet anterior/posterior ratios were unchanged. Despite generalized and regional bone loss, vertebral shape was unaffected. PolGD257A mice showed a 10–20 % reduction of IVD thickness at both thoracic and lumbar levels, with only minimal histopathological changes. IVD thickness was negatively correlated with anterior/posterior ratios of trabecular bone parameters, as well as with more coronally oriented facet joints, but negatively correlated with the anterior/posterior ratio of cortical bone thickness. ConclusionsAging-induced regional changes of vertebral trabecular and cortical bone did not lead to altered vertebral shape in PolgD257A mice but may indirectly cause hyperkyphosis through reduction of IVD thickness. These findings suggest a limited role for aging-induced bone loss in spinal hyperkyphosis and warrants further research on the involvement of paraspinal muscle degeneration.

Integrative and complementary practices in dentistry: acupuncture in temporomandibular disorders

The temporomandibular disorder (TMD) consists of the functional alteration of the orofacial muscles, the temporomandibular joints, or both. Among the therapeutic options available for treating TMD, acupuncture appears as a relevant therapy to relieve pain and reduce the symptoms of clicking and discomfort of the temporomandibular joint. This study investigated the use of acupuncture as an auxiliary therapy in pain management in patients with TMD. A narrative review of the literature was performed using PubMed, Scielo, Bireme, LILACS, the American Association of Pain and the descriptor acupuncture, temporomandibular joint disorders, quality of life, dentistry, limited to the Portuguese, Spanish and English covering the publication period of 2012 to 2022. The highest prevalence rate of TMD is among women (about 80%) and the dysfunction appears after the age of 30. The main causes of TMD are related to behavioral, psychosocial and hormonal factors. Studies evaluating acupuncture for TMD treatment are limited. In contrast, significant short-term pain improvement was expressed in 26% of the articles. Taking into account that the disorder is mainly characterized by pain (algia), the reduction of this condition is of paramount importance.

Keap1/Nrf2 pathway in sodium fluoride-induced cardiac toxicity and the prophylactic role of vitamin C versus platelet-rich plasma.

The present study was conducted to investigate the role of vitamin C versus platelet-rich plasma (PRP) against sodium fluoride (NaF)-induced cardiotoxicity and cell death in rats' myocardium. Previous studies suggest that NaF decreased cellular viability and intracellular antioxidant power. The present study revealed that NaF administration caused histological alterations in the cardiac muscle and increased the accumulation of intracellular reactive oxygen species, the expression of inducible nitric oxide synthases and proliferating cell nuclear antigen as well as collagen deposition in cardiac tissue. As supported by colorimetric analysis, an elevation in malondialdehyde level and a decrease in both superoxide dismutase (SOD) and thioredoxin-1 oxidoreductase (TrX) levels were seen, whereas molecular analysis revealed a decrease in Keap1 and an increase in Nrf2 and HO-1 gene expression. Pretreatment with vitamin C and PRP prior to NaF administration significantly improved the altered parameters and enhanced the cellular antioxidant capability of myocardium resulting in protection of cardiac muscle from NaF-induced cytotoxicity and apoptotic cell death. The cyto-protective activity of PRP was found to be comparable to that of the known antioxidant, vitamin C.