Surrounding Muscle Fibers Research Articles

Elevated heart rate and decreased muscle endothelial nitric oxide synthase in early development of insulin resistance.

Insulin resistance (IR) is a risk factor for the development of several major metabolic diseases. Muscle fiber composition is established early in life and is associated with insulin sensitivity. Hence, muscle fiber composition was used to identify early defects in the development of IR in healthy young individuals in the absence of clinical manifestations. Biopsies were obtained from the thigh muscle, followed by an intravenous glucose tolerance test. Indices of insulin action were calculated and cardiovascular measurements, analyses of blood and muscle were performed. Whole body insulin sensitivity (SIgalvin) was positively related to expression of type I muscle fibers (r = 0.49; P < 0.001) and negatively related to resting heart rate (HR, r = -0.39; P < 0.001), which was also negatively related to expression of type I muscle fibers (r = -0.41; P < 0.001). Muscle protein expression of endothelial nitric oxide synthase (eNOS), whose activation results in vasodilation, was measured in two subsets of subjects expressing a high percentage of type I fibers (59 ± 6%; HR = 57 ± 9 beats/min; SIgalvin = 1.8 ± 0.7 units) or low percentage of type I fibers (30 ± 6%; HR = 71 ± 11; SIgalvin = 0.8 ± 0.3 units; P < 0.001 for all variables vs. first group). eNOS expression was 1) higher in subjects with high type I expression; 2) almost twofold higher in pools of type I versus II fibers; 3) only detected in capillaries surrounding muscle fibers; and 4) linearly associated with SIgalvin. These data demonstrate that an altered function of the autonomic nervous system and a compromised capacity for vasodilation in the microvasculature occur early in the development of IR.NEW & NOTEWORTHY Insulin resistance (IR) is a risk factor for the development of several metabolic diseases. In healthy young individuals, an elevated heart rate (HR) correlates with low insulin sensitivity and high expression of type II skeletal muscle fibers, which express low levels of endothelial nitric oxide synthase (eNOS) and, hence, a limited capacity to induce vasodilation in response to insulin. Early targeting of the autonomic nervous system and microvasculature may attenuate development of diseases stemming from insulin resistance.

Isolation of Nuclei from Human Intermuscular Adipose Tissue and Downstream Single-Nuclei RNA Sequencing.

Intermuscular adipose tissue (IMAT) is a relatively understudied adipose depot located between muscle fibers. IMAT content increases with age and BMI and is associated with metabolic and muscle degenerative diseases; however, an understanding of the biological properties of IMAT and its interplay with the surrounding muscle fibers is severely lacking. In recent years, single-cell and nuclei RNA sequencing have provided us with cell type-specific atlases of several human tissues. However, the cellular composition of human IMAT remains largely unexplored due to the inherent challenges of its accessibility from biopsy collection in humans. In addition to the limited amount of tissue collected, the processing of human IMAT is complicated due to its proximity to skeletal muscle tissue and fascia. The lipid-laden nature of the adipocytes makes it incompatible with single-cell isolation. Hence, single nuclei RNA sequencing is optimal for obtaining high-dimensional transcriptomics at single-cell resolution and provides the potential to uncover the biology of this depot, including the exact cellular composition of IMAT. Here, we present a detailed protocol for nuclei isolation and library preparation of frozen human IMAT for single nuclei RNA sequencing. This protocol allows for the profiling of thousands of nuclei using a droplet-based approach, thus providing the capacity to detect rare and low-abundant cell types.

Endomysium determines active and passive force production in muscle fibers

Connective tissues can be recognized as an important structural support element in muscles. Recent studies have also highlighted its importance in active force generation and transmission between muscles, particularly through the epimysium. In the present study, we aimed to investigate the impact of the endomysium, the connective tissue surrounding muscle fibers, on both passive and active force production. Pairs of skeletal muscle fibers were extracted from the extensor digitorum longus muscles of rats and, after chemical skinning, their passive and active force–length relationships were measured under two conditions: (i) with the endomysium between muscle fibers intact, and (ii) after its dissection. We found that the dissection of the endomysium caused force to significantly decrease in both active (by 22.2 % when normalized to the maximum isometric force; p < 0.001) and passive conditions (by 25.9 % when normalized to the maximum isometric force; p = 0.034). These findings indicate that the absence of endomysium compromises muscle fiber’s not only passive but also active force production. This effect may be attributed to increased heterogeneity in sarcomere lengths, enhanced lattice spacing between myofilaments, or a diminished role of trans-sarcolemmal proteins due to dissecting the endomysium. Future investigations into the underlying mechanisms and their implications for various extracellular matrix-related diseases are warranted.

Cellular activation patterns of CD10+ fibro-adipogenic progenitors across acquired disease states in human skeletal muscle biopsies.

Background: Fibro-adipogenic progenitors (FAP) are muscle resident mesenchymal stem cells pivotal for regulation of myofiber repair. Experimental results show in addition involvement in a range of other pathological conditions and potential for pharmacological intervention. FAP histopathology in human muscle biopsies is largely unknown, but has potential to inform translational research. Methods: CD10+ FAPs in 32 archival muscle biopsies from 8 groups (normal, dermatomyositis, inclusion body myositis (IBM), anti-synthetase syndrome, immune-mediated necrotizing myopathy (IMNM), denervation, type 2 atrophy, rhabdomyolysis) were visualized by CD10 immunohistochemistry and their histology compared. Groups are compared by semi-quantitative scoring. Results: Histological activation of endomysial CD10+ FAPs includes prominent expansion of a network of cell processes surrounding muscle fibers, as well as endomysial cell clusters evidencing proliferation. Prominence of periarteriolar processes is a notable feature in some pathologies. FAP activation is often associated with fiber degeneration/regeneration, foci of inflammation, and denervation in keeping with experimental results. Type 2 atrophy shows no evidence of FAP activation. Dermatomyositis and anti-synthetase syndrome associated myositis demonstrate diffuse activation. Conclusion: Assessment of CD10+ FAP activation is routinely possible using CD10 immunohistochemistry and demonstrates several patterns in keeping with preclinical results. Prominent expansion of FAP processes surrounding myofibers suggests enhanced interaction between myofiber/basement membranes and FAPs during activation. The presence of diffuse FAP activation in dermatomyositis biopsies unrelated to fiber repair raises the possibility of FAP activation as part of the autoimmune process. Future diagnostic applications, clinical significance and therapeutic potential remain to be elucidated.

Myopathy as a cause of fatigue in long-term post-COVID-19 symptoms: Evidence of skeletal muscle histopathology.

Background and purposeAmong post‐COVID‐19 symptoms, fatigue is reported as one of the most common, even after mild acute infection, and as the cause of fatigue, myopathy diagnosed by electromyography has been proposed in previous reports. This study aimed to explore the histopathological changes in patients with post‐COVID‐19 fatigue.MethodsSixteen patients (mean age = 46 years) with post‐COVID‐19 complaints of fatigue, myalgia, or weakness persisting for up to 14 months were included. In all patients, quantitative electromyography and muscle biopsies analyzed with light and electron microscopy were taken.ResultsMuscle weakness was present in 50% and myopathic electromyography in 75%, and in all patients there were histological changes. Muscle fiber atrophy was found in 38%, and 56% showed indications of fiber regeneration. Mitochondrial changes, comprising loss of cytochrome c oxidase activity, subsarcollemmal accumulation, and/or abnormal cristae, were present in 62%. Inflammation was found in 62%, seen as T lymphocytes and/or muscle fiber human leukocyte antigen ABC expression. In 75%, capillaries were affected, involving basal lamina and cells. In two patients, uncommon amounts of basal lamina were found, not only surrounding muscle fibers but also around nerves and capillaries.ConclusionsThe wide variety of histological changes in this study suggests that skeletal muscles may be a major target of SARS‐CoV‐2, causing muscular post‐COVID‐19 symptoms. The mitochondrial changes, inflammation, and capillary injury in muscle biopsies can cause fatigue in part due to reduced energy supply. Because most patients had mild–moderate acute affection, the new variants that might cause less severe acute disease could still have the ability to cause long‐term myopathy.

Diversity of extracellular matrix morphology in vertebrate skeletal muscle.

Existing data suggest the extracellular matrix (ECM) of vertebrate skeletal muscle consists of several morphologically distinct layers: an endomysium, perimysium, and epimysium surrounding muscle fibers, fascicles, and whole muscles, respectively. These ECM layers are hypothesized to serve important functional roles within muscle, influencing passive mechanics, providing avenues for force transmission, and influencing dynamic shape changes during contraction. The morphology of the skeletal muscle ECM is well described in mammals and birds; however, ECM morphology in other vertebrate groups including amphibians, fish, and reptiles remains largely unexamined. It remains unclear whether a multilayered ECM is a common feature of vertebrate skeletal muscle, and whether functional roles attributed to the ECM should be considered in mechanical analyses of non-mammalian and non-avian muscle. To explore the prevalence of a multilayered ECM, we used a cell maceration and scanning electron microscopy technique to visualize the organization of ECM collagen in muscle from six vertebrates: bullfrogs (Lithobates catesbeianus), turkeys (Meleagris gallopavo), alligators (Alligator mississippiensis), cane toads (Rhinella marina), laboratory mice (Mus musculus), and carp (Cyprinus carpio). All muscles studied contained a collagen-reinforced ECM with multiple morphologically distinct layers. An endomysium surrounding muscle fibers was apparent in all samples. A perimysium surrounding groups of muscle fibers was apparent in all but carp epaxial muscle; a muscle anatomically, functionally, and phylogenetically distinct from the others studied. An epimysium was apparent in all samples taken at the muscle periphery. These findings show that a multilayered ECM is a common feature of vertebrate muscle and suggest that a functionally relevant ECM should be considered in mechanical models of vertebrate muscle generally. It remains unclear whether cross-species variations in ECM architecture are the result of phylogenetic, anatomical, or functional differences, but understanding the influence of such variation on muscle mechanics may prove a fruitful area for future research.

Nivolumab causes focal muscular inflammation without electrophysiological or muscle magnetic resonance imaging findings

AbstractA 62‐year‐old woman was admitted to our hospital complaining of bilateral shoulder muscle pain after nivolumab treatment. Her laboratory data disclosed elevated serum creatine kinase levels while the magnetic resonance imaging and the electromyography study were unremarkable. A left deltoid muscle biopsy was performed, and the evidence of focal inflammatory cell infiltration surrounding muscle fibers and upregulation of major histocompatibility complex class I was showed. Even mild and transient muscular symptoms after administration of nivolumab can represent immune‐mediated muscular inflammation.

Effects of Biowastes Released by Mechanically Damaged Muscle Cells on the Propagation of Deep Tissue Injury: A Multiphysics Study.

Deep tissue injuries occur in muscle tissues around bony prominences under mechanical loading leading to severe pressure ulcers. Tissue compression can potentially compromise lymphatic transport and cause accumulation of metabolic biowastes, which may cause further cell damage under continuous mechanical loading. In this study, we hypothesized that biowastes released by mechanically damaged muscle cells could be toxic to the surrounding muscle cells and could compromise the capability of the surrounding muscle cells to withstand further mechanical loadings. In vitro, we applied prolonged low compressive stress (PLCS) and short-term high compressive stress to myoblasts to cause cell damage and collected the biowastes released by the damaged cells under the respective loading scenarios. In silico, we used COMSOL to simulate the compressive stress distribution and the diffusion of biowastes in a semi-3D buttock finite element model. In vitro results showed that biowastes collected from cells damaged under PLCS were more toxic and could compromise the capability of normal myoblasts to resist compressive damage. In silico results showed that higher biowastes diffusion coefficient, higher biowastes release rate, lower biowastes tolerance threshold and earlier timeline of releasing biowastes would cause faster propagation of tissue damage. This study highlighted the importance of biowastes in the development of deep tissue injury to clinical pressure ulcers under prolonged skeletal compression.

P.412 - Diagnostic implications of three cases of skeletal muscle light-chain (AL) amyloidosis

A 70-year-old female with a two year history of painless, progressive proximal weakness and markedly elevated CK (>1600 U/l), a 74-year-old male with a year's history of exercise-induced myalgia, including claudicatio masticatoria and fatigue with CK in the normal range and a 79-year-old male with a four month history of myalgia, constipation and weight loss with elevated CK were diagnosed with skeletal muscle amyloidosis by Congo red stain on muscle biopsy samples. They had IgG lambda, IgA lambda and IgG kappa light chain paraproteins, respectively. In the first and third case, sural nerve biopsies showed some, predominately axonal damage, but no amyloidosis. Rectum biopsy in the second as well as colon and gastral biopsy in the third case failed to detected amyloid deposition, too. In case one, the diagnosis of °I plasmocytoma and in case three of suspected multiple myeloma had been established, but prior to the diagnosis of amyloidosis, no treatment was considered necessary. In the second case, the paraprotein was discovered at the time of biopsy. In every case, muscle biopsy showed some aspects of neurogenic damage and nerve conduction studies revealed some abnormalities. In case one, deposition of congophilic, birefringent material was solely vascular, while in case two and three there was some deposition surrounding muscle fibres. In case three only, immunohistochemistry showed activated complement (C5b9) colocalised with amyloid deposition, widespread capillary changes and perimysial pathology. All the clinical and biopsy findings in these cases are in line with the literature. Nerve, rectum and possibly labial salivary gland biopsies are generally considered to have a higher detection rate for amyloidosis. However, we conclude that biopsy analysis of clinically affected muscle should be the standard procedure in patients with muscular complains and paraprotein. A non-conclusive biopsy of another tissue cannot be accepted as a substitute.

Reconstruction of oro-facial region; challenges and opportunities

Event Abstract Back to Event Reconstruction of oro-facial region; challenges and opportunities Ashraf A. Ayoub1, Randa Al Fotawi1, K E. Tanner2, Matthew J. Dalby3 and Kurt Naudi1 1 University of Glasgow, Glasgow Dental Hospital & School, United Kingdom 2 University of Glasgow, Biomedical Engineering Division, School of Engineering, United Kingdom 3 University of Glasgow, Institute of Molecular, Cell and Systems Biology, College of Medical, Veterinary and Life Sciences, United Kingdom Background: Surgical reconstruction of functional and aesthetic defects, particularly following ablative cancer surgery, is often compromised by limited vascularity and the associated donor site morbidity. A compromised vascular bed is a major obstacle for the successful uptake of a micro-vascular flap. Aim: Investigate a novel approach of using an injectable scaffolding into a pedicled muscle flap for reconstruction of a critical size mandibular defect. Materials and Methods: Under general anesthesia bone marrow was aspirated from both the rabbit’s anterior iliac crest. Cells were cultured and expanded according to a validated standard protocol before application in the surgical defect[1]. A critical size bony defect, 20mm x 15mm, was created in the rabbit’s mandibular body[2]. A fixation plate was applied at the inferior border to maintain the mandibular integrity, while the superior border was maintained. A pedicled masseter muscle flap was rotated and adapted to fill the created surgical defect. An injectable calcium sulfate/hydroxyapatite scaffolding material (Cerament Spine Support) loaded with BMP-7 and mesnechymal stem cells was injected into the muscle flap to induce bone formation. Animals were sacrificed at three months following surgery. The quality of bone regeneration was assessed using Cone Beam Computerised Tomography (CBCT), micro CT and histological assessment. Results: In all the cases sporadic areas of bone regeneration were detected within the muscle flap. In some cases the volume of newly formed bone was more than the volume of bone resected to the create the defect. Bone formation was in close proximity to the injectable scaffold material. Micro CT showed a different trabecular pattern in the regenerated bone to the native bone tissue. Fig 1 Micro CT showing new bone formed in the defect. Histologically, the regenerated tissue consisted of a mixture of mature bone with clear Haversion structure and areas of woven bone. Some areas of fibrous tissue “muscle metaplasia” was detected between the newly generated bone and the surrounding muscle fibres. New bone formation was either from the defect edges or Fig 2 Undecalcified section stained with Goldner’s trichrome, showing resorption of the graft material and new bone formation. Conclusions: The muscle flap acted as a bioreactor for bone induction under the influence of calcium sulfate/hydroxyapatite, stem cells and BMP-7. Three months is insufficient for complete restoration of the bony defect. The new bone formation concentrated around the areas of the injected cells and material. Randa Alfotawi was funded by King Saud University, Ministry of Higher Education; Bone Support AB (Lund, Sweden) is thanked for provision of the Cerament™ bone cements

Botulinum toxin B increases intrinsic muscle activity in organotypic spinal cord-skeletal muscle co-cultures.

In organotypic spinal cord-skeletal muscle co-cultures, motoneurons are driven by locomotor commands and induce contractions in surrounding muscle fibres. Using these co-cultures, it has been shown that effects of organophosphorus compounds on neuromuscular synapses can be determined in vitro. In the present study we aimed to extend this in vitro tool for pharmacologic testing of botulinum toxin B. This neurotoxin is widely used for the treatment of dystonia. Besides its effects on the neuromuscular junction, botulinum toxins may also act at centrally located synapses. Incubation with botulinum toxin B (Neurobloc(®)) induced a significant increase in muscular activity after 24, 48 and 72h. Application of the NMDA- and AMPA-receptor antagonists AP5 (20μM) and CNQX (15μM) induced a similar augmentation of muscle activity after 48 and 72h, respectively. Administration of the glycine- and GABA(A)-receptor antagonists strychnine (1μM) and bicuculline (100μM) did not alter intrinsic muscle activity. In contrast, application of a non-depolarizing muscle relaxant rocuronium bromide reduced the muscle activity in a dose-dependent manner. Our findings suggest that glutamatergic synapses in the spinal cord are more sensitive to botulinum toxin B than synaptic contacts between spinal motoneurons and muscle fibres.

A Cystic Mass in the Popliteal Fossa and Its Differential Diagnosis.

A Cystic Mass in the Popliteal Fossa and Its Differential Diagnosis.

Mest but Not MiR-335 Affects Skeletal Muscle Growth and Regeneration.

When skeletal muscle fibers are injured, they regenerate and grow until their sizes are adjusted to surrounding muscle fibers and other relevant organs. In this study, we examined whether Mest, one of paternally expressed imprinted genes that regulates body size during development, and miR-335 located in the second intron of the Mest gene play roles in muscle regeneration. We generated miR-335-deficient mice, and found that miR-335 is a paternally expressed imprinted microRNA. Although both Mest and miR-335 are highly expressed during muscle development and regeneration, only Mest+/- (maternal/paternal) mice show retardation of body growth. In addition to reduced body weight in Mest+/-; DMD-null mice, decreased muscle growth was observed in Mest+/- mice during cardiotoxin-induced regeneration, suggesting roles of Mest in muscle regeneration. Moreover, expressions of H19 and Igf2r, maternally expressed imprinted genes were affected in tibialis anterior muscle of Mest+/-; DMD-null mice compared to DMD-null mice. Thus, Mest likely mediates muscle regeneration through regulation of imprinted gene networks in skeletal muscle.

Assessing the microstructural response to applied deformation in porcine passive skeletal muscle

The passive micro-structural mechanical response of muscle tissue is important for numerous medical applications. However, the recently observed tension/compression asymmetry in porcine muscle remains poorly explained. In particular there remains a lack of understanding of how external tension or compression applied in the fibre or cross-fibre direction translates internally to deformation of muscle fibres and the extra-cellular matrix. Accordingly, fresh porcine skeletal muscle tissue was harvested, deformed by 30% in uniaxial tension or compression in both the fibre and cross-fibre directions and prepared for optical microscope, polarised light microscope and SEM analysis. The average deformed specimen results were compared to the average control results in each case. For compressive or tensile stretch applied in the muscle fibre direction the average measured muscle fibre cross-sectional area changes are in close correspondence with predictions based on global Poisson’s ratio measurements and these deformation modes did not cause shape changes in the muscle fibre cross-sections. However, muscle tissue reacted to the applied cross-fibre direction deformations as follows: compression flattened muscle fibre cross-sections, aligning them perpendicular to the direction of the applied deformation while tensile deformations stretched the cross-sections of muscle fibres, aligning them parallel to the direction of applied deformation. No evidence of structural reorganisation of endomysium collagen fibres in response to applied stretch was observed. The observed micro-structural responses do not appear to be influenced by the surrounding endomysium, but appear to be significantly influenced by proximity to the perimysium network. It is hypothesised that the perimysium and its interaction with the surrounding muscle fibres is therefore likely to be predominantly responsible for the tension/compression asymmetry observed in macroscopic tests of passive skeletal muscle stress strain behaviour.

Patients with chronic myosteatosis have a reduction in muscle fiber force production and disrupted myofibril architecture (1163.18)

A persistent atrophy of muscle fibers and an accumulation of fat, collectively referred to as myosteatosis, commonly occurs in patients with chronic muscle tears. The rotator cuff muscle group develops substantial myosteatosis after chronic tears, and patients with these injuries often have marked reductions in upper extremity function and quality of life. As the etiology of myosteatosis has not been well characterized in humans, our objective was to determine changes in muscle fiber structure and function in patients with chronic rotator cuff tears. We hypothesized that muscles from patients with chronic rotator cuff tears have reduced muscle fiber force production, disordered myofibrils and an accumulation of inflammatory macrophages.Compared with control muscles, there was no difference in muscle fiber cross‐sectional area, but torn supraspinatus muscles had a 30% reduction in maximum isometric force production and a 29% reduction in normalized force. Using electron microscopy and histology, disordered sarcomeres were noted, along with an accumulation of lipid‐laden macrophages in the extracellular matrix surrounding muscle fibers. The size of the tear correlated well (R2=0.49, P&lt;0.01) with reductions in force production. The results of the study indicate that patients with myosteatosis have marked reductions in muscle fiber force production, disrupted myofibril architecture and an accumulation of inflammatory macrophages in the muscle extracellular matrix. This work will help to establish future therapies to restore muscle function for patients with myosteatosis.

EGFR and Notch signaling respectively regulate proliferative activity and multiple cell lineage differentiation of Drosophila gastric stem cells

Quiescent, multipotent gastric stem cells (GSSCs) in the copper cell region of adult Drosophila midgut can produce all epithelial cell lineages found in the region, including acid-secreting copper cells, interstitial cells and enteroendocrine cells, but mechanisms controlling their quiescence and the ternary lineage differentiation are unknown. By using cell ablation or damage-induced regeneration assays combined with cell lineage tracing and genetic analysis, here we demonstrate that Delta (Dl)-expressing cells in the copper cell region are the authentic GSSCs that can self-renew and continuously regenerate the gastric epithelium after a sustained damage. Lineage tracing analysis reveals that the committed GSSC daughter with activated Notch will invariably differentiate into either a copper cell or an interstitial cell, but not the enteroendocrine cell lineage, and loss-of-function and gain-of-function studies revealed that Notch signaling is both necessary and sufficient for copper cell/interstitial cell differentiation. We also demonstrate that elevated epidermal growth factor receptor (EGFR) signaling, which is achieved by the activation of ligand Vein from the surrounding muscle cells and ligand Spitz from progenitor cells, mediates the regenerative proliferation of GSSCs following damage. Taken together, we demonstrate that Dl is a specific marker for Drosophila GSSCs, whose cell cycle status is dependent on the levels of EGFR signaling activity, and the Notch signaling has a central role in controlling cell lineage differentiation from GSSCs by separating copper/interstitial cell lineage from enteroendocrine cell lineage.

Development of biologic scaffolds for reconstructive surgery from decellularized human skeletal muscle

The development of engineered skeletal muscle tissues has recently been proposed as a potential solution for replacement of volumetric muscle losses. Experimental studies available in literature have mainly been performed in animals. The aim of the present work was to evaluate the possibility of obtaining homologous acellular scaffolds from decellularization of human skeletal muscle, also through a comparison with rats and rabbits, and evaluating the capability of muscle scaffolds to repair defects of the abdominal wall. Muscle samples of rats, rabbits and humans were treated with two different decellularization methods. Surgical tests were also performed in rabbits, implanting the decellularized scaffold in the abdominal wall of animal with surgical defects of the abdominal wall. Human skeletal muscles were sampled from body parts removed during surgery and given to the Body Donation Program of the Institute of Human Anatomy of the University of Padua. Histological stainings confirmed the effectiveness of decellularization, resulting in cell-free scaffolds with no residual cells in the matrix. The complex three-dimensional networks of collagen (azan-Mallory) and elastic fibers (Van Gieson) were maintained, in the absence of nuclear material (DAPI staining and DNA extraction/quantification). Ultrastructural analyses with transmission and scanning electron microscopy also showed the preservation of collagen and elastic fibres, together with proteoglycan components. The vascular structures in the tissue were also still visible, with preservation of collagen and elastic wall components and loss of endothelial (anti-CD31 and –CD34 immunohistochemistry) and smooth muscle (anti-alpha smooth muscle actin) cells. Scaffold implantations in rabbits gave good results in terms of integration with surrounding structures (in vivo US analyses and post mortem macro/ microscopic analyses), although recellularization by surrounding muscle cells was not satisfactory. In conclusion, not only animal (rat and rabbit) skeletal muscles but also human samples may be decellularized to obtain complex 3D scaffolds preserving tissue architecture potentially suitable for recellularization. In rabbits, these scaffolds have maintained some biomechanical properties once implanted, although spontaneous recellularization was not achieved. Further analyses will be necessary to verify the possibility of in vitro recolonization of scaffolds by homologous myoblasts and autologous satellite cells, before in vivo re-implantation.

Effects of Orexin A on Thermal Behaviour: Substantial Evidences for Thermoregulatory Role of Orexin A

Intramuscular lipomas are uncommon benign mesenchymal tumors which infiltrate skeletal muscle. It is very rarely encountered in head and neck region and often located in limbs. A consistent feature is infiltration with dissociation of the surrounding muscle fibers which makes it difficult to distinguish from well-differentiated liposarcomas. Its recurrence is very high. Imaging such as CT, MRI and ultrasonography gives valuable diagnostic information which seldom requires histopathology for diagnosing these lesions. Here, we report a case of an intramuscular lipoma of the masseter muscle in a 50-year-old male patient who presented with a growing mass in the left cheek. The radiographic imaging features are also discussed.

Tenderization effect of soy sauce on beef M. biceps femoris

This study was conducted to evaluate the tenderization effect of soy sauce on beef M. biceps femoris (BF). Five marinades were prepared with 4% (w/v) sodium chloride and 25% (w/v) soy sauce solutions (4% salt concentration) and mixed with the ratios of 100:0 (S0, pH 6.52), 75:25 (S25, 5.40) 50:50 (S50, 5.24), 25:75 (S75, 5.05), and 0:100 (S100, 4.85), respectively. The BF samples which were obtained from Hanwoo cows at 48h postmortem (n=24) were marinated with five marinades for 72h at 4°C (1:4 w/w), and the effects of soy sauce on tenderness were evaluated. Soy sauce marination resulted in a decrease in the pH value of the BF sample. However, there were no significant differences in the water holding capacity (P<0.05). The S100 treatment showed the significant (P<0.05) increase in collagen solubility and myofibrillar fragmentation index, contributing to decreased shear force compared to S0 (control). Reduction in intensity of few myofibrillar protein bands were observed for S100 treatment compared to control using SDS–PAGE. Scanning electron microscopy revealed breakdown of connective tissue surrounding muscle fibers of the S100 treatment. The tenderization effect of soy sauce may attribute various mechanisms such as increased collagen solubility or proteolysis which depend on soy sauce level in marinade.

Study of human adult parotid duct in the area of penetration through buccinator muscle and their functional relationship as a sphincter.

The adult human parotid duct is roughly 6-8 cm long. From the parotid gland, parotid duct traverses through masseter muscle, penetrates through buccinator muscle, and opens into the oral cavity. This unique form of the parotid duct is likely correlated with the function of the duct, directly affected by the movement of the buccinator muscle during mastication and swallowing. Histological structure of the duct is known to be different in each region, and details of smooth muscle present in the parotid duct are mostly unclear. In this study, we conducted SEM and histological observations of the area where the parotid duct penetrates the buccinator muscle, and an observation of smooth muscle to investigate its existence using alpha-smooth muscle antibody. We confirmed the presence of an abundance of skeletal muscle bundles likely originating from the buccinator muscle under the epithelium of the parotid duct wall in the region where it penetrates the buccinator muscle. We also observed that some of the muscle fibers were completely attached to the epithelium. We observed a lack of smooth muscle in this region of the duct wall. From these results, we suggest that the area of the duct penetrating buccinator muscle plays a role in regulating the salivary passage through the contraction of the surrounding buccinator muscle fibers.