Properties Of Muscle Cells Research Articles

Modelling the mechanoreceptor's dynamic behaviour

All sensory receptors adapt, i.e., they constantly adjust their sensitivity to external stimuli to match the current natural environment [1]. Electrophysiological responses of sensory receptors from widely different modalities seem to exhibit common features related to adaptation, and these features can be used to examine the underlying sensory transduction mechanisms [1,2]. Among the principal senses, mechanosensation remains the least understood at the cellular level [3]. To gain greater insights into mechanosensory signalling, we investigated if mechanosensation displayed adaptive dynamics that could be explained by similar biophysical mechanisms in other sensory modalities. To do this, we adapted a fly photoreceptor model [4] to describe the primary transduction process for a stretch-sensitive mechanoreceptor, taking into account the viscoelastic properties of the accessory muscle fibres [5] and the biophysical properties of known mechanosensitive channels (MSCs). The model's output is in remarkable agreement with the electrical properties of a primary ending of an isolated decapsulated spindle; ramp-and-hold stretch evokes a characteristic pattern of potential change, consisting of a large dynamic depolarization during the ramp phase and a smaller static depolarization during the hold phase [6]. The initial dynamic component is likely to be caused by both the mechanical properties of the muscle fibres and a refractory state of MSCs. Consistent with literature, the current model predicts that the dynamical component is due to a rapid stress increase during the ramp [7]. More novel predictions from the model are the mechanisms to explain the initial peak in the dynamical component. At the onset of the ramp, all MSCs are sensitive to external stimuli, but as they become refractory (clipped inactivated state), fewer MSCs are able to respond to the continuous stretch, causing a sharp decrease after the peak response. The same mechanism could contribute a faster component in 'sensory habituation' of a mechanoreceptor, in which a receptor responds more strongly to the first stimulus episode during repetitive stimulation [8].

Single muscle fibre contractile properties differ between body-builders, power athletes and control subjects.

What is the central question of this study? Do the contractile properties of single muscle fibres differ between body-builders, power athletes and control subjects? What is the main finding and its importance? Peak power normalized for muscle fibre volume in power athletes is higher than in control subjects. Compared with control subjects, maximal isometric tension (normalized for muscle fibre cross-sectional area) is lower in body-builders. Although this difference may be caused in part by an apparent negative effect of hypertrophy, these results indicate that the training history of power athletes may increase muscle fibre quality, whereas body-building may be detrimental. We compared muscle fibre contractile properties of biopsies taken from the vastus lateralis of 12 body-builders (BBs; low- to moderate-intensity high-volume resistance training), six power athletes (PAs; high-intensity, low-volume combined with aerobic training) and 14 control subjects (Cs). Maximal isotonic contractions were performed in single muscle fibres, typed with SDS-PAGE. Fibre cross-sectional area was 67 and 88% (P<0.01) larger in BBs than in PAs and Cs, respectively, with no significant difference in fibre cross-sectional area between PAs and Cs. Fibres of BBs and PAs developed a higher maximal isometric tension (32 and 50%, respectively, P<0.01) than those of Cs. The specific tension of BB fibres was 62 and 41% lower than that of PA and C fibres (P<0.05), respectively. Irrespective of fibre type, the peak power (PP) of PA fibres was 58% higher than that of BB fibres (P<0.05), whereas BB fibres, despite considerable hypertrophy, had similar PP to the C fibres. This work suggests that high-intensity, low-volume resistance training with aerobic exercise improves PP, while low- to moderate-intensity high-volume resistance training does not affect PP and results in a reduction in specific tension. We postulate that the decrease in specific tension is caused by differences in myofibrillar density and/or post-translational modifications of contractile proteins.

Mitochondria-targeted antioxidant preserves contractile properties and mitochondrial function of skeletal muscle in aged rats.

Mitochondrial dysfunction plays a central role in the pathogenesis of sarcopenia associated with a loss of mass and activity of skeletal muscle. In addition to energy deprivation, increased mitochondrial ROS damage proteins and lipids in aged skeletal muscle. Therefore, prevention of mitochondrial ROS is important for potential therapeutic strategies to delay sarcopenia. This study elucidates the pharmacological efficiency of the new developed mitochondria-targeted ROS and electron scavenger, XJB-5-131 (XJB) to restore muscle contractility and mitochondrial function in aged skeletal muscle. Male adult (5-month old) and aged (29-month old) Fischer Brown Norway (F344/BN) rats were treated with XJB for four weeks and contractile properties of single skeletal muscle fibres and activity of mitochondrial ETC complexes were determined at the end of the treatment period. XJB-treated old rats showed higher muscle contractility associated with prevention of protein oxidation in both muscle homogenate and mitochondria compared with untreated counterparts. XJB-treated animals demonstrated a high activity of the respiratory complexes I, III, and IV with no changes in citrate synthase activity. These data demonstrate that mitochondrial ROS play a causal role in muscle weakness, and that a ROS scavenger specifically targeted to mitochondria can reverse age-related alterations of mitochondrial function and improve contractile properties in skeletal muscle.

Intracellular Ca(2+)-handling differs markedly between intact human muscle fibers and myotubes.

BackgroundIn skeletal muscle, intracellular Ca2+ is an important regulator of contraction as well as gene expression and metabolic processes. Because of the difficulties to obtain intact human muscle fibers, human myotubes have been extensively employed for studies of Ca2+-dependent processes in human adult muscle. Despite this, it is unknown whether the Ca2+-handling properties of myotubes adequately represent those of adult muscle fibers.MethodsTo enable a comparison of the Ca2+-handling properties of human muscle fibers and myotubes, we developed a model of dissected intact single muscle fibers obtained from human intercostal muscle biopsies. The intracellular Ca2+-handling of human muscle fibers was compared with that of myotubes generated by the differentiation of primary human myoblasts obtained from vastus lateralis muscle biopsies.ResultsThe intact single muscle fibers all demonstrated strictly regulated cytosolic free [Ca2+] ([Ca2+]i) transients and force production upon electrical stimulation. In contrast, despite a more mature Ca2+-handling in myotubes than in myoblasts, myotubes lacked fundamental aspects of adult Ca2+-handling and did not contract. These functional differences were explained by discrepancies in the quantity and localization of Ca2+-handling proteins, as well as ultrastructural differences between muscle fibers and myotubes.ConclusionsIntact single muscle fibers that display strictly regulated [Ca2+]i transients and force production upon electrical stimulation can be obtained from human intercostal muscle biopsies. In contrast, human myotubes lack important aspects of adult Ca2+-handling and are thus an inappropriate model for human adult muscle when studying Ca2+-dependent processes, such as gene expression and metabolic processes.Electronic supplementary materialThe online version of this article (doi:10.1186/s13395-015-0050-x) contains supplementary material, which is available to authorized users.

Scientific Discoveries: What Is Required for Lasting Impact.

I have been involved in two scientific discoveries of some impact. One is the discovery of long-term potentiation (LTP), the phenomenon that brief, high-frequency impulse activity at synapses in the brain can lead to long-lasting increases in their efficiency of transmission. This finding demonstrated that synapses are plastic, a property thought to be necessary for learning and memory. The other discovery is that nerve-evoked muscle impulse activity, rather than putative trophic factors, controls the properties of muscle fibers. Here I describe how these two discoveries were made, the unexpected difficulties of reproducing the first discovery, and the controversies that followed the second discovery. I discuss why the first discovery took many years to become generally recognized, whereas the second caused an immediate sensation and entered textbooks and major reviews but is now largely forgotten. In the long run, discovering a new phenomenon has greater impact than falsifying a popular hypothesis.

Inappropriate interpretation of surface EMG signals and muscle fiber characteristics impedes understanding of the control of neuromuscular function

as the final common pathway from the nervous system to muscle, the motor unit transmits an activation signal generated by the nervous system to engage the contractile proteins and produce the muscle forces needed for reflex responses, automatic behaviors, and voluntary actions ([11][1]). The net

Modelling the mechanoreceptor's dynamic behaviour

All sensory receptors adapt, i.e. they constantly adjust their sensitivity to external stimuli to match the current demands of the natural environment. Electrophysiological responses of sensory receptors from widely different modalities seem to exhibit common features related to adaptation, and these features can be used to examine the underlying sensory transduction mechanisms. Among the principal senses, mechanosensation remains the least understood at the cellular level. To gain greater insights into mechanosensory signalling, we investigated if mechanosensation displayed adaptive dynamics that could be explained by similar biophysical mechanisms in other sensory modalities. To do this, we adapted a fly photoreceptor model to describe the primary transduction process for a stretch-sensitive mechanoreceptor, taking into account the viscoelastic properties of the accessory muscle fibres and the biophysical properties of known mechanosensitive channels (MSCs). The model’s output is in remarkable agreement with the electrical properties of a primary ending in an isolated decapsulated spindle; ramp-and-hold stretch evokes a characteristic pattern of potential change, consisting of a large dynamic depolarization during the ramp phase and a smaller static depolarization during the hold phase. The initial dynamic component is likely to be caused by a combination of the mechanical properties of the muscle fibres and a refractory state in the MSCs. Consistent with the literature, the current model predicts that the dynamic component is due to a rapid stress increase during the ramp. More novel predictions from the model are the mechanisms to explain the initial peak in the dynamic component. At the onset of the ramp, all MSCs are sensitive to external stimuli, but as they become refractory (inactivated), fewer MSCs are able to respond to the continuous stretch, causing a sharp decrease after the peak response. The same mechanism could contribute a faster component in the ‘sensory habituation’ of mechanoreceptors, in which a receptor responds more strongly to the first stimulus episode during repetitive stimulation.

Forgotten research from 19th century: science should not follow fashion.

The fine structure of cross-striated muscle and its changes during contraction were known already in considerable detail in the 19th century. This knowledge was the result of studying birefringence properties of muscle fibres under the polarization microscope, a method mainly established by Brücke (Denk Kais Akad Wiss Math Naturwiss Cl 15:69–84, 1858) in Vienna, Austria. The knowledge was seemingly forgotten in the first half of the 20th century before it was rediscovered in 1954. This rediscovery was essential for the formulation of the sliding filament theory which represents the commonly accepted concept of muscle contraction (A.F. Huxley and Niedergerke, Nature 173:971–973, 1954; H.E. Huxley and Hanson, Nature 173:973–976, 1954). The loss of knowledge was the result of prevailing views within the scientific community which could be attributed to “fashion”: it was thought that the changes of cross-striations, which were observed under the microscope, were inconsequential for contraction since other types of movements like cell crawling and smooth muscle contraction were not associated with similar changes of the fine structure. The basis for this assumption was the view that all types of movements associated with life must be caused by the same mechanisms. Furthermore, it was assumed that the light microscopy was of little use, because the individual molecules that carry out life functions cannot be seen under the light microscope. This unfortunate episode of science history teaches us that the progress of science can severely be retarded by fashion.

The effect of housing conditions on Biceps femoris muscle fibre properties, fatty acid composition, performance and carcass traits of slow-growing rabbits

The aim of the present work was to evaluate the effect of stocking density on the biceps femoris (BF) muscle fibre properties, meat quality, the growth performance and carcass traits of Czech White rabbits. A total of 20 rabbits (40 days old, 10 rabbits per treatment, sex ratio 1/1) were reared in cages at different stocking densities (10 rabbits/m2 or 4 rabbits/m2) for 49 days. Stocking density had no significant effect on the growth performance. There were no significant differences between groups with regard to hot carcass weight (HCW) or dressing-out percentage. The proportions of both perirenal (9.5 vs. 15.9 g/kg HCW; P=0.010) and total dissectible fat (14.9 vs. 25.1 g/kg HCW; P=0.001) were lower in rabbits reared at the lower stocking density. No significant differences in ultimate pH values, meat colour or proximate composition were observed. The hind leg meat of rabbits reared at the lower stocking density contained significantly less lauric (4.6 vs. 6.7 mg/100 g of muscle; P=0.008) and myristic acid (52.2 vs. 64.4 mg/100 g of muscle; P=0.033). Significantly higher percentages of βR fibres (16.3 vs. 6.5 %, P=0.001) and αR fibres (24.5 vs. 14.2 %; P=0.001) and a significantly lower percentage of αW fibres (59.2 vs. 79.3 %; P=0.001) were also observed in these rabbits. The mean cross-sectional area (1882 vs. 2744 μm2; P=0.001) and diameter (47.9 vs. 58.5 μm; P=0.001) of βR fibres were smaller in rabbits reared at the lower stocking density. Thus, the lower stocking density favourably affected the medium-chain fatty acid profile of meat and fibre characteristics of the rabbits' biceps femoris muscle.

The Response of Denervated Muscle to Long-Term Stimulation (1985, Revisited here in 2014).

In 1985, at a meeting in Abano, I presented results showing that direct stimulation of skeletal muscles with appropriate stimulus patterns prevents the effects of denervation on non-junctional properties of muscle fibers. Hence, it appeared unnecessary to postulate that unknown nerve-derived trophic factors control such properties, as posited by the (anterograde) neurotrophic hypothesis. Here I discuss this conclusion in the light of what we know today, particularly with respect to the many lines of evidence that were then taken to support the trophic hypothesis, but which today have alternative interpretations consistent with control by evoked impulse activity. Despite much effort, no one has yet identified any nerve-derived factor consistent with the neurotrophic hypothesis. Reports favoring the existence of neurotrophic factors were numerous before 2000. Now they have essentially disappeared from the literature, including original research papers, textbooks and handbooks, suggesting that the hypothesis is no longer arguable. Thus, the results that I presented in our paper in 1985 seem to have held up rather well.

Thixotropy of Muscle Fibers Probed with Sinusoidal Oscillations

Mechanical properties of individual muscle fibers from rabbit psoas were probed by applying sinusoidal length changes at one end of the fiber and measuring the resulting force at the other end. At frequencies above 1 Hz, this oscillation resulted in a history-dependent reduction in muscle fiber stiffness in activated muscle fibers. Such a reduction in muscle stiffness in response to force is referred to as thixotropy. Perturbing the actin-myosin interaction by treatment with EDTA and blebbistatin caused this effect to disappear, suggesting that this thixotropy results from cross-bridge interactions. At frequencies less than 1 Hz, oscillation resulted in a history-dependent increase in muscle fiber stiffness in activated fibers. Disruption of actin-myosin interactions has no effect on this negative thixotropy, suggesting a different mechanism is at play.

Effects of Exercise on Fiber Properties in the Denervated Rodent Diaphragm

In a unilaterally denervated diaphragm, atrophy of fast-twitch glycolytic (FG) fibers, but not of fast-twitch oxidative glycolytic (FOG) or slow-twitch oxidative (SO) fibers, occurs. The inhibition of atrophy in FOG and SO fibers may be due to the effects of stretch stimuli caused by respiratory contraction of the contralateral diaphragm. We examined the effects of exercise (treadmill running) on the histochemical and biochemical properties of muscle fibers of the costal diaphragm in three groups. Eighteen rats were distributed in (i) a denervation + treadmill running (Dn ex) group, (ii) a denervation (Dn) group, and (iii) a control (Ct) group. After 4 weeks of running, we measured the expression of myosin heavy chain (MHC) isoforms and cross-sectional area of the diaphragm muscle. The expression of MHC 1 and MHC 2a increased 4 weeks after denervation. In contrast, the expression of MHC 2d decreased significantly. After 4 weeks of running, the cross-sectional area of FG fibers increased significantly (85.5%; P < 0.05) compared with that in the Dn group. We suggest that exercise enhances the morphological properties and myosin heavy chain isoforms of the denervated diaphragm. This exercise-mediated adaptation may be associated with the improvement of FG fibers in the denervated diaphragm.

Heterogeneity of Viscoelastic Properties of Myocardial Muscle Fiber: Mathematical Model

Mathematical model describing the processes of mechanical stress development in response to strain of heterogeneous muscle fiber is created. The numerical algorithm to calculate viscoelastic properties of muscle fiber of arbitrary length is developed. In numerical experiments by the model it is shown that the local heterogeneity of geometrical and mechanical parameters of structural units of the model significantly influences in resulting mechanical response of whole fiber. Also it is established the close connection between parameters of mechanical and geometrical heterogeneity compensating each other. It is supposed that the mechanism may modulate the myocardial remodeling under changing load.

Expression of the Embryonic Cav1.1 Splice Variant in Adult Mice Alters Excitation-Contraction Coupling but Does not Cause Dystrophic Myotonia

CaV1.1e is the calcium channel splice variant of embryonic skeletal muscle. It functions as voltage sensor in EC coupling, but in contrast to the adult CaV1.1a variant it also supports sizeable calcium currents activating at the same membrane potential as SR calcium release. Mis-splicing of CaV1.1 results in elevated levels of the CaV1.1e variant in mature muscle that correlate with the severity of muscle weakness in patients suffering from dystrophic myotonia. Therefore we hypothesize that exclusive expression of CaV1.1e in exon 29 knockout mice will cause muscle weakness. In muscles of wildtype mice expression of CaV1.1e declines after birth. However, two weeks after sciatic nerve resection CaV1.1e transcript levels are upregulated in paralyzed muscles, indicative of an activity-dependent regulation of CaV1.1e splicing. Quantitative RT-PCR analysis demonstrates that exon 29 knockouts express exclusively the CaV1.1e splice variant at levels comparable to total CaV1.1 in wildtype muscle. Combined voltage clamp and fluorescence calcium recordings of isolated muscle fibers from exon 29 knockout mice revealed a substantial influx-dependent component of the calcium transient. This not only alters myoplasmic calcium handling, but is further expected to prolong the muscle action potential and consequently reduce the tetanic fusion frequency. Surprisingly, these severe alterations of the muscle fiber properties were not accompanied by a dystrophic myotonia phenotype in knockout mice. A battery of behavioral tests (home-cage activity, voluntary and forced running, grip strength and rotarod tests) revealed no signs of muscle weakness or altered motor activity compared to wildtype siblings. Thus, development of dystrophic myotonia may require the combinatorial action of several mis-spliced genes. Alternatively, strong compensatory mechanisms may cause the absence of the disease phenotype in exon 29 knockout mice. Support: FWF P23479, W1101, OTKA-NN107765, TAMOP-4.2.2./B.-10/1-2010-0024.

Histological characteristics of the musculus longissimus lumborum et thoracis muscle fibres in pigs in relation to selected RYR1, MYOG, MYOD1 and MYF6 genotypes

Histochemical and biochemical muscle fibre properties are the factors that influence the quantitative and qualitative characteristics of pork meat. The aim of the study was to assess the influence of genetic effects of selected genetic markers MyoD genes and RYR1 on the achieved indicators of muscle fibres in the musculus longissimus lumborum et thoracis (MLLT). The study included a total number of 216 hybrid pigs with the mean slaughter weight of 123 kg. Gene polymorphism was determined by the PCR-RFLP method. The gene polymorphism was determined in the RYR1, MYOD1, MYOG, and MYF6 genes. Muscle fibre types from MLLT were identified. Concerning the RYR1 gene, the study found that homozygous-dominant animals reached a lower number of type I (8.35 vs. 10.52; P &lt; 0.05) and a higher number of IIA (3.66 vs. 2.10; P &lt; 0.05) and a higher number of IIB (76.61 vs. 67.91; P &lt; 0.05). The maximum number in all types of muscle fibres reached BB genotype of the MYOG gene (type I: 14.02; IIA: 18.47; IIB: 83.08; P &lt; 0.05). The AA genotype of the MYOD1 gene showed the lowest (P &lt; 0.05) number of muscle in all fibre types (type I: 9.20; IIA: 0.85; IIB: 69.23). The influence of individual genotypes of selected genes on the selected muscle fibre characteristics was proven. The obtained results confirm the possibility of affecting the quality of pork with genomic selection of MyoD genes family.

The passive properties of muscle fibers are velocity dependent

The passive properties of skeletal muscle play an important role in muscle function. While the passive quasi-static elastic properties of muscle fibers have been well characterized, the dynamic visco-elastic passive behavior of fibers has garnered less attention. In particular, it is unclear how the visco-elastic properties are influenced by lengthening velocity, in particular for the range of physiologically relevant velocities. The goals of this work were to: (i) measure the effects of lengthening velocity on the peak stresses within single muscle fibers to determine how passive behavior changes over a range of physiologically relevant lengthening rates (0.1–10Lo/s), and (ii) develop a mathematical model of fiber viscoelasticity based on these measurements. We found that passive properties depend on strain rate, in particular at the low loading rates (0.1–3Lo/s), and that the measured behavior can be predicted across a range of loading rates and time histories with a quasi-linear viscoelastic model. In the future, these results can be used to determine the impact of viscoelastic behavior on intramuscular stresses and forces during a variety of dynamic movements.

Mechanical properties of respiratory muscles.

Striated respiratory muscles are necessary for lung ventilation and to maintain the patency of the upper airway. The basic structural and functional properties of respiratory muscles are similar to those of other striated muscles (both skeletal and cardiac). The sarcomere is the fundamental organizational unit of striated muscles and sarcomeric proteins underlie the passive and active mechanical properties of muscle fibers. In this respect, the functional categorization of different fiber types provides a conceptual framework to understand the physiological properties of respiratory muscles. Within the sarcomere, the interaction between the thick and thin filaments at the level of cross-bridges provides the elementary unit of force generation and contraction. Key to an understanding of the unique functional differences across muscle fiber types are differences in cross-bridge recruitment and cycling that relate to the expression of different myosin heavy chain isoforms in the thick filament. The active mechanical properties of muscle fibers are characterized by the relationship between myoplasmic Ca2+ and cross-bridge recruitment, force generation and sarcomere length (also cross-bridge recruitment), external load and shortening velocity (cross-bridge cycling rate), and cross-bridge cycling rate and ATP consumption. Passive mechanical properties are also important reflecting viscoelastic elements within sarcomeres as well as the extracellular matrix. Conditions that affect respiratory muscle performance may have a range of underlying pathophysiological causes, but their manifestations will depend on their impact on these basic elemental structures.

Time course of diaphragm function recovery after controlled mechanical ventilation in rats

Controlled mechanical ventilation (CMV) is known to result in rapid and severe diaphragmatic dysfunction, but the recovery response of the diaphragm to normal function after CMV is unknown. Therefore, we examined the time course of diaphragm function recovery in an animal model of CMV. Healthy rats were submitted to CMV for 24-27 h (n = 16), or to 24-h CMV followed by either 1 h (CMV + 1 h SB, n = 9), 2 h (CMV + 2 h SB, n = 9), 3 h (CMV + 3 h SB, n = 9), or 4-7 h (CMV + 4-7 h SB, n = 9) of spontaneous breathing (SB). At the end of the experiment, the diaphragm muscle was excised for functional and biochemical analysis. The in vitro diaphragm force was significantly improved in the CMV + 3 h SB and CMV + 4-7 h SB groups compared with CMV (maximal tetanic force: +27%, P < 0.05, and +59%, P < 0.001, respectively). This was associated with an increase in the type IIx/b fiber dimensions (P < 0.05). Neutrophil influx was increased in the CMV + 4-7 h SB group (P < 0.05), while macrophage numbers remained unchanged. Markers of protein synthesis (phosphorylated Akt and eukaryotic initiation factor 4E binding protein 1) were significantly increased (±40%, P < 0.001, and ±52%, P < 0.01, respectively) in the CMV + 3 h SB and CMV + 4-7 h SB groups and were positively correlated with diaphragm force (P < 0.05). Finally, also the maximal specific force generation of skinned single diaphragm fibers was increased in the CMV + 4-7 h SB group compared with CMV (+45%, P < 0.05). In rats, reloading the diaphragm for 3 h after CMV is sufficient to improve diaphragm function, while complete recovery occurs after longer periods of reloading. Enhanced muscle fiber dimensions, increased protein synthesis, and improved intrinsic contractile properties of diaphragm muscle fibers may have contributed to diaphragm function recovery.

Aging-associated exacerbation in fatty degeneration and infiltration after rotator cuff tear

Rotator cuff tears are one of the most common musculoskeletal complaints and a substantial source of morbidity in elderly patients. Chronic cuff tears are associated with muscle atrophy and an infiltration of fat to the area, a condition known as "fatty degeneration." To improve the treatment of cuff tears in elderly patients, a greater understanding of the changes in the contractile properties of muscle fibers and the molecular regulation of fatty degeneration is essential. Using a full-thickness, massive supraspinatus and infraspinatus tear model in elderly rats, we measured fiber contractility and determined changes in fiber type distribution that develop 30 days after tear. We also measured the expression of messenger RNA and micro-RNA transcripts involved in muscle atrophy, lipid accumulation, and matrix synthesis. We hypothesized that a decrease in specific force of muscle fibers, an accumulation of type IIb fibers, and an upregulation in atrophic, fibrogenic, and inflammatory gene expression would occur in torn cuff muscles. Thirty days after the tear, we observed a reduction in muscle fiber force and an induction of RNA molecules that regulate atrophy, fibrosis, lipid accumulation, inflammation, and macrophage recruitment. A marked accumulation of advanced glycation end products and a significant accretion of macrophages in areas of fat accumulation were observed. The extent of degenerative changes in old rats was greater than that observed in adults. In addition, we identified that the ectopic fat accumulation that occurs in chronic cuff tears does not occur by activation of canonical intramyocellular lipid storage and synthesis pathways.

SP0090 Steroid myopathy - do molecular mechanisms bring us closer to novel treatment strategies?

Introduction of glucocorticoids in the treatment of inflammatory myopathies and other inflammatory conditions in the 1950s had a major impact on survival and morbidity. However, it was already early recognized...