SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
The peptide map obtained by electrophoresis after digestion of purified myosin heavy chains from pectoralis muscle of embryonic chicken with the Staphylococcus aureus V8 protease, produces a peptide pattern very similar but not identical to that of adult fast myosin. In fact, some components that are present in a small amount in the map of slow adult myosin are visible in the embryonic pattern.
An analysis of the physiology, morphology, and position of endplates on identified fibers in the Xenopus laevis pectoralis muscle has revealed the following. 1. The percentage of fibers with one endplate is lower in large muscles, and within the same muscle, singly innervated fibers are smaller than dually innervated fibers. 2. Single junctions tend to be stronger than junctions on dually innervated fibers. 3. Single junctions typically are located near the middle of their fibers, while the endplates on dually innervated fibers are located toward either end and usually are separated by at least 20% of the total fiber length. A significant proportion of dually innervated fibers appears to be innervated by the same axon at both junctions. 4. Junctions on the same dually innervated fiber tend to be more similar in length than do junctions on different fibers of the same input resistance. This observation is the same whether both junctions on a given fiber are formed by the same or different axons. There is no corresponding tendency for greater similarity in physiological strength of paired junctions, which frequently show large differences in endplate potential amplitude. 5. The total terminal length on dually innervated fibers of equivalent input resistance is inversely correlated with the mean release per unit length and total release of both junctions. There is no apparent correlation between the distance separating endplates and their strength or length. The data support a model of synaptic regulation in which nerve terminals are attracted, grow, and are maintained in proportion to the amount of a substance supplied by muscle fibers. Our findings suggest that such a substance is produced or distributed uniformly throughout each fiber in amounts proportional to the fiber size and inversely proportional to the total transmitter output of all junctions innervating the fiber. A form of competitive interaction between the terminals which helps to determine synaptic spacing may involve local depletion or inactivation of this substance.
Torn pectoralis major muscles are either treated acutely by orthopedic surgeons or, if neglected, result in deformities of the pectoralis muscle. These deformities are visible, with pectoralis muscle asymmetry, especially on muscle contraction. Bodybuilders prone to this injury accentuate the asymmetry by contracting the pectoralis muscles together. Late repair is not usually possible, and cosmetic improvement relies on removing the bulging, unattached muscles or camouflaging the underlying exposed ribs with a customized implant. Similar customized implants are used to repair pectus excavatum. Techniques must take into consideration the desire for accentuation of the pectoralis muscle with minimal visible scarring. The surgeon and the anesthesiologist should be aware of the possibility of anabolic steroid ingestion in the male body-builder.
Ventricular-like and fast myosin heavy chains (VL-MHC and FMHC) are transiently expressed during slow skeletal muscle development. The influence of innervation on repression of these MHC isoforms is investigated over an 84-day time course in: (1) normal anterior latissimus dorsi (N-ALD) muscles, (2) regenerating ALD (R-ALD) muscles, (3) denervated ALD (D-ALD) muscles, and (4) regenerating and denervated ALD (RD-ALD) muscles. Western blotting demonstrates that the VL-MHC is expressed in R-, D-, and RD-ALD muscles, but not in N-ALD muscles. Expression of the VL-MHC is transient in R-ALD muscles. In contrast, VL-MHC expression persists in RD-ALD muscles, and appears with time in D-ALD muscles. FMHC was not detected in N-ALD muscles by Western blotting. Two FMHCs are seen in R-ALD and RD-ALD muscles, and in 13-day embryonic ALD muscles. The slower migrating FMHC (FMHCA) comigrates with developmentally regulated FMHCs in fast pectoralis muscle, while the faster migrating FMHC (FMHCB) comigrates with the faster migrating FMHC in embryonic ALD muscle (13 days in ovo). FMHCB decreases in amount over the time course in R-ALD muscles, while FMHCA persists. In contrast, substantial levels of both FMHCs persist in RD-ALD muscles, and appear with time in D-ALD muscles. The cellular distribution of MHCs is followed by immunocytochemistry. Regenerating cells expressing VL-MHC and FMHC are replaced by a mature population in R-ALD muscles. Some of the mature myofibers in R-ALD muscles express FMHC, but not VL-MHC. In RD-ALD and D-ALD muscles, both regenerating and mature muscle cells are seen which express VL-MHC and FMHC. Our results indicate that innervation is required for the repression of VL-MHC and FMHCB during regeneration of slow muscle.
Two molecular recombinants (EU-8 and K-3) constructed from ring-necked pheasant virus and UR2AV, the helper virus associated with avian sarcoma virus UR2, caused a high incidence of a hitherto unreported pathological condition in chick skeletal muscle. A disease spectrum was observed in which muscle was infiltrated by proliferating fibroblasts and caused white streaks, white diffuse areas, or well-defined elongated tumors. Fibroblast proliferation was progressive, and the gross presentation depended on the rapidity and extent of proliferation. There was evidence of anaplasia but not frankly malignant disease or metastases. The disease was produced at a high frequency when 10-day-old embryos were infected. Breast muscle (pectoralis major and minor) was affected with variable severity in all birds, thigh muscles were affected occasionally, while other thoracic, external abdominal, and wing muscles were affected very rarely. Progression of proliferative muscle lesions was demonstrated by sequential necropsies and microscopic examination of muscle samples. The disease appeared before 2 weeks of age, and thin white streaks with minimal cellular proliferation were the earliest lesions observed. Elongated, spindle-shaped tumors were the most advanced form of proliferation observed. The advanced lesions showed cellular anaplasia and signs of rapid growth, and appeared most commonly at 6 weeks of age or later. Histologically, mild proliferation correlated with normal appearing fibroblasts producing collagen. Severe proliferation correlated with anaplastic, rapidly dividing cells producing little collagen and a high mitotic index. A decrease in the virus dose resulted in less severe fibromatosis, but at least one chicken infected with a low virus dose showed severe disease. When 10- or 35-day-old hatched chicks were injected in the breast muscle with EU-8 or K-3, a low incidence of lymphoid leukosis was observed, but no fibromatosis resulted during an observation period of 27 weeks. Infectious virus was extracted from the fibromatosis in the breast muscle, and extracted virus caused the same disease when injected in 10-day-old embryos. No transforming activity was observed on normal chick embryo fibroblast monolayers. Cell cultures were established from areas in the breast muscle affected by fibromatosis, and from discrete tumors. These cells did not show any signs of transformation in culture. Supernatants obtained from these cell cultures caused fibromatosis when injected into 10-day-old embryos, but did not transform normal chick embryo fibroblasts.
Effects of embryonic imprinting with growth hormone (GH) on growth and myosin heavy chain (MyHC) isoforms in pectoralis muscle were determined by injecting turkey embryos with ovine growth hormone (oGH) at a dose of 10 micrograms three times a day. Injections were made on days 20 and 26 (Treatment 1), days 14 and 20 (Treatment 2) or days 14 and 26 (Treatment 3) of incubation. In Treatment 1 poults, plasma GH concentrations were elevated at 3 days posthatch and in Treatment 3 poults, plasma GH concentrations were elevated at 15 days posthatch, as compared to control poults. At 4 weeks of age, in males, body weights, shank length and weights of pectoralis, gastrocnemius and sartorius muscles were increased in Treatment 3, and in females, body weights, shank length and weights of gastrocnemius muscle of female turkeys were increased in Treatment 1. The growth rate of female turkeys from 4 weeks through 16 weeks was increased by Treatment 1. Treatment 1 resulted in a delay in the transition from the embryonic MyHC isoform to the neonatal MyHC isoform and to the adult MyHC isoform. Treatment 3 induced an earlier appearance of the adult MyHC isoform. No effects on body and muscle growth and MyHC isoforms were observed by Treatment 2.
As a postural behavior, gliding and soaring flight in birds requires less energy than flapping flight. Slow tonic and slow twitch muscle fibers are specialized for sustained contraction with high fatigue resistance and are typically found in muscles associated with posture. Albatrosses are the elite of avian gliders; as such, we wanted to learn how their musculoskeletal system enables them to maintain spread-wing posture for prolonged gliding bouts. We used dissection and immunohistochemistry to evaluate muscle function for gliding flight in Laysan and Black-footed albatrosses. Albatrosses possess a locking mechanism at the shoulder composed of a tendinous sheet that extends from origin to insertion throughout the length of the deep layer of the pectoralis muscle. This fascial "strut" passively maintains horizontal wing orientation during gliding and soaring flight. A number of muscles, which likely facilitate gliding posture, are composed exclusively of slow fibers. These include Mm. coracobrachialis cranialis, extensor metacarpi radialis dorsalis, and deep pectoralis. In addition, a number of other muscles, including triceps scapularis, triceps humeralis, supracoracoideus, and extensor metacarpi radialis ventralis, were found to have populations of slow fibers. We believe that this extensive suite of uniformly slow muscles is associated with sustained gliding and is unique to birds that glide and soar for extended periods. These findings suggest that albatrosses utilize a combination of slow muscle fibers and a rigid limiting tendon for maintaining a prolonged, gliding posture.
Wound healing is the response of tissue to injury that results in scar formation. Tissue regeneration would be a more ideal response. Previously, we have isolated a population of cells from avian, rodent, and rabbit skeletal muscle capable of differentiating into multiple mesodermal phenotypes. The present experiments were designed to determine whether a similar population of cells exist in human skeletal muscle. Separate cell preparations from skeletal muscle on an amputated leg of a 75-year-old female and the pectoralis muscle of a 27-year-old male were enzymatically dissociated and cultured to confluence in Eagle's minimal essential medium with 10 per cent preselected horse serum, then trypsinized, filtered, and slowly frozen in 7.5 per cent dimethylsulfoxide to -80 degrees C. The cells were thawed and plated with the same media plus dexamethasone (a nonspecific differentiation agent) at 10(-10) - 10(-6) M concentrations for up to 6 weeks. Immunological and histochemical staining assays were performed. Phenotypes observed included stem cells with typical stellate morphology (control), skeletal myotubes (anti-myosin), smooth muscle (anti-a-actin), bone (von Kossa stain), cartilage (Alcec blue), and fat (Sudan black B). These experiments establish the existence of a population of mesenchymal stem cells in human skeletal muscle capable of differentiating into multiple mesodermal phenotypes. The possibility exists of manipulating the mesenchymal stem cells to achieve appropriate regeneration of mesenchymal tissues in the injured patient.
Phosphorus-31 nuclear magnetic resonance (31P-NMR) analysis was performed on normal (line 412) and dystrophic (line 413) superficial pectoralis muscles excised from chickens between 15 and 116 days after hatching. An apparent alteration in dystrophic muscle energy metabolism was abolished by pretreatment with curare and was attributed to muscle hyperexcitability. Time-dependent 31P-NMR studies demonstrated no apparent difference in the overall tissue adenosine triphosphatase (ATPase) activity of dystrophic as compared to normal muscle. After 55 days of age, a resonance signal attributed to serine ethanolamine phosphodiester (SEPDE) was observed only in dystrophic muscle. Adding the paramagnetic cation Mn2+ to the buffer surrounding the muscle resulted in an approximate 80% decrement in the dystrophic SEPDE signal without apparent alteration of the other phosphatic signals in either the normal or dystrophic muscle. This would argue against any generalized membrane defect in dystrophic chicken muscle and suggest that SEPDE is in a compartment accessible to Mn2+.
The influence of the Ca2+ ionophores, ionomycin and A23187 upon the incorporation of [35S]methionine into proteins of cultured chicken pectoralis muscle was studied during differentiation of myoblasts into multinucleated myotubes. Fusion was reversibly arrested by growing cells in low-calcium media from the time of plating. Exposure of normal and fusion blocked cultures to 10-6-10-5 M ionomycin or A23187 for 2-6 h on the second to fourth day of growth, resulted in a selective increase in the incorporation of [35S]methionine into two proteins of about 100 000 and 80 000 dalton. When 10-5 M ionomycin or A23187 were added to older cultures, all large myotubes contracted and detached from the plate. Only the adhering myoblasts and small myotubes incorporated [35s[methionine into the muscle proteins and showed increased incorporation of label into 100 000 and 80 000 proteins. After ionophore pulse, the adhering cells retained the ability to differentiate and accumulate myosin. The effect of Ca2+ ionophores upon the rate of protein synthesis is presumably related to increased influx of extracellular Ca2+ with a rise in the Ca2+ concentration of the cytoplasm. We conclude that Ca2+ sensitive mechanisms may regulate the synthesis of a select group of muscle proteins.
An avian uncoupling protein (UCP) gene homolog was recently sequenced from skeletal muscle and was proposed to have a role in thermogenesis in chickens, ducks and hummingbirds. Since mammalian UCP 2 and UCP 3 also appear to have functions associated with energy and substrate partitioning and body weight regulation, the purpose of this study was to further characterize chicken UCP under conditions of nutritional stress and/or leptin administration. Male 3-week-old chickens were starved for 24 or 48 h and then half of each group was refed for an additional 24 h. In a follow-up experiment, chickens were fed or starved for 48 h with or without leptin administration. Feed deprivation increased UCP mRNA expression in skeletal muscle by up to 260% (P<0.001), and in a time-dependent manner in pectoralis muscle. Refeeding for 24 h normalized muscle UCP mRNA levels. Leptin administration had no effect on muscle UCP. Chicken muscle UCP mRNA levels were highly correlated with plasma triglyceride and non-esterified fatty acid (NEFA) concentrations, and with circulating levels of insulin, insulin-like growth factor (IGF)-I and IGF-II. These results suggest that, as in mammals, avian UCP is up-regulated during feed deprivation and is highly correlated with increased fatty acid oxidation and flux into skeletal muscle.
The electron microscopic study shows that in 10 days chick embryo parenchymal elements of the gastrocnemius and pectoralis muscles are myotubes with sparse mitochondria, and that they do not differ morphologically. Up to the 18th day in ovo muscle fibers in the future oxidative muscle grow up faster than those in the future glycolytic one. There is no relation between the mitochondrial density and distribution within sarcoplasm and the capillary location but they are in good correlation with the myofibrillar parameters. As muscle fibers mature the energy delivery of myofibrils (mitochondria-to-myofibrils volume density ratio) increases due to mitochondrial density rather than their size.
Skeletal muscles in developing chick embryos were tested for responsiveness to adenosine 5'-triphosphate (ATP), a substance known to depolarize chick skeletal muscle in culture. The sensitivity to extracellular ATP was tested at various stages of development in five different muscles; pectoralis superficia, anterior latissimus dorsi, posterior latissimus dorsi, sartorious, and gastrocnemius. At the earliest time that muscles were tested (Embryonic Day 6, stage 30 of Hamburger and Hamilton, 1951) application of ATP(50-100 microM) elicited vigorous contractions in all five muscles, but within a few days (Embryonic Day 17, stage 43) none of the muscles contracted in response to ATP. Sensitivity declined at approximately the same time in all five of these muscles. Intracellular recordings made from muscle fibers near the time of hatching (Embryonic Days 18-21 or Postnatal Days 1-2) indicated that the loss of the ability to contract in response to ATP was due to the total loss of responsiveness to ATP. Surgical denervation of the anterior latissimus dorsi and posterior latissimus dorsi was performed in a series of chicks 1-2 days after hatching, and the ability of these muscles to contract in response to ATP was tested 3-10 days after the surgery. Contractions in response to ATP were present in many of the muscles. Thus denervation of muscles in newly hatched chicks led to the reappearance of sensitivity to ATP. The disappearance of ATP responsiveness shortly after muscles become innervated and the reappearance of ATP responsiveness following denervation suggest that the expression of ATP responsiveness is regulated by motor neurons.
A monoclonal antibody (McAb) specific for actin depolymerizing factor (ADF) was prepared. With this and previously prepared anti-cofilin McAb (MAB-22) and other antibodies, the expression of cofilin and ADF in the muscles of dystrophic (NH-413) chicken and dystrophic (C57BL/6J dy/dy) mice was compared with that in normal control animals by immunoblotting and immunocytochemical methods. Since cofilin expression is down-regulated during normal postnatal development of skeletal muscles [Abe et al. (1989) J. Biochem. 106, 696-702], cofilin was detected in the breast (pectoralis) muscle of normal adult chicken and the leg (femoris and tibialis anterior) muscles of normal mice only at a low level. ADF was not detectable in adult skeletal muscles. However, a significant increase of cofilin amount, but not of ADF amount, was observed in these muscles of the dystrophic animals, when the symptom of muscular dystrophy became evident. In order to localize cofilin in individual muscle fibers, serial cryosections of the dystrophic chicken muscle were examined with anti-cofilin antibody (MAB-22). The antibody stained cells of different size in the dystrophic muscle, indicating that cofilin expression was induced in the regenerating muscle cells as well as in the pre-existing myofibers. We suggest that cofilin is involved in disassembly or reorganization of actin in the dystrophic muscle.
The radioligand dihydropyridine [methyl-3H]PN 200-110 binds to contracting myotubes in culture derived from chick embryo pectoralis muscle. [methyl-3H]PN 200-110 binds specifically to high-affinity sites, with nonspecific binding only between 15 and 30% of the total binding. A Scatchard plot of the specific binding revealed a single high-affinity binding site with a KD (dissociation constant) of 0.5 nM +/- 0.2 nM and Bmax (number of binding sites) of 100 fmol/10(6) nuclei. We employed this sensitive assay to probe the appearance of high-affinity [methyl-3H]PN 200-110 binding sites during myogenesis. The time course of appearance of high-affinity binding sites lags behind that of fusion. Low-calcium media prevented the differentiation of myoblasts and blocked the appearance of high-affinity sites. Chelation of intracellular calcium before or after fusion of myoblasts with the calcium indicator Quin 2 prevented the appearance of dihydropyridine binding sites. These findings are consistent with the view that the expression of dihydropyridine receptors is modulated by the intracellular calcium.
The research in the vascularisation of myocutaneous flaps of the pectoralis major muscle was conducted on the human cadavers. After the injection of the arteries 20 myocutaneous flaps were created. The main artery which is the source of vascularization of this muscle is pectoralis branch of thoraco-acromial artery. The objective of the research was to find out the direction of run of this artery. The direction variability was defined. The variability in the run of the branch of the thoraco-acromial artery refers to the place of departure from the thoraco-acromial artery, does not influence usefulness of the pectoral major muscle in creating the myocutaneous flap, considering the constant pathway of run of the distal part of this artery. The results of our research was compared with the classical description of the vascularisation given by the creator of this flap as well as with the works of authors dealing with the same issue.
The vanadate-induced crystallization of Ca2+-ATPase was analyzed on sarcoplasmic reticulum vesicles isolated between 10 and 28 days of development from pectoralis muscles of chicken. After exposure to Na3VO4 in a Ca2+-free medium, Ca2+-ATPase crystals begin to appear on portions of the surface of a few vesicles, isolated at 18 days of development. Thereafter, the number of vesicles containing Ca2+-ATPase crystals rapidly increases and after 1 week of postnatal development (28 days), it reaches the adult level of about 30% of the vesicle population. These observations are discussed with reference to the mechanism of Ca2+-ATPase crystallization and the regulation of sarcoplasmic reticulum biosynthesis.
In an attempt to understand the mechanism of calcium accumulation in myopathies, changes in the major calcium-binding protein, calmodulin, was studied in genetically dystrophic chickens. Measurements by radioimmunoassay revealed an increase in the calmodulin concentration of dystrophic chicken muscles. Poly A-containing RNA(s) of fast and slow muscles from the normal and dystrophic chicks were hybridized with [32P]-labeled calmodulin cDNA probe by the dot-hybridization technique. Densitometric scan of the autoradiogram showed that the calmodulin mRNA levels of dystrophic fast muscles (pectoralis and posterior latissimus dorsi) were approximately two-fold higher than those of the corresponding normal muscles. No significant change in calmodulin and calmodulin messenger RNA of slow muscle (ALD) was found in dystrophic chickens. Our results suggest that increased calcium flux within the dystrophic muscle may be modulated by calmodulin.