bluuebunny/crossref_metadata_2025_split huggingface dataset:
The effect of stretch removal on muscle weight and proteolytic enzyme activity in normal and dystrophic chicken muscles
Authors: Day Ronald K. , Ashmore C. Robert , Lee Yu Bang 
Published: January 2005

AbstractHypertrophy was induced in the patagialis (PAT) muscle of 6‐week‐old normal and dystrophic chicks by passive stretch for 1 week. Stretch was then removed and muscle weights and activities of the proteolytic enzymes cathepsin C, cathepsin D, and leucine aminopeptidase (LAPase) were measured after 3, 5, 7, 10, and 14 days. In both genotypes, weights of stretch‐released muscles dropped progressively for 7 days relative to control muscles, after which they were not significantly different. At the time of stretch release, proteolytic enzyme activities were approximately twice as high in stretched normal muscles as in normal control muscles. In dystrophic chicks there was no difference in activities between stretched and control muscles. However, the activities of the enzymes in dystrophic muscles were already about 4 times higher than in normal control muscles. After stretch release, the enzyme activities in normal muscle progressively fell for 10 days, after which they were not different from normal control muscles. In dystrophic muscles the enzyme activities remained elevated and were not different from dystrophic control muscle activities at any time. We conclude that degradative enzyme activities in normal muscle closely parallel changes in muscle weight, whereas in dystrophic muscle proteolytic enzymes remain elevated and constant whether the muscle is gaining or losing weight.
Gastroparesis in neonatal myotonic dystrophy
Authors: Bodensteiner John B. , Grunow John E. 
Published: January 2005

AbstractMyotonic dystrophy in the neonate is commonly accompanied by facial diplegia, generalized muscular hypotonia, talipes equinovarus, and muscular respiratory failure. The gastrointestinal manifestations of this disease include poor sucking, choking, regurgitation, aspiration, and swallowing difficulties. Gastroparesis can be a major contributor to the feeding difficulties experienced by these infants. We report on an infant with congenital myotonic dystrophy in whom a severe gastric motility problem was alleviated by metoclopramide therapy. This smooth muscle manifestation may be an important and potentially remediable source of morbidity in these infants.
A freeze‐fracture analysis of intramembrane particle densities on dystrophic hamster heart sarcolemma
Authors: Graham Kathryn A. , Shivers Richard R. , Atkinson Burr G. 
Published: January 2005

AbstractThe intramembrane particle (IMP) profile of control and dystrophic (Bio 14.6) hamster cardiac muscle plasma membrane was assessed in freeze‐fracture replicas to determine whether this animal model of muscular dystrophy exhibits the same membrane characteristics found in skeletal muscle from other more thoroughly studied dystrophic animals, and to test the hypothesis that the plasma membrane of the cardiac muscle cell is the site of a defect associated with the disease. Samples of cardiac muscle tissue from hamsters ranging in age from 1 to 13 months were freeze‐fractured. Intramembrane particle numbers were determined for all tissue samples by counting randomly selected areas of Phyphen; and E‐face surfaces. Up to the age of 1 month, the particle density was the same in both strains of hamster, after which time, the population of IMPs was about 30% lower in dystrophic than in normal heart sarcolemma. This 30% difference in particle frequency in dystrophic hamster heart membrane is consistent with values published for cell membrane from other muscular dystrophies and supports the theory that there is a defect in the plasma membrane of dystrophic cells. In addition, this study has shown for the first time that a presumed membrane defect related to muscular dystrophy (reduced number of IMPs) may be present throughout the life of the animal (1–13 months), and expressed in every cell sampled.
Phosphoglycerate kinase deficiency myopathy: Biochemical and immunological studies of the mutant enzyme
Authors: Bresolin Nereo , Miranda Armand , Chang Hai Won , Shanske Sara , DiMauro Salvatore 
Published: January 2005

AbstractA new phosphoglycerate kinase variant (PGK New Jersey) has been purified from muscle and cultured fibroblasts of a patient with recurrent myoglobinuria. The mutant enzyme had higher than normal affinity for adenosine triphosphate (ATP) and 3‐phosphoglycerate, and a shift of the pH optimum towards the acidic side. Antibodies raised against PGK purified from normal muscle were used to evaluate the presence of immunologically cross‐reacting enzyme protein in tissues from the patient. Immunodiffusion and an antibody consumption test showed the presence of reduced amounts of cross‐reacting material in the patient's muscle. Several PGK variants have been characterized in asymptomatic individuals or in patients with hemolytic anemia. The biochemical features of PGK New Jersey, the only known variant associated with recurrent myoglobinuria, distinguish this mutant enzyme from others.
Healing‐over in skeletal muscles of the guinea pig following induced injury
Authors: Furukawa Kenichiro 
Published: January 2005

AbstractElectrical membrane properties of cremaster muscle fibers of the guinea pig were determined before and after sectioning, using the microelectrode method. After sectioning, the membrane was depolarized to a maximum level within 5 minutes and the original level was reverted to within 60 minutes. Following restoration of the membrane potential, the spatial distribution of electrotonic potential indicated an electrical sealing at the cut end, and an action potential could be evoked. Therefore, it would appear that the cremaster muscle possesses the healing‐over phenomenon. This process was dependent on temperature and [Ca2+]0 and was not affected by pretreatment of actinomycin D, a protein synthesis inhibitor. This healing‐over process also occurs in the extensor digitorium longus (EDL) muscle of the guinea pig but not in the diaphragm. These results indicate that some mammalian skeletal muscle fibers possess the healing‐over phenomenon, as is observed in cardiac muscle fibers.
Congenital canine myasthenia gravis: I. Deficient junctional acetylcholine receptors
Authors: Oda Kenichiro , Lambert Edward H. , Lennon Vanda A. , Palmer Anthony C. 
Published: January 2005

AbstractThe neuromuscular junction was studied during growth in two breeds of dog with a congenital familial from of myasthenia gravis (CMG): the Jack Russell terrier and the springer spaniel. Light microscopy revealed no difference in endplate size or nerve terminal morphology in agematched CMG dogs and unaffected littermates. At all ages there was in individual muscle fibers of CMG dogs an approximately 75% lower postsynaptic membrane density of acetylcholine receptors (AChR). There was no evidence that this abnormality had an autoimmune basis. Measurements of miniature endplate potential amplitude in relation to fiber diameter revealed that the low density of AChR in the postsynaptic membrane of CMG dogs remained constant and did not change with the marked progression of muscle weakness during growth. Antigenic determinants of AChR were deficient in CMG muscle to the same extent as α‐bungarotoxin (αBT) binding sites. Thus, a low density of AChR in the muscle's postsynaptic membrane appears to be the principal abnormality of CMG. The data suggest that the normal increase in number of acetylcholine (ACh) quanta released by nerve impulse may not fully compensate for the reduction in depolarization produced by a single quantum as the muscle fiber diameter increases. This could cause progression of weakness during growth. In addition to being a useful animal model of a rare form of CMG that resembles one form of human CMG, canine CMG offers a unique model for investigating events of synaptogenesis at the neuromuscular junction.
Congenital canine myasthenia gravis: II. Acetylcholine receptor metabolism
Authors: Oda Kenichiro , Lennon Vanda A. , Lambert Edward H. , Palmer Anthony C. 
Published: January 2005

AbstractAcetylcholine receptor (AChR) metabolism was studied in muscle from juvenile and adult dogs with congenital myasthenia gravis (CMG) and their unaffected littermates. Although the amount of AChR in the junctional region of innervated CMG muscle fibers was 25% of normal, or less, denervation of CMG fibers resulted in the appearance of AChR in extrajunctional membranes at as high a concentration as in denervated normal fibers. The rate of degradation of junctional AChR in CMG fibers explanted to organ culture did not differ significantly from normal. In monolayer cultures derived from enzyme‐dissociated CMG muscle, myotubes of normal morphology developed, and the synthesis and degradation of AChR did not differ from normal. Addition of sera from dogs with the acquired autoimmune form of MG accelerated the degradation of AChR on cultured myotubes, but CMG dog sera were without effect. These data suggest that the low junctional membrane density of AChR in CMG does not reflect a primary inability of muscle to synthesize AChR, nor an accelerated degradation of AChR in the postsynaptic membrane, but rather a low insertion rate of AChR in the postsynaptic membrane.
Control of myofibrillar ATPase activity and force in myodystrophic muscle
Authors: Mobley Bert A. , Reddy Y. S. , Feeback Daniel L. , Bodensteiner John B. , Bokhari Masuda , Robinson R. D. , Clark Ronald 
Published: January 2005

AbstractMyofibrillar ATPase activity was measured as a function of the free calcium concentration in skeletal muscles of control and myodystrophic mice. In addition, the force developed in skinned extensor digitorum longus (EDL) fibers of control and myodystrophic mice was measured as a function of the free calcium concentration, and a histomorphometric study was performed on soleus and EDL muscles of control and myodystrophic mice. The results showed that the myofibrillar ATPase activity and the force‐generating mechanisms of control and myodystrophic muscles were controlled to the same relative degree by equivalent concentrations of calcium ions. Upon maximal activation of the ATPase activities, we measured 18% less activity in myodystrophic muscles than in control muscles. Maximal activation of the force‐generating capacity in skinned fibers showed there was no significant difference in force produced in the control compared to myodystrophic fibers. The histomorphometric study revealed no alteration in the relative distribution of different fiber types in myodystrophic compared to control muscles. However, the histomorphometry did reveal a larger slow (type 1) relative cellular area compared to total cross‐sectional area in myodystrophic muscle than in controls. We propose that the lower ATPase activity but equal force‐generating capacity of myodystrophic muscles compared to control muscles is due to myodystrophic muscles being composed of a greater fraction of myofibrils from slow (type 1) fibers than control muscles.
Morphology of stable muscle grafts of rats: Effects of gender and muscle type
Authors: Clark Kathryn I. , White Timothy P. 
Published: January 2005

AbstractOur purpose was to quantify morphological characteristics of extensor digitorum longus (EDL) and soleus (SOL) muscle grafts in female (N =8) and male (N = 8) rats. Muscles were grafted orthotopically, with the nerve remaining intact, and were studied 56 days later. The mass of EDL and SOL grafts and control muscles of females was 60% to 65% of male values; this difference was directly related to gender differences in body mass. The fiber composition of EDL and SOL grafts did not differ from control, and no gender effects were noted. The mean fiber area (MFA) of control EDL and SOL muscles of females averaged 65% of male values. The MFA of grafts did not differ due to gender, and averaged 60% of control value for SOL and 70% for EDL grafts. We conclude there are no substantial differences in the regenerative capacity of EDL and SOL muscles grafted with the nerve intact.
Effects of isaxonine on skeletal muscle reinnervation in the rat: An electrophysiologic evaluation
Authors: Pecot‐Dechavassine Monique , Mira Jean‐Claude 
Published: January 2005

AbstractElectrophysiologic detection of the first signs of gastrocnemius muscle reinnervation shows that after a single localized freezing of the rat sciatic nerve, isaxonine does not significantly increase the rate of axonal regeneration. However, this drug does significantly enhance axonal sprouting, as it induces an increase of 50% in the number of muscle fibers with multiple innervation 10–30 days after freezing. After 30 days, the proportion of multiinnervated fibers decreases in both the control and isaxonine‐treated rats, and the differences between them gradually disappear.
Parvalbumin in cross‐reinnervated and denervated muscles
Authors: Müntener Markus , Berchtold Martin W. , Heizmann Claus W. 
Published: January 2005

AbstractThe extensor digitorum longus (EDL) muscle was cross‐reinnervated by the soleus (SOL) nerve, leading to the well‐known transformation toward a slow muscle. Nine weeks after the operation, the quantitative analysis of the Ca2+‐binding protein, parvalbumin (PV), using highperformance liquid chromatography, showed a threefold reduction of PV in the cross‐reinnervated EDL muscle. Denervation of the EDL muscle, which leads to an increase of the half‐relaxation time, resulted in a 20% decrease of the PV concentration within 4 days. This significant lower PV level was detectable prior to any change of the myofibrillar adenosine triphosphatase (ATPase). Normal PV concentrations were reached after 9 weeks following self‐reinnervation of the EDL muscle. The experiments support the view that PV is involved in the relaxation of rat fast skeletal muscles and that its expression is dependent on nerve—muscle interaction. Since PV changes preceded histochemical changes after denervation, this protein may be a sensitive marker for early stages of neuromuscular disturbances.
Differential effects of α‐latrotoxin on mouse nerve endings and fibers
Authors: Mallart Alberto , Haimann Claudia 
Published: January 2005

AbstractThe action of α‐latrotoxin (α‐LTx), the major toxic component from black widow spider venom, was studied on mammalian motor nerve endings and fibers. Electrophysiologic recordings of presynaptic and postsynaptic responses at early stages after the application of different doses of α‐LTx showed massive transient increases in transmitter release and changes in the configuration of presynaptic currents. Later, a loss of invasion of terminals by nerve impulses occurred, whereas the impulse conduction in nerve fibers was unmodified. These results support the idea of a selective effect of α‐LTx on presynaptic membrane excitability.
Localization of calcium‐activated neutral protease (CANP) in the peripheral nerve
Authors: Kamakura Keiko , Ishiura Shoichi , Fujita Takehisa , Nonaka Ikuya , Sugita Hideo 
Published: January 2005

AbstractLocalization of calcium‐activated neutral protease (CANP) in the rat peripheral nerve was studied by an indirect immunofluorescent method, using rabbit antiserum against CANP extracted from chicken skeletal muscle. Its specificity to CANP, as well as its cross‐reactivity with rat CANP, were confirmed by the Ouchterlony immunodiffusion procedure and immunoreplica method. CANP was demonstrated in the axon, but not in the myelin sheath or endoneurium. We could not conclude whether or not CANP in axons exists in association with neurofilaments.
Phospholipid methylation in skeletal muscle membranes
Authors: Kuncl Ralph W. , Drachman Daniel B. , Kishimoto Yasuo 
Published: January 2005

AbstractPhospholipid methylation is thought to modulate such vital cellular processes as calcium transport, receptor function, and membrane microviscosity. As these processes are fundamental to the function of muscle cells and are thought to be altered in disease states, we have characterized several features of phospholipid methylation reactions in skeletal muscle and have defined appropriate assay conditions. In rat leg muscle, methyltransferase activity was assayed radiometrically by measuring the incorporation of methyl groups from S‐adenosyl‐L‐[methyl‐3H]methionine into membrane phospholipids, the methylated derivatives of which were separated by thin‐layer chromatography. Contrary to previous investigations of whole muscle, phospholipid methyltransferase activity was clearly present in skeletal muscle membranes, being highly localized in sarcoplasmic reticulum and present to a lesser extent in sarcolemma. Both the reaction products and the reaction kinetics were consistent with sequential methylation of phospholipids by two methyltransferase enzymes. S‐adenosylhomocysteine and its analogues were potent inhibitors of phospholipid methylation in sarcoplasmic reticulum. The predominant localization of phospholipid methytransferase activity in sarcoplasmic reticulum suggests that its functional role in skeletal muscle may be in calcium transport.
In vivo P‐NMR spectroscopy: Muscle energy exchange in paramyotonia patients
Authors: Lehmann‐Horn Frank , Höpfel Dieter , Rüdel Reinhardt , Ricker Kenneth , Küther Gerald 
Published: January 2005

AbstractUsing phosphorus nuclear magnetic resonance spectroscopy, we studied the muscle metabolism in four patients with paramyotonia congenita as reflected in the PC/Pi and PC/ATP ratios. At normal body temperature, all results were indistinguishable from controls. After cooling to 29°C muscle temperature and a single 2‐sec maximum contraction, the forearm muscles were stiff. At this stage, no decrease in the ATP content could be detected. In >50% of the experiments with patients, an additional peak occurred transiently at the resonant frequency for monophosphates. After a working period at 29°C muscle temperature, the paramyotonic muscles were paralyzed, but displayed spectra similar to those obtained at normal body temperature and full working capability. Intracellular pH was close to 7 in paramyotonic muscle under all conditions examined.
Isolated myofibers from rat skeletal muscle in suspension: Cellular morphology and calcium homeostasis
Authors: Zuurveld Judith G. E. M. , Veerkamp Jacques H. , Wirtz Peter 
Published: January 2005

AbstractMyofiber suspensions with 80% viability (morphological intactness) were prepared from rat m. flexor digitorum brevis by a 6‐hour collagenase treatment. The viable fibers had intact sarcolemmas and generally showed continuous basal laminae. The intracellular compartments exhibited normal muscular morphology. The suspended myofibers showed good tolerance against extracellular calcium (up to 30 mM), but were susceptible to 15mM EGTA. Calcium ionophore A23187 induced contraction, with loss of viability in both calcium‐containing and nominally calcium‐free Krebs‐Ringer medium. EGTA prevented the ionophore effect, but the muscle cells collapsed as soon as calcium was replenished. A calcium paradox, as observed with perfused heart, could not be induced in isolated skeletal myocytes. This suspended cell system should provide a useful tool for investigating relationships between metabolic parameters and muscle physiology. The extracellular environment can be manipulated easily, and cellular responses of individual skeletal muscle fibers can be measured and visualized.
Post‐tetanic responses in creatine‐depleted rat edl muscle
Authors: Mainwood Graham W. , De Zepetnek Joanne Totosy 
Published: January 2005

AbstractThe total creatine content of rat extensor digitorum longus (EDL) muscles is reduced from 26.7 m̈mol·g−1 to 5.2 m̈mol·g−1 after 4 weeks on a diet containing b̃‐guanidinopropionate. The resting muscles of these animals contain only 5% of the normal creatine phosphate and about 30% of the normal adenosine triphosphate (ATP). Isometric twitch and brief tetanic responses are not significantly different from normal. However, following a 1‐second tetanus, the normal twitch potentiation (+80%) is reversed in depleted muscles (−40%). The initial suppression lasts 1–2 seconds and is followed by a small delayed potentiation (+25%). Relaxation rate, which is normally increased following a tetanus, is considerably reduced in depleted muscles. Reversal of potentiation appears to be due to a suppression of twitch activation. The suppression may result from a transient fall in ΔGATP, which is thought to be a critical parameter in the uptake of Ca++ by the sarcoplasmic reticulum (SR).
Sequential urinary Nτ‐methylhistidine to creatinine ratios in premature infants
Authors: Burgoyne Judith L. , Fitzgerald Anne , Dahlenburg Geoffrey W. , Haslam Ross R. , Tomas Frank M. , Ballard F. John 
Published: January 2005

AbstractThe present study was undertaken to establish normal values of the Nτ‐methylhistidine to creatinine excretion ratio in very premature infants, to observe changes with postnatal age, and to determine whether or not reliable data on this index of myofibrillar protein breakdown could be obtained from untimed urine samples without recourse to the 24‐ hour collections used previously. The normal range (95% confidence limits) of the molar excretion ratio for unstressed infants was established to be between 0.0248 and 0.0440. Narrower limits of variability occurred when nutrient intake was controlled at a satisfactory level or when comparisons were between sequential urine samples from single infants. No diurnal changes could be detected. We conclude that analyses of Nτ‐methylhistidine and creatinine on spot urine samples permit the calculation of an excretion ratio that is reproducible both within and between individual infants and that should be useful in assessing changes in myofibrillar protein breakdown caused by differences in clinical, pharmacologic, or nutritional status.
31P‐NMR Studies on an animal model of human defective muscle glycolysis
Authors: Kuwabara Takeo , Yuasa Tatsuhiko , Miyatake Tadashi 
Published: January 2005

AbstractSequential metabolic changes in leg muscles of a model of defective muscle glycolysis that was produced by intraaortic injection of sodium iodoacetate were observed by in vivo 31P‐NMR spectroscopy with a surface coil. Spectra obtained from iodoacetate‐treated muscles presenting exercise‐induced cramp showed decreased levels of phosphocreatinine (PCr) and adenosine triphosphate (ATP) and an accumulation of sugar phosphate. The chemical shift of inorganic phosphate (Pi) resonance, which reflects the intracellular pH of the contracted muscles, showed a milder shift to the acidic condition than those of controls. In vivo 31P‐NMR study showed dynamic information on the muscle energetics under defective glycolytic conditions.
Insulin binding in denervated muscle
Authors: Donaldson Deirdre , Evans Owen B. , Harrison Robert W. 
Published: January 2005

AbstractInsulin binding was measured in rat muscle following denervation. There was a 40% reduction in the number of high‐affinity insulin receptors, with no change in the insulin binding Kd. Selected muscles showed a 40%–60% reduction in weight during this period. The down regulation in the number of insulin receptors may contribute to the mechanism of muscle atrophy following denervation.