bluuebunny/crossref_metadata_2025_split huggingface dataset:
Electrical properties of commercial concentric EMG electrodes
Authors: Dorfman Leslie J. , McGill Kevin C. , Cummins Kenneth L. 
Published: January 2005

AbstractFive electrical characteristics—impedance, broadband noise generation, line interference sensitivity, signal distortion, and common‐mode conversion—were measured in five electromyographic (EMG) concentric needle electrodes (CNEs) from each of six commercial manufacturers. Untreated CNEs showed considerable variation in impedance and broadband noise characteristics, both within and among manufacturers. Electrolytic treatment reduced impedances by a factor between 1.5 and 4.0 and lessene within manufacture variability Average post‐treatment impedances at 100Hz ranged from 31 to 436 kOhms, reflecting in part the range of core surface areas. Treatment also reduced the broadband noise to the level of the instrumentation noise for all but the highest impedance CNEs. Distortion and common‐mode conversion were negligible for the lowest impedance CNEs. Line interference from a nearby power cord was completely suppressed only by those CNEs with fully shielded cables, and then only when the electromyographer also was grounded; there was no measurable benefit when the shield was driven, as opposed to grounded. We conclude that (1) there are consistent differences in the properties of CNEs from different manufacturers, reflecting differences in materials, design, and construction; (2) electrolytic treatment temporarily improves the performance of all CNEs, and tends to lessen the differences among them, most likely through a surface electrochemical effect; and (3) both active and passive cable shields are effective in reducing extraneous line interference.
Free‐energy carriers in human cultured muscle cells
Authors: Bolhuis P. A. , de Zwart H. J. D. , Ponne N. J. , de Jong J. M. B. V. 
Published: January 2005

AbstractCreatine phosphate (CrP), adenosine triphosphate (ATP), creatine kinase (CK), adenylate kinase (AK), protein, and DNA were quantified in human muscle cell cultures undergoing transition from dividing myoblasts to multinucleate myotubes. CrP is negligible in cultures grown in commonly applied media but increases rapidly when sufficient exogeneous creatine is available. The rise in CrP content precedes the rapid increase of CK and cessation of DNA synthesis found during cell fusion. The addition of creatine has no significant effect on the CK and protein content and on the fusion of the human muscle cells. ATP, AK, and protein increase gradually during proliferation and differentiation. When expressed per milligram of protein, ATP and AK are in the same range as in human skeletal muscle and are not correlated to the cell fusion. In contrast, CrP and CK per milligram protein are much higher in myotubes than in myoblasts but remain much lower than in muscle. These data indicate that only an early differentiation phase has been reached in the muscle cell cultures.
Endoneurial potassium is increased and enhances spontaneous activity in regenerating mammalian nerve fibers—implications for neuropathic positive symptoms
Authors: Low Phillip A. 
Published: January 2005

AbstractThe endoneurial fluid potassium [K+]e has potent effects on membrane potential and excitability but direct measurements have not been reported. The [K+]e was measured with K+ ion‐sensitive microelectrodes in normal, demyelinated, and regenerating rat peripheral nerve fibers. The mean value in normal nerve was 3.7 mM. The [K+]e was consistently elevated in regenerating nerves and infrequently elevated in demyelinated nerves. The time course of [K+]e was studied in the left tibial nerve of 22 rats 2 days to 3 months in the extended crush model. The [K+]e was increased and peaked in the first 2 weeks, with a progressive decline toward control values after that. Single fiber recordings were made from the tibial division of the sciatic nerve in 13 animals. The mean number of single fibers studied per rat was 55.5 (SD 24.6). Spontaneous activity (SA) was present in all regenerating nerves and was maximal in the first 2–4 weeks. Endoneurial K+ was further increased by intraarterial injection of potassium into the saphenous artery. Spontaneous activity was enhanced when [K+]e began to rise; there were further superimposed bursts of SA with the administration of additional boluses. These findings suggest that [K+]e increase is a factor in enhancing SA in damaged nerve fibers.
Acoustic myography: A noninvasive monitor of motor unit fatigue
Authors: Barry Daniel T. , Geiringer Steven R. , Ball Richard D. 
Published: January 2005

AbstractAcoustic myography is the recording of sounds produced by contracting muscle. These sounds become louder with increasing force of contraction. We have compared muscle sounds with surface EMG to monitor the dissociation of electrical from mechanical events (presumably, the loss of excitation–contraction coupling) which occur with motor unit fatigue. Acoustic signals were amplified using a standard phonocardiograph, recorded on FM magnetic tape, and digitally analyzed. Muscles were examined at rest, with intermittent contractions, and with sustained contractions. We found that with fatigue, the acoustic amplitude decayed, but the surface EMG amplitude did not. With decreased effort, however, the acoustic and the surface EMG amplitudes declined simultaneously. By simultaneously recording acoustic signals and needle EMG, individual motor units were resolved acoustically in two muscles with decreased numbers of motor units and increased motor unit size. Fasciculations also produced acoustic signals, although no acoustic signal has yet been found that correlates with fibrillations. Analysis of acoustic signals from muscle provides a noninvasive method for monitoring motor unit fatigue in vivo. It may also be useful in distinguishing muscle fatigue from decreased volition.
Acquired versus familial demyelinative neuropathies in children
Authors: Miller Robert G. , Gutmann Ludwig , Lewis Richard A. , Sumner Austin J. 
Published: January 2005

AbstractThe electrophysiologic differences between chronic acquired demyelinative neuropathy and the demyelinative form of Charcot‐Marie‐Tooth disease have recently been reported. The present report extends these observations to include the genetically determined demyelinating neuropathies seen in metachromatic leukodystrophy, Krabbe's leukodystrophy, and Cockayne's syndrome. The electrophysiologic features of metachromatic leukodystrophy (five patients), Krabbe's (four patients), and Cockayne's syndrome (three patients) were all similar. There was uniform slowing of conduction (both in different nerves and in different nerve segments), and conduction block was not seen. These findings are consistent with a uniform degree of demyelination in multiple nerves and throughout the entire length of individual axons. Thus, uniform slowing of nerve conduction constitutes strong evidence for a familial demyelinative neuropathy, as opposed to the multifocal slowing seen in acute and chronic acquired demyelinative neuropathy.
Response of satellite cells to focal skeletal muscle injury
Authors: Schultz Edward , Jaryszak Debra L. , Valliere Charles R. 
Published: January 2005

AbstractThe time course and pattern of the initiation of satellite cell mitoses was studied following a crush injury of the distal third of the 30‐day‐old rat extensor digitorum longus, a muscle in which myofibers run the entire length of the belly. Satellite cell mitotic activity was monitored using autoradiography after injection of 3H‐thymidine. Satellite cell labeling rose above control values by 15 hours post injury at the injured site and by 20 hours in the middle third or adjacent undamaged portion of the muscle. Labeling decreased in the proximal third of the muscle, so that by 25 hours post injury, a gradient of labeling was established along the muscle length. Electron microscopy (EM) quantitation showed that the reduced labeling in the proximal third resulted from a reduction in satellite cell numbers. The results suggest that mitotic activity of satelite cells after localized injury occurs mainly at or near the site of injury, but that many of the dividing cells have migrated from undamaged areas distant from the lesion site.
Lysosomal changes in mouse skeletal muscle during the repair of exercise injuries
Authors: Salminen Antero , Kihlström Markku 
Published: January 2005

AbstractLysosomal changes of mouse skeletal muscle during the repair of exercise injuries were studied with biochemical, histochemical, and electron microscopic methods. Treadmill running for 4 hours and 9 hours increased the activities of cathepsin C and β‐glucuronidase, but not that of β‐glycerophosphatase in mouse quadriceps femoris muscle. The highest activities occurred 3 days after exertion and were higher after the longer duration of exertion. Similar changes that were highly correlated with the activities of lysosomal enzymes occurred in the activities of glucose‐6‐phosphate dehydrogenase and 6‐phosphogluconate dehydrogenase and in the concentration of DNA. The activities of lysosomal enzymes correlated significantly with the severity of histopathologic injuries. Histochemical stainings of β‐N‐acetylglucosaminidase and β‐glucuronidase showed a strong increase in the staining intensity 3 and 5 days after exertion, both in inflammatory phagocytes and in surviving muscle fibers in the injured area, and staining intensities increased in parallel with the severity of injuries. Electron microscopy showed an increased number of autophagic vacuoles, lysosomelike bodies, and Golgi complexes in the fibers adjacent to necrotic foci, coinciding with the highest histochemical staining pattern. Lysosomal changes in surviving muscle fibers in close proximity to injured muscle fibers could, by autophagic degradation, provide structural elements for the regeneration of injured muscle fibers.
The free cytoplasmic Ca2+ levels in duchenne muscular dystrophy lymphocytes
Authors: Klip Amira , Elder Brian , Ruiz‐Funes Hugo P. , Buchwald Manuel , Grinstein Sergio 
Published: January 2005

AbstractAn increased cellular Ca2+ content has been associated with Duchenne muscular dystrophy (DMD). However, estimates of the free cytoplasmic Ca2+ concentration ([Ca2+]i) in cells of DMD patients were not available. We compared the [Ca2+]i levels of normal and DMD peripheral blood lymphocytes and Epstein‐Barr virus‐transformed lymphoblasts using the novel probe, quin 2, an internally trapped fluorescent indicator. The [Ca2+]i levels of normal and DMD cells were not significantly different.
Fatigue trends in and the diagnosis of myasthenia gravis by frequency analysis of EMG interference patterns
Authors: Yaar Israel , Mitz Andrew R. , Pottala Erik W. 
Published: January 2005

AbstractTwenty patients with myasthenia gravis were studied. Needle interference patterns at maximal isometric contractions were recorded from the biceps brachii muscles. Each recording lasted for 30 seconds and induced som fatigue. The EMG signals were transformed into power spectra and were analyzed for differences between control and myasthenic fatigue trends and were tested for the power of the frequency variables to classify unknown subjects. Both groups showed a similar averaged spectra for the first 5 seconds. Thereafter, the controls manifested continuous increase in power, and a power peak frequency shift toward low frequencies. The myasthenics showed an initial increase throughout the frequency ranges; however, later, there was a marked decrease in power and their peak frequency shifted toward the lower frequencies. These fatigue trends differed significantly from one another. Discriminant analysis correctly classified 83% of the subjects. This technique may be helpful in the diagnosis of myasthenia gravis.
Evidence for the identities of five proteins decreased in skeletal muscle of dystrophic mice
Authors: Jasch Laura G. , Moase Elaine H. 
Published: January 2005

AbstractIn a previous study,16 protein distributions in normal and dystrophic soleus and EDL were examined using polyacrylamide isoelectric focusing. Whereas normally protein distributions in these two muscles were characteristically different, in dystrophic muscles they were strikingly similar. The soleus‐specific proteins were identified as the myosin light chains LC1s and LC2s. The EDL‐amplified proteins were the myosin light chains LC1f, LC2f, the phosphorylated form of LC2f (LC2f‐P), and LC3f. In addition, evidence is presented that one protein, which had not been identified in two‐dimensional gels, is parvalbumin. The decreased proportion of parvalbumin, LC2f‐P, and LC3f in the dystrophic EDL was also shown in other fast‐twitch muscles of the mouse. We suggest that these changes in protein distributions in dystrophic muscles reflect a loss of their acquired state of differentiation.
Regeneration of frog twitch and slow muscle fibers after mincing
Authors: Schmidt Heinz , Emser Wendelin 
Published: January 2005

AbstractIliofibularis muscles of Rana temporaria were minced and allowed to regenerate in the iliofibularis or the sartorius bed of the same frog. Regenerated muscles were examined for the presence of slow muscle fibers using electrophysiologic, histochemical, and contractile parameters. Muscle regeneration from sartorius mince was also studied. Regeneration was more successful from iliofibularis than from sartorius mince, and the iliofibularis bed was more favorable for regeneration than the sartorius bed for both types of muscle. Twitch fibers regenerated within a few months, but slow fibers could not be identified earlier than 14 months after muscle destruction. Slow muscle fibers regenerated only from iliofibularis mince, both orthotopically and heterotopically. All regenerates capable of maintaining a K‐contracture contained histochemically identified slow fibers; the membrane properties of electrophysiologically identified slow fibers were normal. It is concluded that slow muscle fibers regenerate only from the remnants of a muscle that contains slow fibers. The results are discussed with respect to the role of innervating nerve fibers.
Postpoliomyelitis muscle pseudohypertrophy
Authors: Bertorini Tulio E. , Igarashi Masanori 
Published: January 2005

AbstractA 62‐year‐old patient who had had acute paralytic poliomyelitis in early childhood developed bilateral lower limb muscle pseudohypertrophy. The pseudohypertrophy was caused primarily by an enormous excess of adipose tissue replacing muscle fibers, and, in part, by work hypertrophy of muscle fibers.
Beta‐oxidation enzymes in normal human muscle and in muscle from a patient with an unusual form of myopathic carnitine deficiency
Authors: Trevisan Carlo P. , Reichmann Heinz , DeVivo Darryl C. , DiMauro Salvatore 
Published: January 2005

AbstractIn a reported patient with myopathic carnitine deficiency, addition of exogenous carnitine to muscle homogenates failed to correct palmitate oxidation, and oral carnitine was of no clinical benefit.27 In a muscle biopsy from this patient, we found that, in contrast to the marked deficiency of free carnitine (3% of normal) short‐ and medium‐chain acylcarnitines were in the normal range and long‐chain acylcarnitine was increased almost four times. As this result confirmed the hypothesis of a muscle defect of mitochondrial oxidation of palmitate, all eight enzymes of beta‐oxidation were measured spectrophotometrically in the muscle extract. None of them was found to be defective. These data suggest that the underlying biochemical abnormality in this patient may be a deficiency of the carnitine–acylcarnitine translocase system or a defective interaction between acyl‐CoA dehydrogenase and its flavoprotein coenzyme.
Tissue culture studies of muscle disorders: Part 1. Techniques, cell growth, morphology, cell surface
Authors: Witkowski J. A. 
Published: January 2005

AbstractTissue culture has been used extensively in studies of human inherited disorders, and its application in the field of the neuromuscular disorders has increased rapidly in recent years. This review, covering the period 1977 to 1984, deals with tissue culture studies of both human and animal muscle disorders, although Duchenne muscular dystrophy (DMD) figures prominently because of the overwhelming interest in that disorder. The review is in two parts. In the first part, I discuss technical innovations in the field, the morphology and growth of cells, and a variety of studies related to the cell surface. Important findings in relation to DMD include reports of abnormal growth rates and reduced lifespan of DMD cells, hypersensitivity to DNA‐damaging agents, abnormal cell‐to‐cell and cell‐to‐substratum adhesion, and a more “fluid” cell membrane. However, these findings are controversial or have so far been reported only by single laboratories.
Tissue culture studies of muscle disorders: Part 2. Biochemical studies, nerve‐muscle culture, metabolic myopathies, and animal models
Authors: Witkowski J. A. 
Published: January 2005

AbstractThis review continues with studies of protein, lipid, and purine metabolism of Duchenne muscular dystrophy (DMD) cells in vitro and of muscle cells in combined culture with nerve cells. In vitro studies of human metabolic myopathies are tabulated. Results using the hamster, chicken, and mouse (dy25, dy, mdg, and mdx) myopathies are discussed. Interesting findings include suggestions of altered collagen synthesis by DMD cells. Analysis of cell proteins by two‐dimensional gel electrophoresis and the use of combined nerve‐muscle cultures remain important areas of development. It is disappointing that so few attempts have been made to repeat significant findings in this field, and when a number of laboratories have examined the same phenomenon, the results are often contradictory. It remains to be shown how these various abnormalities found in cells in vitro are related to each other and to those pathologic features of diseased muscle observed in vivo.
Effector mechanisms in myasthenia gravis: End‐plate function after passive transfer of IgG, Fab, and F(ab′)2 hybrid molecules
Authors: Sterz Raimund , Hohlfeld Reinhard , Rajki Klara , Kaul Martin , Heininger Kurt , Peper Klaus , Toyka Klaus V. 
Published: January 2005

AbstractUsing the quantitative ionophoresis technique and the mouse passive transfer model of myasthenia gravis, end‐plate function was measured in mice transferred with myasthenic lgG, Fab, or F(ab')2 hybrid molecules prepared by recombination of one acetylcholine receptor (AChR) specific Fab and one Fab directed against irrelevant antigen. The Hill coefficient (a measure for the cooperativity between AChR subunits) and the apparent dissociation constant K for the ACh‐AChR interaction were essentially unaltered after passive transfer of lgG or lgG fragments. In contrast, myasthenic lgG and Fab, but not control lgG or Fab, markedly reduced the mean number of end‐plate channels. A similar effect was observed after passive transfer of F(ab')2 hybrid molecules. These results show that passive transfer of myasthenic lgG or lgG fragments leads to a quantitative reduction of ACh‐controlled end‐plate channels, whereas the function of the remaining receptors/channels remains unchanged. The results suggest further that crosslinking of AChR by divalent antibody may not be an absolute requirement for the reduction of AChR at the functional neuromuscular synapse.
Promiscuous expression of myosin in myotonic dystrophy
Authors: Moore Gudrun E. , Roses Allen D. , Pericak‐vance Margaret A. , Garrett William E. , Schachat Frederick H. 
Published: January 2005

AbstractThe pathologic changes in myotonic dystrophy (DM) skeletal muscle biopsies have been analyzed at both the histochemical and molecular level. A histochemical stain for pretyping single fibers in conjunction with sodium dodecyl sulphat—polyacrylamide gel electrophoresis allowed biochemical differences to be pinpointed in specific histochemical fiber types. These biochemical differences can be related to histochemical changes in fiber type observed in cross‐section of the DM biopsies. Such changes included, specific fiber type atrophy, hypertrophy, and disproportion. The pathogenesis of DM appears to be characterized by a large increase in the number of promiscuous fibers, that is, those fibers that express both fast and slow myosins. This promiscuity, which is rare in control muscle (<2%), is also prevalent at high levels in some family members at risk for DM. The observed promiscuity, although probably not a primary effect of DM, appears to be linked to the histochemical changes in fiber type observed in the DM biopsies.
Delayed nerve regeneration in streptozotocin diabetic rats
Authors: Longo F. M. , Powell H. C. , Lebeau J. , Gerrero M. R. , Heckman H. , Myers R. R. 
Published: January 2005

AbstractNerve regeneration across a 10‐mm gap was delayed in streptozotocin diabetic rats 3 and 4 weeks after transecting the sciatic nerve. Opposite ends of each cut nerve were introduced into a silicone tube, leaving a 10‐mm gap. Electron microscopy was used to evaluate the progress of regeneration in sections at 2‐mm intervals across the 10‐mm gap. After 3 weeks, control axons had bridged the 10‐mm gap, and myelin sheaths extended for 6–8 mm. By contrast, axons and their myelin sheaths were seen no further than 2 mm from the proximal stump in diabetic animals. By 4 weeks, axons had bridged the gap in diabetics; however, they appeared immature and showed dystrophic changes. The findings suggest that although regeneration does occur in diabetic nerves, it is significantly delayed and qualitatively impaired.
Skeletal muscle acetylcholinesterase molecular forms in amyotrophic lateral sclerosis
Authors: Fernandez Hugo L. , Stiles Joel R. , Donoso J. Alejandro 
Published: January 2005

AbstractAcetylcholinesterase (AChE) molecular forms in muscle biopsies from control and amyotrophic lateral sclerosis (ALS) patients were extracted under low (G: globular forms) and high (A: asymmetric forms) ionic strength conditions and were evaluated by velocity sedimentation analysis. Total AChE activity in endplate‐containing ALS muscle sections was reduced by an average of 65% of control muscle levels. This decrement resulted from an almost complete disappearance of 9.5S (G4) and 8.0S (A4) AChE and significant decreases in the 3.8S (G1), 12.1S (A8), and 15.8S (A12) forms (66%, 9%, and 25% of control, respectively). In most of the ALS biopsies examined, ultrastructural‐cytochemical analysis revealed large reductions in AChE reaction product of both synaptic infoldings (extracellular) and sarcoplasmic reticulum (intracellular) of the muscles' motor endplate regions. These data are compatible with the view that alterations observed in AChE forms from ALS muscles are related to disturbances in the normal “trophic” interactions between nerve and muscle.
Ganglioside therapy in diabetic neuropathy
Authors: Horowitz Steven H. 
Published: January 2005

AbstractCronassial, a combination of four different cerebral gangliosides, was administered intramuscularly (40 mg daily) in a double‐blind controlled study of 28 patients with moderate to severe diabetic neuropathy. Clinical neurologic and near‐nerve electrophysiologic studies were performed. The 14 patients receiving gangliosides experienced statistically significant improvement in their clinical scores due to an increase in lower extremity sensory perception. No other clinical or electrophysiologic changes were present. No side effects were noted. Further studies employing greater numbers of patients and higher doses are required to confirm the efficacy of gangliosides in diabetic neuropathy.