bluuebunny/crossref_metadata_2025_split huggingface dataset:
Sensory group la proximal conduction velocity
Authors: Eisen Andrew , Hoirch Maureen , White James , Calne Donald 
Published: January 2005

AbstractThe fastest median and ulnar velocities derived by recording motor and mixed nerve action potentials, F waves, H‐reflexes, and somatosensory evoked potentials (SEPs) were compared. H‐reflex recording was facilitated by employing selective group la excitation during voluntary muscular contraction. Mixed nerve, SEP, and H velocities, considered to predominantly reflect group la conduction, measured 63.2 ± 3.2 m/sec, 63.4 ± 4.5 m/sec, and 67.2 ± 4.3 m/sec, respectively, between the wrist and elbow. Conventional motor conduction velocity was significantly slower (58.3 ± 5.1 msec), but F velocity, which although nonuniform is also a measure of motor conduction, was 68.4 m/sec. Mean F latency was considered more reliable and representative than minimum F latency. F and H velocities accelerated proximally by 4.5 m/sec. They complement each other when evaluating motor and sensory group la conduction. The H‐reflex and SEP use identical stimulus characteristics and when simultaneously recorded allow direct comparison of the fastest conducting peripheral and central sensory pathways.
Nifedipine relieves exercise‐exacerbated myalgias
Authors: Sufit Robert L. , Peters Henry A. 
Published: January 2005

AbstractThree women with exercise‐exacerbated myalgias refractory to usual medications are described who responded favorably when the calcium channel blocker, nifedipine, was administered. The side effects were dose‐related and prevented complete resolution of the symptoms. Three potential mechanisms of action are suggested for these effects.
An insulin receptor defect in murine muscular dystrophy
Authors: Hofmann William W. 
Published: January 2005

AbstractA study has been made of the I125 insulin binding and postbinding effects on excised soleus muscles from the 129 ReJ strain of dystrophic mice. Results are compared with those in sex‐ and weight‐matched controls. The data suggest that, in the range of physiological hormone concentrations, the affinity of insulin receptors on dystrophic muscles is less than normal and that the insulin‐dependent uptake of both 2‐deoxyglucose (2‐DG) and aminoisobutyric acid (AIB) is impaired. These findings are taken to indicate that many of the biochemical and electrophysiological abnormalities observed in murine dystrophy could arise from some genetic defect in the receptor proteins controlling uptake of raw materials.
Conduction block in compression neuropathy: Recognition and quantification
Authors: Olney Richard K. , Miller Robert G. 
Published: January 2005

AbstractPrevious reports of conduction block in compression neuropathy have used the amplitude difference of the compound muscle action potential (CMAP) comparing proximal with distal stimulation. The present study was undertaken to determine if area reduction of the proximal CMAP provides diagnostic information that is not included in amplitude reduction, particularly in distinguishing conduction block from temporal dispersion. Digitized, integrated area measurements were compared with amplitude and, as a convenient estimate of area, the calculated Mindex (1/2 duration x amplitude). Amplitude reduction did not reliably distinguish conduction block from temporal dispersion in compression neuropathy. Both in the investigation of conduction block and in the management of compression neuropathy, integrated area measurement allows for the more accurate identification and quantification of conduction—a usually reversible cause for weakness in compression neuropathy.
The interaction of unregulated actin and myosin in avian muscular dystrophy
Authors: Feit Howard , Farrell Cathy 
Published: January 2005

AbstractThe presence of an altered form of the heavy chain component of myosin subfragment‐1 (S‐1) in avian dystrophic pectoral muscle was confirmed by Triton‐urea‐acetic acid polyacrylamide gel electrophoresis. The potential functional significance of this altered form of S‐1 was evaluated by measuring the ATPase activity of the unregulated acto‐S‐1 complex using all possible pairwise combinations of actin and S‐1 from normal (N) and dystrophic (D) muscle. (NN, DD, ND, DN, where the first letter designates the actin and the second letter the S‐1). With conventionally purified actin and S‐1, NN ≠ DD ≠ ND ≠ DN, implying both N actin ≠ D actin and N S‐1 ≠ D S‐1 functionally. An alternate purification scheme for atin resulted in preparations from normal and dystrophic muscles of actin Mg‐polymers with the same rheology (viscosity vs shear rate) and critical concentration for polymerization. When these actins were combined with more highly purified preparations of S‐1, the adenosine triphosphatase (ATPase) activity of the acto‐S‐1 complex did not vary with changes in the pairwise composition and responded similarly to variation of the actin or adenosine triphosphate (ATP) concentration. In experiments with actin activation of intact myosin, no differences were observed between myosin from normal vs dystrophic muscle. The different isozymes of myosin present in normal and dystrophic chicken pectoral muscles are functionally equivalent as ATPases in their interactions with unregulated actin.
Muscle development in mdx mutant mice
Authors: Dangain Josette , Vrbova Gerta 
Published: January 2005

AbstractMechanical and contractile properties of tibialis anterior (TA) muscles from X‐linked muscular dystrophic (mdx) mutant mice at different stages of development are compared to those of muscles from normal control animals. There is no difference between the tension output, speeds of contraction and relaxation, and weight of TA muscles from mutant adults and normal control animals. However, it is found that in 3–4‐week‐old mutant animals, tension output and muscle weight are very much reduced and half relaxation time is prolonged. Thus, during this stage of development, muscles from mdx mice do not function properly. Histological examination of these muscles provides further evidence that, in these animals, rapid muscle destruction occurs at a particular time of development and that it is followed by complete recovery. This new mutant therefore presents an interesting case of muscle destruction and rapid regeneration. However, it is not an adequate model for Duchenne muscular dystrophy.
Granular nuclear inclusion body disease: Fine structure of tibial muscle and sural nerve
Authors: Schröder Johann Michael , Krämer Klaus Günter , Hopf Hanns Christian 
Published: January 2005

AbstractFine granular (hyaline) intranuclear inclusion bodies were found in perivascular cells of a muscle and a sural nerve biopsy from a 32‐year‐old woman with slowly progressive motor disturbances. The hyaline nuclear inclusion bodies could be distinguished from other intranuclear hyaline inclusions by their granularity, the size of the granules (approximately 5–15 nm), and the positive iron staining reaction. They were not seen in muscle fibers or Schwann cells. Because of these apparently pathognomonic structural features the patient appears to present a condition that has not been described before.
Passive transfer of the Lambert‐Eaton myasthenic syndrome: Neuromuscular transmission in mice injected with plasma
Authors: Kim Yong I. 
Published: January 2005

AbstractMice were given 1 to 67 daily injections of whole plasma from a control subject and a patient with the Lambert‐Eaton myasthenic syndrome (LES), and the parameters of neuromuscular transmission in diaphragm muscles were studied in vitro. In animals that received 41 to 59 injections of LES plasma, mean quantum content of the endplate potentials, as measured under the conditions of low [Ca2+]0 (1.2 mM) and high [Mg2+]0 (10 mM), was reduced to 30% of the control, or 40% of the value found in normal untreated mice. When [K+]0 was elevated from 5 mM to 17.5 mM, the frequency of spontaneous miniature endplate potentials increased by a factor of 98 and 105 respectively in the control and normal mice but only 39 times in the LES plasma recipients. Despite these presynaptic abnormalities, no evidence of postsynaptic deficit, nerve conduction failure, or inability of the muscle fibers to produce normal action potentials was found. These electrophysiologic features in mice thus represent a reproduction of the human condition, supporting the concept of humoral involvement in the pathophysiology of LES. Passively transferred LES in mice is a faithful animal model of the human disease which will be useful in exploring the molecular basis of the presynaptic impairment.
Morphometric anlysis of intramuscular nerves
Authors: Madriaga Evelyn P. , Osame Mitsuhiro , Fukuoka Tadahiro , Sato EiiChi , Gamez Gilberto L. , Igata Akihiro 
Published: January 2005

AbstractIntramuscular nerves were obtained at autopsy from five adult controls and were morphometrically analyzed. The number of myelinated fibers was directly proportional to the diameter of the fascicles. The fascicles were grouped into six sizes according to diameter. For each group, the normal range of distribution of the number of myelinated fibers could be estimated. Fiber size distribution and myelinated fiber density were also calculated. A unimodal fiber size distribution was observed for the small fascicles (<50m̈m in diameter), and bimodal pattern was observed for the large fascicles. Total myelinated fiber density was high in the small fascicles, and it decreased as the fascicles became larger in size, approaching the values observed In the large peripheral nerves. This study will be helpful in objectively evaluating morphological changes of intramuscular nerves in adult neuromuscular disorders.
Basement membrane component changes in nerve allografts and isografts
Authors: Gulati Adarsh K. , Zalewski Andrew A. 
Published: January 2005

AbstractThis study describes immunocytochemical changes in laminin, which is an integral basement membrane (BM) component, during axonal regeneration through antigenic nerve allografts and nonantigenic nerve isografts. In normal rat nerve, laminin was localized in the BM of Schwann cells and the perineurium. During nerve allograft rejection, the perineurium and Schwann cells disappeared. However, the Schwann cell BMs persisted and became distorted and collapsed. In isografted nerves, the perineurium and Schwann cells were present, and only a few Schwann cell BMs appeared to be distorted; however, the staining for laminin was faint, indicating a possible BM breakdown. A new BM appeared as small rings around the Schwann cells after they had become associated with regenerated axons. Because only a limited axonal regeneration occurred in allografts as compared to isografts, it is concluded that the viable Schwann cells, and their BM architecture, are essential for regeneration through long nerve grafts.
Rabies virus binding to cellular membranes measured by enzyme immunoassay
Authors: Lentz Thomas L. , Chester Janice , Benson Robin J. J. , Hawrot Edward , Tignor Gregory H. , Smith Abigail L. 
Published: January 2005

AbstractThe binding of rabies virus to cellular membranes was measured using an enzyme‐linked immunosorbent assay (ELISA). Virus binding to membranes adsorbed to the wells of microtiter plates was detected with rabies virus antibody and alkaline phosphatase‐linked second antibody. The greatest degree of binding was to myotube, neuroblastoma, and salivary gland membranes; intermediate levels occurred in striated muscle and nerve membranes; and low levels of binding were found in other membranes, including those of most parenchymal organs. Binding of rabies virus to myotube membranes was saturable, dependent on pH (with an optimum of pH 6.0), facilitated by the divalent cations Ca++, Mn++, and Mg++, and was temperature dependent. Binding was greatly reduced by inactivation of virus with β‐propiolactone or treatment of virus with trypsin. In embryonic chick myotubes, total acetylcholine receptor content and acetylcholinesterase activity undergo marked changes during development, first increasing and then decreasing at the time of hatching. Binding of rabies virus followed a similar pattern, indicating that the virus may interact with the acetylcholine receptor or other surface molecules undergoing similar developmental changes.
Contribution of the Na+‐K+ pump to membrane potential in familial periodic paralysis
Authors: Martin A. Robert , Levinson S. Rock 
Published: January 2005

AbstractThe possibility has been raised that in familial periodic paralysis, the relatively large depolarization of the muscle fiber membrane seen during periods of paralysis might be attributable to a reduction in activity of the electrogenic Na+‐K+ pump. The theoretical analysis presented here shows that although such hypotheses are qualitatively correct, the quantitative contribution of the electrogenic pump is too small to account entirely for the changes in membrane potential observed between the paralytic and interictal states.
Surface recording of orthodromic sensory nerve action potentials in median and ulnar nerves in normal subjects
Authors: Andersen Kjeld 
Published: January 2005

AbstractReference values of sensory nerve compound action potentials (CAP) were established in 50 healthy subjects by examination with surface electrodes placed in a transverse and a longitudinal position at the wrist. Longitudinal electrodes record potentials of larger amplitude and shorter duration than transversally recorded CAPs. Both amplitude and duration were increased by an increase of interelectrode distance. The use of amplitude and duration as variables is encouraged by the well‐defined biologic variation obtained when fixed interelectrode distance is used and when values are corrected for age and temperature. The strong correlation between amplitude and duration might indicate that the decrease of amplitude with age is caused by the reduction of conduction velocity rather than axonal loss. The ulnar nerve CAPs differ from those of the median nerve mostly with regard to influence of age and temperature. The reasons for this are discussed.
Mononeuropathy multiplex (AAEE case report #11)
Authors: Parry Gareth J. G. 
Published: January 2005

AbstractMononeuropathy multiplex is a syndrome of diverse causes, the most common of which is nerve ischemia due to microangiopathy associated with diabetes or the collagen‐vascular diseases. The acquired inflammatory demyelinating neuropathies invariably are multifocal, although the clinical manifestations of these and other multifocal neuropathies may appear symmetrical. The identification of multifocal neuropathies is important because of the frequent therapeutic implications. A case of mononeuropathy multiplex associated with polyarteritis nodosa is described.
Endoneurial injection of antisera to myelin antigens
Authors: Hughes Richard A. C. , Powell Henry C. , Braheny Sherry L. , Brostoff Steven 
Published: January 2005

AbstractWhen antisera to purified myelin antigens were injected into rat sciatic nerves, some produced significant demyelination, whereas others merely induced an inflammatory infiltrate. Extensive demyelination was produced by antisera to galactocerebroside and the peripheral nerve glycoprotein P0. Demyelination resulting from injections of antisera to ganglioside GM1, P2, myelin basic protein, sulfatide, and glucocerebroside did not exceed that produced by normal rabbit serum. Addition of guinea pig complement had no effect. It is of interest that the greatest demyelination followed injection of antisera to two molecules, galactocerebroside and P0, the main antigenic determinants of which present at the Schwann cell surface.
The relation between blood lactate and ammonia in ischemic handgrip exercise
Authors: Sinkeler Sytze P. T. , Daanen Hein A. M. , Wevers Ron A. , Oei T. Lian , Joosten Ed M. G. , Binkhorst Rob A. 
Published: January 2005

AbstractSubjects with myopathies associated with certain enzyme defects often show abnormal concentrations of lactate (LA) and ammonia (NH3) in blood after ischemic exercise. Myoadenylate deaminase (MAD) deficient patients produce only small amounts of NH3, whereas LA rises to normal levels. On the other hand, patients with certain enzyme deficiencies in the glyco(geno)lytic pathway show the opposite. However, the concentrations in blood are dependent on the exercise performed. Standardization of tests for screening purposes, therefore, is necessary. For ischemic contractions, experiments were performed to find the optimal combination for force and frequency, using the highest LA and NH3 concentrations in blood as criteria. Eleven healthy subjects performed ischemic isometric contractions with a handgrip dynamometer at frequencies of 30 and 50/min−1 and force levels of 50%, 65%, and 80% of maximal voluntary contraction (MVC). A combination of 30/min−1 and 80% MVC was found to give the best results.
Mitral valve prolapse in myotonic dystrophy
Authors: Streib Erich W. , Meyers David G. , Sun Sallie F. 
Published: January 2005

AbstractForty‐three patients with myotonic dystrophy (MyD) and 43 age‐ and sex‐matched controls were prospectively evaluated for mitral valve prolapse (MVP) using both cardiac auscultation and echocardiography (ECHO). Prevalence of MVP was significantly increased in MyD patients when using either abnormal auscultation plus abnormal ECHO (23.3%, P < 0.02) or abnormal ECHO alone (30%, P < 0.01) as diagnostic criteria for MVP. Frequency of MVP was even more increased in patients with a thin, flat chest compared with patients with normal physical appearance (P < 0.007). These findings are in support of the concept that the increased frequency of MVP in neuromuscular disorders is likely due to geometrical changes of the heart caused by thorax deformities, rather than structural changes of the mitral valve. For this reason, MVP in MyD probably belongs to the entity of so‐called benign, secondary MVP. This is further supported by the absence of symptoms of “systemic” complications of MVP in our patient population.
Postnatal histochemical fiber type differentiation in normal and hypothyroid rat soleus muscle
Authors: Sugie Hideo , Verity M. Anthony 
Published: January 2005

AbstractWe have analyzed the effect of 6‐propylthiouracil‐induced hypothyroidism on neonatal fiber type differentiation in the rat soleus muscle. Body weight, total soleus fiber number, histochemical fiber type differentiation, and morphometry were determined at 7, 14, 21, and 28 days. Neonatal hypothyroidism (1) inhibits the apparent ∼50% increase in soleus muscle fiber number occurring at 14–21 days, (2) blocks the transformation of type 2C to type 2A fibers occurring between 14 and 21 days, (3) preferentially inhibits the increase in type 2 fiber diameter, and (4) retards the development of sarcoplasmic reticulum. Immature muscle fibers reveal type 1 and type 2 fiber myosin adenosine triphosphatase (ATPase) differentiation at pH 10.3, which drops to pH 9.4 with maturation. No myosin ATPase differentiation was found at pH 9.4 in the hypothyroid animals, even at 28 days.
Modified methods for preparation of cryostat sections of skeletal muscle
Authors: Wu Ju‐Sung , Hogan Gwendolyn R. , Morris Jerry D. 
Published: January 2005

AbstractWe developed two modified methods for the preparation of cryostat sections of skeletal muscle: one using solid carbon dioxide and the other using the ultra‐low freezer to prepare 2‐methylbutane (isopentane) for freezing of skeletal muscle. The results were quite satisfactory, with good preservation of cellular details and histochemical properties. Freezing artifacts were minimal when compared with the standard liquid nitrogen method.
Fiber type‐specific autoantibodies in a dog with eosinophilic myositis
Authors: Shelton G. Diane , Cardinet George H. , Bandman Everett , Cuddon Paul 
Published: January 2005

AbstractSerum from a 2‐year‐old male Belgian sheepdog with eosinophilic myositis, which particularly affects the masticatory muscles, was tested for the presence of muscle‐specific autoantibodies. Control type 2 temporalis muscle fibers were selectively stained following incubation with the patient's serum and staphylococcal protein A conjugated to horseradish peroxidase (SPA‐HRPO). Likewise, type 2 fibers in the patient's temporalis muscle were selectively stained with SPA‐HRPO. The same staining procedures applied to limb muscle did not result in fiber staining. Proteins isolated from the temporalis and triceps brachii muscles of a normal dog were separated under denaturing conditions by onedimensional sodium dodecyl sulfate‐polyacrylamide gel electrophoresis. The separated proteins were transferred onto nitrocellulose paper and incubated with either sera from the patient, normal dogs, or neuromuscular disease controls. Subsequent incubation with peroxidase‐conjugated goat anti‐dog lgG demonstrated antibodies to at least four proteins of the temporalis muscle (myosin heavy chain and three unidentified proteins) when incubated with the patient's serum but not with the controls. Under all conditions, antibodies to the proteins of the triceps brachii were not detected. These findings establish the presence of autoantibodies to specific temporalis muscle proteins that may initiate the myonecrosis and inflammatory response as well as limit the distribution of the response.
Myosin transitions in chronic stimulation do not involve embryonic isozymes
Authors: Hoffman Rebecca K. , Gambke Brigitte , Stephenson Larry W. , Rubinstein Neal A. 
Published: January 2005

AbstractChronic low‐frequency stimulation of a fast skeletal muscle effects a transition of myosin isozymes from those characteristic of a fast muscle to those characteristic of a slow muscle. This transformation involves changes in both myosin heavy and light chains. During development, muscles usually change directly from embryonic to neonatal to fast or from embryonic to neonatal to slow isozymes. We have questioned whether chronic stimulation of the adult fast muscle results in a direct fast‐to‐slow isozyme shift or whether transformation requires reexpression of the developmental isozymes prior to the synthesis of adult slow isozymes. We have examined these alternatives in the chronically stimulated dog diaphragm using adenosine triphosphatase (ATPase) histochemistry, pyrophosphate gel electrophoresis of native isozymes, peptide mapping of myosin heavy chains, immunoblotting with an antibody specific to embryonic myosin heavy chain, and solid‐phase radioimmunoassay. We have demonstrated that a transition from adult fast to adult slow isozymes during chronic stimulation does not involve a recapitulation of embryonic isozymes.
A morphological/biochemical study on the actions of corticosteroids on rat skeletal muscle
Authors: Kelly Frank J. , McGrath Josephine A. , Goldspink David F. , Cullen Michael J. 
Published: January 2005

AbstractFour corticosteroid hormones were administered (5 mg/kg/day) to rats over 6 to 10 days. Both biochemical and microscopic techniques were employed to determine the influence of these corticosteroids on the fine structure and growth of five striated muscles. Throughout, dexamethasone and triamcinalone were more potent than prednisone or cortisone in influencing muscle growth. The corticosteroids' action on the heart was anabolic, increasing its RNA and protein content. In contrast, the same corticosteroids were catabolic against fast‐twitch muscles (e.g., extensor digitorum longus), inducing appreciable atrophy. However, slow‐twitch muscles (e.g., soleus) were more resistant to these hormones, exhibiting an intermediate response between that of the heart and fast‐twitch muscles. Only minor morphological changes were found in both fast and slow muscles 10 days after the corticosteroid treatments. The hormones′ atrophic effects on skeletal muscle primarily arose from the corticosteroid's ability to inhibit protein synthesis, via decreases in the muscles′ ribosomal capacities. Whole‐body protein synthesis was also suppressed by these corticosteroids, but to a lesser extent than in the whole skeletal musculature.