bluuebunny/crossref_metadata_2025_split huggingface dataset:
Nerve conduction changes and fine structural alterations of extra‐ and intrafusal muscle and nerve fibers in streptozotocin diabetic rats
Authors: Weis Joachim , Schröder J. Michael , Dimpfel Wilfried 
Published: January 2005

AbstractStreptozotocin‐induced diabetes mellitus in known to cause a reduction of both conduction velocity and axon caliber in sciatic nerves and also a decrease in muscle fiber size. The present study investigates whether the distal parts of the peripheral nervous system, including extra‐ and intrafusal muscle fibers, are more severely affected than the proximal segments in the diabetic state. Proximal and distal sensory nerve conduction velocities were monitored during a period of 3 months in rats rendered diabetic by injection of streptozotocin. Segments of the sciatic and ventral coccygeal nerves, and of the biceps femoris and lumbrical muscles, were studied by light and electron microscopy, including morphometric analysis. In contrast to previous studies, daily suboptimal insulin injections were given to prevent acute metabolic complications. Sensory conduction velocity in the ventral coccygeal nerve was significantly (P > 0.05) decreased in the diabetic rats compared to controls. Proximal and distal nerve segments were equally affected. Mean cross‐sectional axon area of the sciatic nerve was moderately, but significantly (P < 0.05), smaller in insulin‐treated diabetic rats than in controls. In both the sciatic nerve and the terminal, intrafusal nerve segments, occasional axons showed moderate dystrophic changes. Fibers of the intrafusal nerve segments appeared to be equally affected compared to the fibers in the sciatic nerve, although no quantitative comparison was made. The increase of small caliber skeletal muscle fibers in experimental streptozotocin‐induced diabetes was confirmed. These findings indicate that proximal and distal segments of peripheral nerves are affected equally in the early stages of experimental diabetic neuropathy.© 1995 John Wiley &Sons, Inc.
Classic neurogenic thoracic outlet syndrome in a competitive swimmer: A true scalenus anticus syndrome
Authors: Katirji Bashar , Hardy Russell W. 
Published: January 2005

AbstractNeurogenic thoracic outlet syndrome (TOS) is caused by compression of the lower branchial plexus usually by a cervical rib or a fibrous band. We describe a 16‐year‐old girl with weakness and wasting of her right hand, which progressed over the ensuing years. She had been a competitive long distance freestyle and butterfly swimmer since age 8 years. A neurological exam at age 20, revealed severe atrophy and weakness of all intrinsic right hand muscles, more so of the thenar muscles, and hypesthesia along the ulnar aspect of the hand and forearm. EMG, which showed a severe chronic axon loss lower trunk brachial plexopathy with minimal fibrillations, was typical for classic neurogenic TOS. Chest and cervical spine X‐rays and MRI of the cervical spine were normal. A supraclavicular exploration confirmed the absence of a cervical rib or band. The lower trunk was thickened under the scalenus anticus which was sectioned. Neurolysis was also done. She was advised to abandon swimming. A clinical and EMG follow‐up 2.5 years later showed no significant changes. This is the first case of true neurogenic TOS caused by scalenus anticus compression occurring in a competitive swimmer.© 1995 John Wiley &Sons, Inc.
Can the size principle be detected in conventional emg recordings?
Authors: Ertas Mustafa , Stålberg Erik , Falck Björn 
Published: January 2005

AbstractAccording to Henneman's size principle, small motor units are recruited before large ones. It is commonly believed that this can be detected in routine conventional EMG recordings even among the earliest recruited motor units. That is, the MUP amplitude, area, and thickness should increase with recruitment order. We studied the first four motor unit potentials (MUPs) recruited within the pickup area of the electrodes. Data were obtained from 179 different sites in monopolar recordings and in 153 concentric recordings from 5 health subjects. In the pooled material, amplitude, area, and thickness increased slightly between consecutively recruited MUPs. However, at individual recording sites the size of consecutively recruited MUPs varied considerably. At some recording sites the first recruited MUP had the largest amplitude and the later MUPs has successively smaller amplitudes. We conclude that, at individual recording sites, the size principle cannot be detected in low threshold motor units with monopolar or concentric EMG electrodes. The reason for this is the small uptake area of these electrodes in relation to the motor unit territory. © 1995 John Wiley & Sons, Inc.
CT muscle imaging and the clinical assessment of neuromuscular disease
Authors: Swash Michael , Brown Martin M. , Thakkar Chandra 
Published: January 2005

AbstractTwenty patients with neurogenic disorders, polymyositis, or muscular dystrophies were assessed clinically and by CT imaging of limb, limb girdle, and trunk muscles, using a standard protocol. On each side of these patients 26 movements were graded by the MRC scale, and 20 muscles were assessed by CT imaging. The clinical and CT findings could be compared, in a blind evaluation, in 10 muscles on each side. A quantitative assessment of the CT muscle images were also made. The CT images showed striking abnormalities, even in many muscles of normal strength by clinical testing. Asymmetrical involvement of muscles was found in all the disorders studied, even when not suspected on clinical examination. Muscles in patients with muscular dystrophy were more abnormal than those in patients with neurogenic disorders. In polymyositis the attenuation values were intermediate to the other two groups. A “washed‐out” appearance with very low attenuation values was very suggestive of muscular dystrophy. Involvement of paraspinal and rectus abdominis muscles was uncommon in neurogenic disorders. The gracilis muscle was relatively resistant to degeneration. CT imaging can enhance the clinical assessment of patients with neuromuscular disease, often revealing unexpected abnormalities. © 1995 John Wiley & Sons, Inc.
AAEM minimonograph #16: Instrumentation and measurement in electrodiagnostic medicine–part II
Authors: Gitter Andrew J , Stolov Walter C. 
Published: January 2005

AbstractA review of instrumentation and measurement in electrodiagnostic medicine is continued in this Part II which focuses on digital instrumentation principles, gain and sweep effects, noise, nerve stimulation, and conduction measurement limitations. With the adoption of microprocessor‐based equipment, the neurophysiologic signal must undergo analog‐to‐digital conversion (ADC) before analysis and display on a video monitor. ADC resolution and sampling rates affect accuracy and measurement precision. Following waveform display, the visual assessment of latency and duration may be influenced by sweep and gain settings, often overlooked sources of error. Undesired signal or noise typically originates from power‐line interference, electronic amplifier noise, background muscle activity, or nerve stimulation artifact. Noise often interferes with clinical studies but techniques exist to reduce noise to acceptable levels in virtually all situations. An awareness and understanding of these technical issues will lead to an appreciation of the limitations of electrodiagnostic testing and improve interpretation and clinical decision‐making. © 1995 John Wiley & Sons, Inc.
High‐frequency fatigue in rat skeletal muscle: Role of extracellular ion concentrations
Authors: Cairns Simeon P. , Dulhunty Angela F. 
Published: January 2005

AbstractHigh‐frequency fatigue (HFF), the decline of force during continuous tetanic stimulation (lasting 4–40 s), was studied in isolated bundles of rat skeletal muscle fibers. HFF was slower in slow‐twitch soleus fibers than in fast‐twitch red or white sternomastoid fibers; denervation accelerated fatigue in soleus. Maximal 200‐mmol/L potassium contractures of normal amplitude were induced in fatigued fibers, suggesting that crossbridge cycling and the voltage activation of excitation–contraction coupling could still occur maximally, but that activation by action potentials was impaired. An increase in [Na+]o slowed HFF, while a small increase in [K+]o or reduction in [Cl−]o accelerated HFF. Increasing the tetanic stimulation frequency exacerbated fatigue. Recovery from HFF proceeded rapidly since force increased markedly within a few seconds when stimulation ceased. These results support the hypothesis that a redistribution of Na+, K+, and Cl− across the transverse tubular membranes during repeated action potential activity induces fatigue by reducing the amplitude and conduction of action potentials. © 1995 John Wiley & Sons, Inc.
Conduction velocity distributions compared to fiber size distributions in normal human sural nerve
Authors: van Veen Benno K. , Schellens Ronald L. L. A. , Stegeman Dick F. , Schoonhoven Ruurd , Gabreëls‐Festen Anneke A. W. M. 
Published: January 2005

AbstractCompound action potentials (CAPs) were recorded from the sural nerve of healthy volunteers. A mathematical technique (inverse modeling) was used to compute conduction velocity (CV) histograms from the data. Results were compared to the morphology of age‐matched normal sural nerve biopsies. Coefficients of variation (CoVs) revealed the statistical relationship between morphological data (diameter histograms) and electrophysiological data (CV histograms and conventional CAP parameters). No differences were found for the thick fiber group when comparing the CoVs of the diameter histogram parameters with the corresponding CV histogram parameters. Apparently, the same inherent biological interindividual variability is encountered. The CoVs of the CVs of the CAP's main phases are in good agreement with the CoVs of the estimated mean velocity of the thick fiber group. Inverse modeling increases the reliability of the estimation of the number of active fibers as compared to direct CAP amplitude interpretation.© 1995 John Wiley & Sons, Inc.
Effect of β‐endorphin on the contractile responses in mouse skeletal muscle
Authors: Khan Salim , Smith Margaret E. 
Published: January 2005

AbstractTension development in response to direct and indirect electrical stimulation was studied in an isolated phrenic nerve hemidiaphragm preparation of the mouse. β‐Endorphin (β‐EP) caused an increase in the preparation of the mouse. β‐Endorphin (β‐EP) caused an increase in the response to low frequency stimulation of the nerve. Upon direct stimulation of the muscle the peptide had no effect. The actions of β‐EP were abolished in the presence of the opioid antagonist naloxone and mimicked by β opioid agonists. Upon high frequency stimulation of the nerve, β‐EP caused an increase in the initial, maximum, and mean tension. It also prevented the fall in the final tension seen in the control preparations with repeated periods of stimulation. The findings are consistent with β‐EP having a role to improve neuromuscular function and deley fatigue, and indicate the possible therapeutic potential of opioid substances in conditions where muscle weakness is present. © John Wiley & Sons, Inc.
Myogenic cells derived from rat bone marrow mesenchymal stem cells exposed to 5‐azacytidine
Authors: Wakitani Shigeyuki , Saito Tomoyuki , Caplan Arnold I. 
Published: January 2005

AbstractThe compound 5‐azacytidine has been previously shown to convert cells of the rat embryonic fibroblastic cell line, C3H/10T1/2, into myoblasts, adipocytes, and chondrocytes. Rare, resident cells of bone marrow and periosteum, referred to as mesenchymal stem cells, have been shown to differentiate into a number of mesenchymal phenotypes including bone, cartilage, and adipocytes. Rat bone marrow‐derived mesenchymal stem cells were exposed to 5‐azacytidine beginning 24 h after seeding twice‐passaged cells into culture dishes. After an exposure of 24 h, long, multinucleated myotubes were observed in some of the dishes 7–11 days later. Cells containing Sudan black‐positive droplets in their cytoplasm were also observed. Thus, culture‐propagated rat bone marrow mesenchymal stem cells appear to have the capacity to be induced to differentiate in vitro into myogenic and adipocytic phenotypes, although nonmesenchymal cells (rat brain fibroblasts) cannot be so induced. Taken together, these observations provide support for the suggestion that mesenchymal stem cells in the bone marrow of postnatal organisms may provide a source for myoprogenitor cells which could function in clinically relevant myogenic regeneration. © 1995 John Wiley & Sons, Inc.
Applications of manganese‐enhanced magnetic resonance imaging (MEMRI) to imaging of the heart
Authors: Wendland Michael F. 
Published: January 2005

AbstractThe use of manganese‐based MRI contrast materials, either manganese salts or chelates, has spanned the entire timeframe of cardiac MRI. However interest in Mn compounds for cardiac MRI has been sporadic because of concerns over cardiotoxicity associated with significant concentration of free Mn2+ and notable success of gadolinium chelates in cardiac application. Initial strategies to overcome cardiotoxicity included chelation of Mn2+ to reduce the concentration of the free ion in vivo, and addition of Ca2+ in combination with Mn2+ to competitively reduce binding of Mn2+ to Ca2+ channels in the heart. Both approaches met with mixed success, but were subsequently discontinued in favor of gadolinium‐based approaches. However Mn2+‐based media potentially offer unique advantages for characterizing heart pathology over conventional Gd‐based contrast media because Mn2+ is taken up by heart cells and retained for hours. Cellular uptake occurs through calcium channels so contrast on delayed images may be interpreted according to regional or global functional status. Since Mn2+ is retained in the heart, Mn‐based media can be administered outside the magnet and the contrast pattern measured hours later to provide assessment of uptake. A key issue is whether sufficient accumulation of Mn2+ in heart cells for imaging can occur without cardiotoxicity, and findings to date indicate this is possible. This review examines the current status of Mn2+‐enhanced MRI of heart with particular focus on the hypothesis that Mn2+ uptake can be interpreted in terms of heart function. Copyright © 2004 John Wiley & Sons, Ltd.
Isolation and chemical nature of the receptor for d‐tubocurarine in nerve‐ending membranes of the cerebral cortex
Authors: De Robertis E. , Fiszer Sara , Pasquini Juana M. , Soto E. F. 
Published: January 2005

AbstractThe binding capacity of isolated acetylcholinesterase‐rich nerve‐ending membranes of the cat cerebral cortex for dimethyl‐14C‐d‐tubocurarine (1.5 × 10−6 M) was studied with an in vitro technique. After treatment of the membranes with organic solvents, most of the radioactivity was found in the extract and bound either to the lipids or proteolipids, but not to the gangliosides.Comparing the binding capacity per milligram of proteolipid protein of the M1 1.0 nerve‐ending fraction with that of myelin, there was a tenfold increase in specific activity in the former. This layer cromatography of a lipid extract, previously passed through Sephadex G 25 fine, showed that the radioactivity remained at the point of origin together with the proteolipids. The use of a special technique with Sephadex LH20 demonstrated that the bound dimethyl‐14C‐d‐tubocurarine was eluted together with a protein peak which had no cholesterol and negligible amounts of phospholipids.Experiments using precipitation with ether of the proteolipid protein and passage through the Sephadex LH20 column gave similar results and confirmed that the receptor properties for d‐tubocurarine may be in a special type of proteolipid present in the nerve‐ending membrane, probably at the junctional complex. These results are discussed in relation to previous attempts, reported in the literature, to isolate a cholinergic receptor.
Relationship between catecholamines and serotonin in sympathetic nerves of the rat pineal gland
Authors: Zweig Mark , Axelrod Julius 
Published: January 2005

AbstractSympathetic nerves of the pineal gland contain both serotonin and norepinephrine. Inhibition of norepinephrine synthesis with a tyrosine hydroxylase inhibitor, α‐methyl‐p‐tyrosine (αMPT), causes an elevation of pineal serotonin. The administration of dopamine or norepinephrine blocks the elevation of pineal serotonin by αMPT. When sympathetic nerves to the pineal are interrupted αMPT no longer causes a rise in pineal serotonin. Tryptophan causes a marked increase in pineal serotonin; αMPT enhances and norepinephrine blocks this rise.
Acetoxycycloheximide effect on synthesis and metabolism of glucosamine‐containing macromolecules in brain and in nerve endings
Authors: Barondes Samuel H. , Dutton Gary R. 
Published: January 2005

AbstractCarbohydrate‐containing macromolecules of brain were substantially labeled after intracerebral injection of C14‐glucosamine. The “half‐life” of the labeled macromolecules, as measured in these experiments, was about one week. Acetoxycycloheximide inhibited incorporation of C14‐glucosamine into these substances. This appears to be secondary to inhibition of synthesis of polypeptide chains which act as “acceptors” for carbohydrate residues. Acetoxycycloheximide inhibited incorporation of C14‐glucosamine (and its derivatives) into the soluble carbohydrate‐containing macromolecules of nerve endings far less than that of the other subcellular fractions of brain. This suggests that the polypeptide “acceptors” of carbohydrate residues at nerve endings are not synthesized locally but are transported to the nerve endings. Final incorporation of carbohydrates into carbohydrate‐containing macromolecules occurs at nerve endings. The “turnover” of these substances in nerve endings was found to be relatively rapid. Evidence suggesting reversible incorporation and removal of some carbohydrate residues of carbohydrate‐containing macromolecules of brain was found and the possible regulatory role of this process is considered.
Nerve electrical activity; depression by puromycin not related to inhibited protein synthesis
Authors: Dahl Nancy Ann 
Published: January 2005

AbstractPuromycin (1 mM) causes a reversible decrease in spike potential and positive after potential amplitudes of rabbit vagus nerve in vitro. This failure is independent of the rate of stimulation in contrast to the failure following sodium pump inhibition by ouabain. Puromycin does not inhibit brain Na‐K ATPase in vitro. There is no reduction in the action potential by either of the protein synthesis inhibitors, chloramphenicol or cycloheximide. Puromycin inhibits even in the presence of cycloheximide, a compound which blocks the release of abnormal polypeptides by puromycin. Puromycin aminonucleoside does not have the puromycin effect nor does dibutyryl‐cyclic‐3′,5′‐AMP protect the nerve against puromycin.Puromycin can inhibit ribosomal protein synthesis and interfere with purine metabolism but these actions do not appear to be the basis of the action potential decrease. A more likely site of action is interference with glycolipid and glycoprotein formation or a direct effect on the membrane. It is concluded that neither mitochondrial nor ribosomal protein synthesis is critical to the short term maintenance of the action potential.
Neuroplasmic transport in the nervous system of the cockroach Periplaneta americana
Authors: Smith Barry H. 
Published: January 2005

AbstractNeuroplasmic transport phenomena were studied in the nervous system of the cockroach, Periplaneta americana. For proteins, at least two major rates of movement can be resolved by liquid scintillation counting of incorporated C14‐labelled amino acids in serial slices of nerve cord. The slower of the two rates is 1−2 mm/day and appears identical to the “slow” flow well documented for vertebrate neurons. Evidence for an even faster movement is presented.The suitability of the cockroach nerve cord as a model system for the study of the mechanism and control of the movement of the neuroplasmic constituents is discussed.
Post mortem changes in the content and specific radioactivity of several amino acids in four areas of the rat brain
Authors: Shank R. P. , Aprison M. H. 
Published: January 2005

AbstractThe contents of alanine, aspartate, GABA, glutamate, glutamine, glycine, serine, and lactic acid were measured in the cerebral hemispheres, midbrain, cerebellum, and pons‐medulla of rats killed by immersion into liquid nitrogen or by decapitation. The head of each decapitated rat was frozen as described. Only in the cases of lactic acid, alanine and GABA were marked post‐mortem changes observed within a few minutes after death. In rats killed 7 and 15 min after an intraperitoneal injection of (U−14C) glucose, there was a post‐mortem increae in the specific activity of GABA relative to glutamate. These post‐mortem changes in GABA support the idea that of the carbon units oxidized via the tricarboxylic acid cycle approximately 10% pass through the GABA bypath. These data are also consistent with the view that multiple pools of both glutamate and GABA exist in brain tissue.
Subcellular fractionation of cultured glial cells
Authors: Cotman C. , Herschman H. , Taylor D. 
Published: January 2005

AbstractWe have studied the subcellular fractionation of a clonal line of glial cells from rat brain. In comparison to rat brain, more of the total protein is collected in the crude nuclear fraction following differential centrifugation. When a crude mitochondrial fraction is prepared and resolved on a density gradient, we find that like brain the glial cell crude mitochondrial fraction is also heterogenous. On a sucrose density gradient, such as that used for the preparation of synaptosomes, the glial cell crude mitochondrial fraction resolves into two major fractions. One of these bands sediments to the same isopycnic density as synaptosomes. This fraction contains 20% of the protein, and 50% of the Na‐K ATPase and acid phosphatase of the crude mitochondrial fraction, but virtually no cytochrome oxidase or choline esterase. The fraction consists of numerous membrane structures resembling plasma membranes when examined by electron microscopy. Because the sedimentation properties of the glial membranes are very similar to synaptosomes, we conclude that synaptosomes prepared on sucrose gradients are probably contaminated by these membrane fragments. In contrast to the separation achieved on sucrose gradients, glial membranes separate from synaptosomes on Ficoll‐sucrose gradients.
Re‐Innervation of smooth muscle of the vas deferens transplanted into the anterior chamber of the eye
Authors: Malmfors T. , Furness J. B. , Campbell G. R. , Burnstock G. 
Published: January 2005

AbstractPieces of vas deferens were transplanted into the anterior chamber of the eye in guinea pigs. The transplants were observed in vivo and then removed and examined with cellular methods. Changes occurring in smooth muscle cells and in nerves were examined with the electron microscope and with the fluorescence histochemical method. Neuromuscular transmission in the transplant was examined with microelectrode and organ bath methods. Four main phases were distinguished in transplants between 2 days and 14 weeks (the oldest transplants examined): (1) initial degeneration of nerves and muscles; (2) vascularization followed by the onset of regeneration of muscle at 3 to 4 days; (3) re‐innervation by nerves from the iris and muscle‐bundle formation beginning at 1 to 2 weeks; (4) restitution of functional neuromuscular transmission beginning at about 4 weeks. The number of adrenergic nerves grandually increased, but even at 14 weeks, the overall density was less than in a normal adult preparation. Nevertheless, neuromuscular transmission was comparable to that in a normal vas deferens. The factors involved in the regeneration of single muscle fibers, the formation of muscle bundles and neuromuscular relationships, and the regulation of reinnervation density are discussed.