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Charles L Rice - One of the best experts on this subject based on the ideXlab platform.
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Rate modulation of human Anconeus motor units during high-intensity dynamic elbow extensions
Journal of Applied Physiology, 2016Co-Authors: Brianna L Cowling, Brad Harwood, David B. Copithorne, Charles L RiceAbstract:We recorded single MUFRs during a high-intensity fatiguing dynamic elbow extension task. Because of unique features, the Anconeus Muscle (an accessory elbow extensor) facilitates tracking of units ...
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in vivo measurement of fascicle length and pennation of the human Anconeus Muscle at several elbow joint angles
Journal of Anatomy, 2014Co-Authors: Daniel E Stevens, Cameron B Smith, Brad Harwood, Charles L RiceAbstract:Ultrasound imaging has facilitated the reliable measure of the architectural variables fascicle length (LF) and pennation angle (PA), at rest and during static and dynamic contractions in many human skeletal Muscles in vivo. Despite its small size and very modest contribution to elbow extension torque, the Anconeus Muscle has proven a useful model for the study of neuromuscular function in health and disease. Recent single motor unit (MU) studies in the Anconeus have reported discrete and identifiable individual trains of MU potentials from intramuscular electromyography (EMG) recordings during dynamic elbow extensions. It is unknown whether the Anconeus has unique architectural features related to alterations in LF and PA throughout the elbow joint range of motion that may help explain these high-quality recordings. Previous anatomical studies have investigated this Muscle in cadavers and at mainly one elbow joint angle. The purpose of this study was to measure in vivo PA and LF of the Anconeus Muscle in a relaxed state at different degrees of elbow flexion using ultrasonography. Ultrasound images were collected from 10 healthy males (25 ± 3 years) at 135°, 120°, 90°, 45°, and 0° of elbow flexion. Average values of LF decreased by 6 mm (10%), 6 mm (12%), and 4 mm (9%) from 135–120°, 120–90°, and 90–45° of elbow flexion, respectively, whereas average PA values increased by 1° (9%), 1° (8%), and 2° (14%) from 135–120°, 120–90°, and 45–0°, respectively. The results indicate that Anconeus Muscle architecture is dynamic, undergoing moderate changes with elbow joint excursion that are similar to other limb Muscles reported elsewhere. The data obtained here are more comprehensive and representative of architectural changes at various elbow joint positions than those data reported in cadaveric studies. Furthermore, the results of this study indicate that despite experiencing similar relative changes in Muscle architecture to other skeletal Muscles about the elbow joint, the minimal absolute changes in LF of the Anconeus likely contribute to the clarity of intramuscular EMG previously reported in this Muscle.
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Reduced motor unit discharge rates of maximal velocity dynamic contractions in response to a submaximal dynamic fatigue protocol
Journal of Applied Physiology, 2012Co-Authors: Brad Harwood, I. Choi, Charles L RiceAbstract:Fatigability is highly task dependent wherein motor unit (MU) discharge rates and recruitment thresholds are affected differently depending on whether contractions are performed at maximal or submaximal intensities. Although much is described for isometric tasks, the behavior of MU properties during the production of maximal velocity dynamic contractions following submaximal fatiguing contractions is unknown. In seven young men, we evaluated changes in MU recruitment thresholds and MU discharge rates of the Anconeus Muscle during both submaximal and maximal dynamic elbow extensions following a submaximal dynamic fatiguing protocol of moderate intensity to velocity task failure. Velocity and power of the maximal dynamic contractions declined ∼45 and ∼55%, respectively, but these variables were unchanged for the submaximal target velocity contractions. Discharge rates of the 12 MUs at task failure were unchanged for submaximal dynamic contractions, but were decreased ∼20% for maximal dynamic and ballistic i...
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changes in motor unit recruitment thresholds of the human Anconeus Muscle during torque development preceding shortening elbow extensions
Journal of Neurophysiology, 2012Co-Authors: Brad Harwood, Charles L RiceAbstract:Rate of torque development and the subsequent movement velocity are modulated by motor unit (MU) properties, primarily MU discharge rate and MU recruitment threshold (MURT). In isometric conditions...
Ricardo A Maselli - One of the best experts on this subject based on the ideXlab platform.
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Novel delta subunit mutation in slow‐channel syndrome causes severe weakness by novel mechanisms
Annals of Neurology, 2020Co-Authors: Christopher M. Gomez, Ricardo A Maselli, Bhupinder P. S. Vohra, Manuel F. Navedo, Joel R. Stiles, Pierre Charnet, Kelly Schott, Legier V. Rojas, John Keesey, Anthony VerityAbstract:We investigated the basis for a novel form of the slow-channel congenital myasthenic syndrome presenting in infancy in a single individual as progressive weakness and impaired neuromuscular transmission without overt degeneration of the motor endplate. Prolonged low-amplitude synaptic currents in biopsied Anconeus Muscle at 9 years of age suggested a kinetic disorder of the Muscle acetylcholine receptor. Ultrastructural studies at 16 months, at 9 years, and at 15 years of age showed none of the typical degenerative changes of the endplate associated with the slow-channel congenital myasthenic syndrome, and acetylcholine receptor numbers were not significantly reduced. We identified a novel C-to-T substitution in exon 8 of the δ-subunit that results in a serine to phenylalanine mutation in the region encoding the second transmembrane domain that lines the ion channel. Using Xenopus oocyte in vitro expression studies we confirmed that the δS268F mutation, as with other slow-channel congenital myasthenic syndrome mutations, causes delayed closure of acetylcholine receptor ion channels. In addition, unlike other mutations in slow-channel congenital myasthenic syndrome, this mutation also causes delayed opening of the channel, a finding that readily explains the marked congenital weakness in the absence of endplate degeneration. Finally, we used serial morphometric analysis of electron micrographs to explore the basis for the progressive weakness and decline of amplitude of endplate currents over a period of 14 years. We demonstrated a progressive widening and accumulation of debris in the synaptic cleft, resulting in loss of efficacy of released neurotransmitter and reduced safety factor. These studies demonstrate the role of previously unrecognized mechanisms of impairment of synaptic transmission caused by a novel mutation and show the importance of serial in vitro studies to elucidate novel disease mechanisms.
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Exome sequencing detection of two untranslated GFPT1 mutations in a family with limb-girdle myasthenia
Clinical Genetics, 2013Co-Authors: Ricardo A Maselli, Juan Arredondo, Joanna Nguyen, Marian Lara, Fiona Ng, J. M. Pham, Q. Yi, Jeffrey M. Stajich, Kristin K. McdonaldAbstract:The term ‘limb-girdle myasthenia’ (LGM) was first used to describe three siblings with proximal limb weakness without oculobulbar involvement, but with EMG decrement and responsiveness to anticholinesterase medication. We report here that exome sequencing in the proband of this family revealed several sequence variations in genes linked to proximal limb weakness. However, the only mutations that cosegregated with disease were an intronic IVS7-8A>G mutation and the previously reported 3′-UTR c.*22C>A mutation in GFPT1, a gene linked to LGM. A minigene assay showed that IVS7-8A>G activates an alternative splice acceptor that results in retention of the last seven nucleotides of intron 7 and a frameshift leading to a termination codon 13 nucleotides downstream from the new splice site. An Anconeus Muscle biopsy revealed mild reduction of the axon terminal size and postsynaptic fold simplification. The amplitudes of miniature endplate potentials and quantal release were also diminished. The DNA of the mildly affected father of the proband showed only the intronic mutation along with sequence variations in other genes potentially relevant to LGM. Thus, this study performed in the family originally described with LGM showed two GFPT1 untranslated mutations, which may cause disease by reducing GFPT1 expression and ultimately impairing protein glycosylation.
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Congenital myasthenic syndrome associated with epidermolysis bullosa caused by homozygous mutations in PLEC1 and CHRNE
Clinical Genetics, 2010Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Tahseen Mozaffar, S. Skinner, S. Yousif, Rr Davis, Jeffrey P. Gregg, Mark Sivak, Thomas KoniaAbstract:Maselli RA, Arredondo J, Cagney O, Mozaffar T, Skinner S, Yousif S, Davis RR, Gregg JP, Sivak M, Konia TH, Thomas K, Wollmann RL. Congenital myasthenic syndrome associated with epidermolysis bullosa caused by homozygous mutations in PLEC1 and CHRNE. Mutations in the plectin gene (PLEC1) cause epidermolysis bullosa simplex (EBS), which may associate with muscular dystrophy (EBS–MD) or pyloric atresia (EBS–PA). The association of EBS with congenital myasthenic syndrome (CMS) is also suspected to result from PLEC1 mutations. We report here a consanguineous patient with EBS and CMS for whom mutational analysis of PLEC1 revealed a homozygous 36 nucleotide insertion (1506_1507ins36) that results in a reduced expression of PLEC1 mRNA and plectin in the patient Muscle. In addition, mutational analysis of CHRNE revealed a homozygous 1293insG, which is a well-known low-expressor receptor mutation. A skin biopsy revealed signs of EBS, and an Anconeus Muscle biopsy showed signs of a mild myopathy. Endplate studies showed fragmentation of endplates, postsynaptic simplification, and large collections of thread-like mitochondria. Amplitudes of miniature endplate potentials were diminished, but the endplate quantal content was actually increased. The complex phenotype presented here results from mutations in two separate genes. While the skin manifestations are because of the PLEC1 mutation, footprints of mutations in PLEC1 and CHRNE are present at the neuromuscular junction of the patient indicating that abnormalities in both genes contribute to the CMS phenotype.
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Mutations in MUSK causing congenital myasthenic syndrome impair MuSK–Dok-7 interaction
Human Molecular Genetics, 2010Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Jarae J. Ng, Jennifer A. Anderson, Colette Williams, Bae J. Gerke, Betty Soliven, Robert L. WollmannAbstract:We describe a severe congenital myasthenic syndrome (CMS) caused by two missense mutations in the gene encoding the Muscle specific receptor tyrosine kinase (MUSK). The identified MUSK mutations M605I and A727V are both located in the kinase domain of MuSK. Intracellular microelectrode recordings and microscopy studies of the neuromuscular junction conducted in an Anconeus Muscle biopsy revealed decreased miniature endplate potential amplitudes, reduced endplate size and simplification of secondary synaptic folds, which were consistent with postsynaptic deficit. The study also showed a striking reduction of the endplate potential quantal content, consistent with additional presynaptic failure. Expression studies in MuSK deficient myotubes revealed that A727V, which is located within the catalytic loop of the enzyme, caused severe impairment of agrin-dependent MuSK phosphorylation, aggregation of acetylcholine receptors (AChRs) and interaction of MuSK with Dok-7, an essential intracellular binding protein of MuSK. In contrast, M605I, resulted in only moderate impairment of agrin-dependent MuSK phosphorylation, aggregation of AChRs and interaction of MuSK with Dok-7. There was no impairment of interaction of mutants with either the low-density lipoprotein receptor-related protein, Lrp4 (a co-receptor of agrin) or with the mammalian homolog of the Drosophila tumorous imaginal discs (Tid1). Our findings demonstrate that missense mutations in MUSK can result in a severe form of CMS and indicate that the inability of MuSK mutants to interact with Dok-7, but not with Lrp4 or Tid1, is a major determinant of the pathogenesis of the CMS caused by MUSK mutations.
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Mutations in LAMB2 causing a severe form of synaptic congenital myasthenic syndrome
Journal of Medical Genetics, 2008Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Jarae J. Ng, Jennifer A. Anderson, Colette Williams, H. B. Wessel, H. Abdel-hamid, Robert L. WollmannAbstract:Background: We describe a severe form of congenital myasthenic syndrome (CMS) associated with congenital nephrosis and ocular malformations caused by two truncating mutations in the gene encoding the laminin β2 subunit ( LAMB2 ). Methods and results: Mutational analysis in the affected patient, who has a history of a serious untoward reaction to treatment with acetylcholinesterase inhibition, revealed two frame-shifting heteroallelic mutations, a maternally inherited 1478delG and a paternally inherited 4804delC . An Anconeus Muscle biopsy demonstrated a profound distortion of the architecture and function of the neuromuscular junction, which was strikingly similar to that seen in mice lacking laminin β2 subunit. The findings included: pronounced reduction of the axon terminal size with encasement of the nerve endings by Schwann cells, severe widening of the primary synaptic cleft and invasion of the synaptic space by the processes of Schwann cells, and moderate simplification of postsynaptic folds and intact expression of the endplate acetylcholinesterase. The endplate potential quantal content was notably reduced, while the frequencies and amplitudes of miniature endplate potentials were only moderately diminished and the decay phases of miniature endplate potentials were normal. Western blot analysis of Muscle and kidney tissue and immunohistochemistry of kidney tissue showed no laminin β2 expression. Conclusion: This case, which represents a new type of synaptic CMS, exemplifies the wide variability of phenotypes associated with LAMB2 mutations and underscores the fundamental role that laminin β2 plays in the development of the human neuromuscular junction.
Brad Harwood - One of the best experts on this subject based on the ideXlab platform.
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Rate modulation of human Anconeus motor units during high-intensity dynamic elbow extensions
Journal of Applied Physiology, 2016Co-Authors: Brianna L Cowling, Brad Harwood, David B. Copithorne, Charles L RiceAbstract:We recorded single MUFRs during a high-intensity fatiguing dynamic elbow extension task. Because of unique features, the Anconeus Muscle (an accessory elbow extensor) facilitates tracking of units ...
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in vivo measurement of fascicle length and pennation of the human Anconeus Muscle at several elbow joint angles
Journal of Anatomy, 2014Co-Authors: Daniel E Stevens, Cameron B Smith, Brad Harwood, Charles L RiceAbstract:Ultrasound imaging has facilitated the reliable measure of the architectural variables fascicle length (LF) and pennation angle (PA), at rest and during static and dynamic contractions in many human skeletal Muscles in vivo. Despite its small size and very modest contribution to elbow extension torque, the Anconeus Muscle has proven a useful model for the study of neuromuscular function in health and disease. Recent single motor unit (MU) studies in the Anconeus have reported discrete and identifiable individual trains of MU potentials from intramuscular electromyography (EMG) recordings during dynamic elbow extensions. It is unknown whether the Anconeus has unique architectural features related to alterations in LF and PA throughout the elbow joint range of motion that may help explain these high-quality recordings. Previous anatomical studies have investigated this Muscle in cadavers and at mainly one elbow joint angle. The purpose of this study was to measure in vivo PA and LF of the Anconeus Muscle in a relaxed state at different degrees of elbow flexion using ultrasonography. Ultrasound images were collected from 10 healthy males (25 ± 3 years) at 135°, 120°, 90°, 45°, and 0° of elbow flexion. Average values of LF decreased by 6 mm (10%), 6 mm (12%), and 4 mm (9%) from 135–120°, 120–90°, and 90–45° of elbow flexion, respectively, whereas average PA values increased by 1° (9%), 1° (8%), and 2° (14%) from 135–120°, 120–90°, and 45–0°, respectively. The results indicate that Anconeus Muscle architecture is dynamic, undergoing moderate changes with elbow joint excursion that are similar to other limb Muscles reported elsewhere. The data obtained here are more comprehensive and representative of architectural changes at various elbow joint positions than those data reported in cadaveric studies. Furthermore, the results of this study indicate that despite experiencing similar relative changes in Muscle architecture to other skeletal Muscles about the elbow joint, the minimal absolute changes in LF of the Anconeus likely contribute to the clarity of intramuscular EMG previously reported in this Muscle.
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Reduced motor unit discharge rates of maximal velocity dynamic contractions in response to a submaximal dynamic fatigue protocol
Journal of Applied Physiology, 2012Co-Authors: Brad Harwood, I. Choi, Charles L RiceAbstract:Fatigability is highly task dependent wherein motor unit (MU) discharge rates and recruitment thresholds are affected differently depending on whether contractions are performed at maximal or submaximal intensities. Although much is described for isometric tasks, the behavior of MU properties during the production of maximal velocity dynamic contractions following submaximal fatiguing contractions is unknown. In seven young men, we evaluated changes in MU recruitment thresholds and MU discharge rates of the Anconeus Muscle during both submaximal and maximal dynamic elbow extensions following a submaximal dynamic fatiguing protocol of moderate intensity to velocity task failure. Velocity and power of the maximal dynamic contractions declined ∼45 and ∼55%, respectively, but these variables were unchanged for the submaximal target velocity contractions. Discharge rates of the 12 MUs at task failure were unchanged for submaximal dynamic contractions, but were decreased ∼20% for maximal dynamic and ballistic i...
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changes in motor unit recruitment thresholds of the human Anconeus Muscle during torque development preceding shortening elbow extensions
Journal of Neurophysiology, 2012Co-Authors: Brad Harwood, Charles L RiceAbstract:Rate of torque development and the subsequent movement velocity are modulated by motor unit (MU) properties, primarily MU discharge rate and MU recruitment threshold (MURT). In isometric conditions...
Robert L. Wollmann - One of the best experts on this subject based on the ideXlab platform.
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Mutations in MUSK causing congenital myasthenic syndrome impair MuSK–Dok-7 interaction
Human Molecular Genetics, 2010Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Jarae J. Ng, Jennifer A. Anderson, Colette Williams, Bae J. Gerke, Betty Soliven, Robert L. WollmannAbstract:We describe a severe congenital myasthenic syndrome (CMS) caused by two missense mutations in the gene encoding the Muscle specific receptor tyrosine kinase (MUSK). The identified MUSK mutations M605I and A727V are both located in the kinase domain of MuSK. Intracellular microelectrode recordings and microscopy studies of the neuromuscular junction conducted in an Anconeus Muscle biopsy revealed decreased miniature endplate potential amplitudes, reduced endplate size and simplification of secondary synaptic folds, which were consistent with postsynaptic deficit. The study also showed a striking reduction of the endplate potential quantal content, consistent with additional presynaptic failure. Expression studies in MuSK deficient myotubes revealed that A727V, which is located within the catalytic loop of the enzyme, caused severe impairment of agrin-dependent MuSK phosphorylation, aggregation of acetylcholine receptors (AChRs) and interaction of MuSK with Dok-7, an essential intracellular binding protein of MuSK. In contrast, M605I, resulted in only moderate impairment of agrin-dependent MuSK phosphorylation, aggregation of AChRs and interaction of MuSK with Dok-7. There was no impairment of interaction of mutants with either the low-density lipoprotein receptor-related protein, Lrp4 (a co-receptor of agrin) or with the mammalian homolog of the Drosophila tumorous imaginal discs (Tid1). Our findings demonstrate that missense mutations in MUSK can result in a severe form of CMS and indicate that the inability of MuSK mutants to interact with Dok-7, but not with Lrp4 or Tid1, is a major determinant of the pathogenesis of the CMS caused by MUSK mutations.
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Mutations in LAMB2 causing a severe form of synaptic congenital myasthenic syndrome
Journal of Medical Genetics, 2008Co-Authors: Ricardo A Maselli, Juan Arredondo, Órla Cagney, Jarae J. Ng, Jennifer A. Anderson, Colette Williams, H. B. Wessel, H. Abdel-hamid, Robert L. WollmannAbstract:Background: We describe a severe form of congenital myasthenic syndrome (CMS) associated with congenital nephrosis and ocular malformations caused by two truncating mutations in the gene encoding the laminin β2 subunit ( LAMB2 ). Methods and results: Mutational analysis in the affected patient, who has a history of a serious untoward reaction to treatment with acetylcholinesterase inhibition, revealed two frame-shifting heteroallelic mutations, a maternally inherited 1478delG and a paternally inherited 4804delC . An Anconeus Muscle biopsy demonstrated a profound distortion of the architecture and function of the neuromuscular junction, which was strikingly similar to that seen in mice lacking laminin β2 subunit. The findings included: pronounced reduction of the axon terminal size with encasement of the nerve endings by Schwann cells, severe widening of the primary synaptic cleft and invasion of the synaptic space by the processes of Schwann cells, and moderate simplification of postsynaptic folds and intact expression of the endplate acetylcholinesterase. The endplate potential quantal content was notably reduced, while the frequencies and amplitudes of miniature endplate potentials were only moderately diminished and the decay phases of miniature endplate potentials were normal. Western blot analysis of Muscle and kidney tissue and immunohistochemistry of kidney tissue showed no laminin β2 expression. Conclusion: This case, which represents a new type of synaptic CMS, exemplifies the wide variability of phenotypes associated with LAMB2 mutations and underscores the fundamental role that laminin β2 plays in the development of the human neuromuscular junction.
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Presynaptic failure of neuromuscular transmission and synaptic remodeling in EA2
Neurology, 2003Co-Authors: Ricardo A Maselli, Vanessa Dunne, Michael C. Graves, Robert W. Baloh, Robert L. WollmannAbstract:Objective: To further investigate the basis of abnormal neuromuscular transmission in two patients with congenital myasthenic syndrome associated with episodic ataxia type 2 (EA2) using stimulated single fiber EMG (SFEMG) and in vitro microelectrode studies. Methods: Two patients with genetically characterized EA2 previously shown to have abnormal neuromuscular transmission by voluntary SFEMG were studied with stimulated SFEMG and Anconeus Muscle biopsy with microelectrode studies and electron microscopy of the neuromuscular junction. Results: In vivo stimulated SFEMG showed signs of presynaptic failure, with jitter and blocking that improved with increased stimulation frequency. Additional evidence of presynaptic failure was provided by the in vitro microelectrode studies, which showed marked reduction of the end plate potential quantal content in both patients. Of note, the end plate potentials showed high sensitivity to N-type blockade with ω-conotoxin not seen in controls. The ultrastructural studies revealed some evidence of small nerve terminals apposed to normal or mildly overdeveloped postsynaptic membranes, suggesting an ongoing degenerative process. Conclusions: The authors demonstrated presynaptic failure of neurotransmission in patients with heterozygous nonsense mutations in CACNA1A . The contribution of non-P-type calcium channels to the process of neurotransmitter release in these patients likely represents a compensatory mechanism, which is insufficient to restore normal neuromuscular transmission.
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Rapsyn mutations in myasthenic syndrome due to impaired receptor clustering
Muscle & Nerve, 2003Co-Authors: Ricardo A Maselli, Constance M. Bowe, Vanessa Dunne, S.i. Pascual-pascual, Mark A. Agius, Rochelle Frank, Robert L. WollmannAbstract:Rapsyn, a 43-kDa postsynaptic protein, is essential for anchoring and clustering acetylcholine receptors (AChRs) at the endplate (EP). Mutations in the rapsyn gene have been found to cause a postsynaptic congenital myasthenic syndrome (CMS). We detected six patients with CMS due to mutations in the rapsyn gene (RAPSN). In vitro studies performed in the Anconeus Muscle biopsies of four patients showed severe reduction of miniature EP potential amplitudes. Electron microscopy revealed various degrees of impaired development of postsynaptic membrane folds. All patients carried the N88K mutation. Three patients were homozygous for N88K and had less severe phenotypes and milder histopathologic abnormalities than the three patients who were heterozygous and carried a second mutation (either L14P, 46insC, or Y269X). Surprisingly, two N88K homozygous patients had one asymptomatic relative each who carried the same genotype, suggesting that additional genetic factors to RAPSN mutations are required for disease expression. Muscle Nerve 28: 293–301, 2003
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Choline acetyltransferase mutations in myasthenic syndrome due to deficient acetylcholine resynthesis
Muscle & Nerve, 2003Co-Authors: Ricardo A Maselli, Darlene Chen, Delores Mo, Constance M. Bowe, Grace Fenton, Robert L. WollmannAbstract:The myasthenic syndrome due to abnormal acetylcholine resynthesis is characterized by early onset, recessive inheritance, and recurrent episodes of potentially fatal apnea. Mutations in the gene encoding choline acetyltransferase (CHAT) have been found to account for this condition. We have identified five patients from three independent families with features of this disease including, in four patients, a paradoxical worsening of symptoms with cold temperatures. Electrodiagnostic studies demonstrated impaired neuromuscular transmission in all patients. In vitro microelectrode studies performed in the Anconeus Muscle biopsies of two patients showed moderate reduction of quantal release. Electron microscopy of the neuromuscular junction was normal in both patients. Each patient had two heterozygous CHAT mutations including L210P and P211A (family 1), V194L and V506L (family 2), and R548stop and S694C (family 3). Three of these mutations have previously been reported and suggest that, in this syndrome, some molecular defects may be more prevalent than others. Muscle Nerve 27: 180–187, 2003
C. L. Rice - One of the best experts on this subject based on the ideXlab platform.
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Motor unit discharge rates of the Anconeus Muscle during high-velocity elbow extensions
Experimental Brain Research, 2011Co-Authors: B. Harwood, A. W. Davidson, C. L. RiceAbstract:Motor unit recruitment and motor unit discharge rate (MUDR) have been widely studied in isometric conditions but minimally during velocity-dependent contractions. For isometric contractions, surface electromyography (EMG) activity of the elbow extensors plateaus at near maximal torques (Le Bozec et al. 1980 ; Le Bozec and Maton 1982 ). One study (Maton and Bouisset 1975 ) recorded single motor unit (MU) activity at maximal velocities; however, only the rate of the first interspike interval (ISI) was reported and likely was not representative of the average MUDR of the MU train. The purpose was to calculate average MUDRs of the Anconeus during loaded velocity-dependent contractions from zero velocity (isometric) up to maximal velocity (V_max25) through a large range of motion. A Biodex dynamometer was used to record elbow extension torque, position, and velocity. Single MU potentials were collected from the Anconeus with intramuscular EMG, and surface EMG was sampled from the lateral head of the triceps brachii during maximal voluntary isometric contractions (MVCs) and velocity-dependent contractions loaded at 25% MVC over 120° range of motion at five target velocities (0, 25, 50, 75, 100%V_max25). Elbow extension velocities ranged from 93 to 494°/s and average MUDR ranged from 11.8 Hz at 25%MVC to 39.0 Hz at 100%V_max25. Overall average MUDRs increased as a function of velocity, although the root mean square of triceps brachii surface EMG plateaued at 50%V_max25. Piecewise regression analysis revealed two distinct linear ranges each described by a unique equation, suggesting that MUDRs of the Anconeus enter a secondary range of firing, characterized by a steeper slope as velocity approaches maximum.
