The Experts below are selected from a list of 285 Experts worldwide ranked by ideXlab platform
Alfredo Gorio - One of the best experts on this subject based on the ideXlab platform.
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Muscle Reinnervation and IGF-I synthesis are affected by exposure to heparin: an effect partially antagonized by anti-growth hormone-releasing hormone.
Neurochemical research, 2003Co-Authors: L. Madaschi, Anna Maria Di Giulio, Alfredo GorioAbstract:Sciatic nerve crush was performed in 2-day-old rats, then Reinnervation of the extensor digitorum longus muscle, motor neuron survival, and muscle IGF-I production were monitored. In saline-treated rats, the extent of Reinnervation was around 50% and the number of EDL reinnervating motor neurons was significantly reduced. In heparin-treated rats the extent of muscle Reinnervation, the recovery of nerve-evoked muscle twitch tension, and the number of motor neurons reinnervating the extensor digitorum longus muscle were greatly enhanced compared to saline-treated rats. In addition, treatment with heparin increased markedly insulin-like growth factor-I levels in denervated muscles. The concomitant exposure to anti-growth hormone releasing hormone partially abolished the stimulatory action of heparin on muscle Reinnervation and prevented the increase of insulin-like growth factor-I muscle levels.
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Glycosaminoglycan-promoted muscle Reinnervation and insulin-like growth factor-I levels are affected by anti-growth hormone-releasing hormone exposure.
Journal of neuroscience research, 2001Co-Authors: Alfredo Gorio, Eugenio E. Müller, Carmen Citterio, Anna Maria Di GiulioAbstract:The present study shows that exposure to antibodies to growth hormone-releasing hormone (GHRH) partially counteracted the promoting effects of treatment with glycosaminoglycans (GAGs) on muscle Reinnervation. Sciatic nerve crush was performed in 2-day-old rats, and Reinnervation of the extensor digitorum longus muscle was monitored. The extent of Reinnervation was rather poor in saline-treated rats, whereas in GAG-treated rats the extent of muscle Reinnervation, the recovery of nerve-evoked muscle twitch tension, and the number of motor neurons reinnervating the extensor digitorum longus muscle were greatly enhanced. In addition, treatment with glycosaminoglycans increased markedly insulin-like growth factor-I (IGF-I) levels in denervated muscles. Both types of stimulatory action exerted by GAGs were affected by concomitant exposure to anti-GHRH, with abolition of IGF-I muscle increase and a smaller enhancement in muscle Reinnervation. J Neurosci. Res. 66:1112–1117, 2001. © 2001 Wiley-Liss, Inc.
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Muscle Reinnervation following neonatal nerve crush. Interactive effects of glycosaminoglycans and insulin-like growth factor-I
Neuroscience, 1998Co-Authors: Alfredo Gorio, L. Vergani, A.m. Di Giulio, A De Tollis, Antonio Torsello, Lorena Cattaneo, E. E. MüllerAbstract:This study shows that glycosaminoglycans promote muscle Reinnervation following neonatal sciatic nerve injury. Such an effect appears to be mediated by insulin-like growth factor-1. The glycosaminoglycan moiety of proteoglycans is a constituent of the basal lamina active on nerve regeneration by means of the interaction with laminin and with several growth factors. We have previously shown that supplementation of glycosaminoglycans affects neuronal degeneration and regeneration. In this study we report that following neonatal lesion of the rat sciatic nerve glycosaminoglycan treatment promoted extensor digitorum longus muscle Reinnervation with consequent improvement of muscle morphology. In saline-treated rats, Reinnervation was only partial and there was a marked muscle fibre atrophy. In addition glycosaminoglycan treatment of lesioned rats increased insulin-like growth factor-I messenger RNA and protein in the reinnervated muscle, and insulin-like growth factor-I and insulin-like growth factor binding protein-3 plasma levels. Similarly, treatment of nerve lesioned rats with insulin-like growth factor-I promoted muscle Reinnervation and prevention of muscle fibre atrophy, higher levels of insulin-like growth factor-I in the reinnervated muscle and of insulin-like growth factor-I and insulin-like growth factor binding proteins in plasma. These data suggest that glycosaminoglycans are potent stimulants of muscle Reinnervation and that their effects may be mediated by increased levels of insulin-like growth factor-I.
Gerald S. Berke - One of the best experts on this subject based on the ideXlab platform.
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Effects of arytenoid adduction on laryngeal function following ansa cervicalis nerve transfer for vocal fold paralysis in an in vivo canine model
The Laryngoscope, 1994Co-Authors: Sina Nasri, Joel A. Sercarz, Jody Kreiman, Bruce R. Gerratt, Gerald S. BerkeAbstract:Laryngeal Reinnervation with the ansa cervicalis has been proposed as a treatment for human unilateral vocal fold paralysis (UVFP). This study tested the assumption that results from Reinnervation could be improved if combined with medialization surgery. Six canine subjects underwent recurrent laryngeal nerve section and Reinnervation with a branch of the ansa cervicalis. After Reinnervation, vocal function was assessed before and after arytenoid adduction. Although laryngeal function improved significantly following Reinnervation, results were significantly enhanced by the addition of medialization surgery. The implications for the treatment of human unilateral vocal fold paralysis are discussed.
Ramon M. Esclamado - One of the best experts on this subject based on the ideXlab platform.
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results of ansa to recurrent laryngeal nerve Reinnervation
Otolaryngology-Head and Neck Surgery, 2007Co-Authors: Claudio F Milstein, Douglas M Hicks, Lee M Akst, Ramon M. EsclamadoAbstract:Objective We sought to describe the results of ansa cervicalis to recurrent laryngeal nerve (ansa-RLN) Reinnervation for unilateral vocal fold paralysis. Study design A chart review was performed on patients undergoing ansa-RLN Reinnervation for unilateral vocal cord paralysis at a tertiary care center. Patient perceptions of preoperative and postoperative voice quality was surveyed. Acoustic and visual parameters were assessed from videostroboscopy. Results From a total of 25 study patients, 15 patients underwent both preoperative and postoperativ video stroboscopies. In stroboscopies within 6 months, the average improvement in overall severity, roughness, and breathiness was 69, 79, and 100 percent, respectively. In stroboscopies after 6 months, the average improvement in overall severity, roughness, and breathiness was 63, 66, and 100 percent, respectively. Postoperatively, all patients had Reinnervation of the vocal fold. Conclusions Voice outcomes were improved in patients with preoperative and postoperative stroboscopies. Significance Ansa-RLN Reinnervation should be considered as a treatment for unilateral vocal fold paralysis.
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Selective cricothyroid muscle Reinnervation by muscle-nerve-muscle neurotization
Archives of otolaryngology--head & neck surgery, 2001Co-Authors: Hussam K. El-kashlan, William R. Carroll, Norman D. Hogikyan, Douglas B. Chepeha, Paul R. Kileny, Ramon M. EsclamadoAbstract:Objective To determine if selective Reinnervation of the cricothyroid muscle could be achieved with muscle-nerve-muscle neurotization. Design Case series. Setting Tertiary referral center. Patients Three consecutive patients with high vagal lesions that resulted in unilateral laryngeal paralysis. Interventions Patients underwent laryngeal Reinnervation with ansa hypoglossi to recurrent laryngeal nerve anastomosis. In addition, patients underwent selective cricothyroid muscle Reinnervation by muscle-nerve-muscle neurotization technique. Main Outcome Measures Objective and subjective improvement in voice quality and electromyographic evidence of selective Reinnervation of the cricothyroid muscle. Results All patients recovered normal or near-normal speaking voice and had normal objective measures of voice quality. They also showed electromyographic evidence of cricothyroid muscle Reinnervation. Conclusion The muscle-nerve-muscle neurotization technique was successful in providing selective Reinnervation of the cricothyroid muscle in our 3 patients.
S Bauche - One of the best experts on this subject based on the ideXlab platform.
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muscle histone deacetylase 4 upregulation in amyotrophic lateral sclerosis potential role in Reinnervation ability and disease progression
Brain, 2013Co-Authors: Thomas Simonet, S Bauche, Edoardo Malfatti, Nathalie Mandjee, Gaelle Bruneteau, Emmanuelle GirardAbstract:Amyotrophic lateral sclerosis is a typically rapidly progressive neurodegenerative disorder affecting motor neurons leading to progressive muscle paralysis and death, usually from respiratory failure, in 3–5 years. Some patients have slow disease progression and prolonged survival, but the underlying mechanisms remain poorly understood. Riluzole, the only approved treatment, only modestly prolongs survival and has no effect on muscle function. In the early phase of the disease, motor neuron loss is initially compensated for by collateral Reinnervation, but over time this compensation fails, leading to progressive muscle wasting. The crucial role of muscle histone deacetylase 4 and its regulator microRNA-206 in compensatory Reinnervation and disease progression was recently suggested in a mouse model of amyotrophic lateral sclerosis (transgenic mice carrying human mutations in the superoxide dismutase gene). Here, we sought to investigate whether the microRNA-206–histone deacetylase 4 pathway plays a role in muscle compensatory Reinnervation in patients with amyotrophic lateral sclerosis and thus contributes to disease outcome differences. We studied muscle Reinnervation using high-resolution confocal imaging of neuromuscular junctions in muscle samples obtained from 11 patients with amyotrophic lateral sclerosis, including five long-term survivors. We showed that the proportion of reinnervated neuromuscular junctions was significantly higher in long-term survivors than in patients with rapidly progressive disease. We analysed the expression of muscle candidate genes involved in the Reinnervation process and showed that histone deacetylase 4 upregulation was significantly greater in patients with rapidly progressive disease and was negatively correlated with the extent of muscle Reinnervation and functional outcome. Conversely, the proposed regulator of histone deacetylase 4, microRNA-206, was upregulated in both patient groups, but did not correlate with disease progression or Reinnervation. We conclude that muscle expression of histone deacetylase 4 may be a key factor for muscle Reinnervation and disease progression in patients with amyotrophic lateral sclerosis. Specific histone deacetylase 4 inhibitors may then constitute a therapeutic approach to enhancing motor performance and slowing disease progression in amyotrophic lateral sclerosis. * Abbreviations : ALS : amyotrophic lateral sclerosis ALSFRS-R : revised ALS Functional Rating Scale
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Muscle histone deacetylase 4 upregulation in amyotrophic lateral sclerosis: potential role in Reinnervation ability and disease progression.
Brain : a journal of neurology, 2013Co-Authors: Gaelle Bruneteau, Thomas Simonet, S Bauche, Edoardo Malfatti, Marie-laure Tanguy, Nathalie Mandjee, Emmanuelle Girard, Anthony Behin, Frédéric Khiami, Elhadi SarialiAbstract:Amyotrophic lateral sclerosis is a typically rapidly progressive neurodegenerative disorder affecting motor neurons leading to progressive muscle paralysis and death, usually from respiratory failure, in 3-5 years. Some patients have slow disease progression and prolonged survival, but the underlying mechanisms remain poorly understood. Riluzole, the only approved treatment, only modestly prolongs survival and has no effect on muscle function. In the early phase of the disease, motor neuron loss is initially compensated for by collateral Reinnervation, but over time this compensation fails, leading to progressive muscle wasting. The crucial role of muscle histone deacetylase 4 and its regulator microRNA-206 in compensatory Reinnervation and disease progression was recently suggested in a mouse model of amyotrophic lateral sclerosis (transgenic mice carrying human mutations in the superoxide dismutase gene). Here, we sought to investigate whether the microRNA-206-histone deacetylase 4 pathway plays a role in muscle compensatory Reinnervation in patients with amyotrophic lateral sclerosis and thus contributes to disease outcome differences. We studied muscle Reinnervation using high-resolution confocal imaging of neuromuscular junctions in muscle samples obtained from 11 patients with amyotrophic lateral sclerosis, including five long-term survivors. We showed that the proportion of reinnervated neuromuscular junctions was significantly higher in long-term survivors than in patients with rapidly progressive disease. We analysed the expression of muscle candidate genes involved in the Reinnervation process and showed that histone deacetylase 4 upregulation was significantly greater in patients with rapidly progressive disease and was negatively correlated with the extent of muscle Reinnervation and functional outcome. Conversely, the proposed regulator of histone deacetylase 4, microRNA-206, was upregulated in both patient groups, but did not correlate with disease progression or Reinnervation. We conclude that muscle expression of histone deacetylase 4 may be a key factor for muscle Reinnervation and disease progression in patients with amyotrophic lateral sclerosis. Specific histone deacetylase 4 inhibitors may then constitute a therapeutic approach to enhancing motor performance and slowing disease progression in amyotrophic lateral sclerosis.
David L. Zealear - One of the best experts on this subject based on the ideXlab platform.
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Stimulation of denervated muscle promotes selective Reinnervation, prevents synkinesis, and restores function
The Laryngoscope, 2013Co-Authors: David L. Zealear, Rajshri Mainthia, Isamu Kunibe, Akihiro Katada, Cheryl R. Billante, Kenichiro NomuraAbstract:Objectives/Hypothesis Previously, electrical stimulation of denervated canine laryngeal muscle was shown to promote Reinnervation by native over foreign motoneurons. The goal of this study was to assess the effect of different stimulus paradigms on Reinnervation quality and functional recovery. Study Design A prospective study of six canines over 8 to 20 months. Methods A clinical model of laryngeal paralysis was used, where recurrent laryngeal nerves of the animals were sectioned and ventilation compromised. The abductor, posterior cricoarytenoid (PCA) muscles were implanted bilaterally with electrodes from an implantable pulse generator. Animals were randomly assigned to three groups to assess the effect of different stimulus paradigms: 1) 40 pulses per second (pps) train, 2) 10 pps train, 3) no stimulation. Spontaneous vocal fold movement was measured endoscopically during hypercapnia. Exercise tolerance was measured on a treadmill using pulse oximetry. In the terminal session, electromyography (EMG) potentials were recorded during superior laryngeal nerve stimulation to index foreign Reinnervation of the PCA by reflex glottic closure (RGC) motoneurons. Results After Reinnervation started, nonstimulated and stimulated 40 pps animals displayed paradoxical closure of the glottis during hypercapnia and severely decreased exercise tolerance due to faulty Reinnervation. In contrast, stimulated 10 pps animals displayed minimal paradoxical closure and normal exercise tolerance (12 minutes up to 8 mph). EMG findings in this group demonstrated significantly less PCA Reinnervation by foreign RGC motoneurons. Conclusion PCA stimulation with low frequency reduced synkinetic Reinnervation by foreign RGC motoneurons. Paradoxical closure of the glottis with inspiration was reduced and exercise tolerance restored to normal. Level of Evidence N/A. Laryngoscope, 124:E180–E187, 2014
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Physiologic effect of electrical stimulation on Reinnervation of the canine larynx
Otolaryngology–Head and Neck Surgery, 2004Co-Authors: David Harley, Jeremy Dan Vos, Ricardo J. Rodriguez, Akihird Katada, Brad Swelstad, Shashidhar Kusuma, David L. ZealearAbstract:Abstract Problem: Paralysis of the recurrent laryngeal nerve (RLN) leads to significant functional morbidity in affected patients. Methods: Six canines underwent RLN sectioning and reanastomosis. In the experimental group, the posterior cricoarytenoid (PCA) muscle was stimulated using an implantable electrical stimulator. Reinnervation through the RLN was documented through electromyography of the the thyroarytenoid (TA) and PCA muscles during physiologic trials. Results: At 110 days of interrupted stimulation, there was a trend toward enhanced native Reinnervation and reduced foreign Reinnervation. By 140 days of stimulation, this reduction became more significant and even approximated the normal contralateral side. Later, a period of continuous stimulation appeared to inhibit further innervation, both native and foreign, while the control group demonstrated a continued increase in overall innervation. Additionally, all Reinnervation of the PCA, both foreign and native, was shown to occur exclusively through the reanastomosed RLN. Conclusion: Electrical stimulation of the dennervated larynx appears to inhibit the formation of foreign and erroneous Reinnervation after injury to the RLN. When presented intermittently, in a more physiologic fashion, it appears to stimulate proper native Reinnervation. Significance: While laryngeal paralysis poses a difficult problem to correct, electrical stimulation of the paralyzed musculature offers a promising option for future study. By showing that this model produces consistently hopeful results in the canine model, the opportunity exists for significant benefits for patients in the years to come. Support: None reported.
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Anatomic effect of electrical stimulation on the Reinnervation of the paralyzed canine larynx
Otolaryngology–Head and Neck Surgery, 2004Co-Authors: Jeremy Dan Vos, David Harley, Akihird Katada, Brad Swelstad, Shashidhar Kusuma, David L. ZealearAbstract:Abstract Problem: The larynx relies on correct innervation to mediate its normal functions. The aberrantly reinnervated larynx is compromised in its vocalization and airway-protective functions. Methods: Six canines were implanted with electrical stimulation devices, and their recurrent laryngeal nerve sectioned and re-anastomosed on one side. The effects of interrupted chronic muscle stimulation of experimental animals were compared with nonstimulated control animals. Physiologic measures of electromyography of thyroarytenoid (TA) and posterior cricoarytenoid (PCA) muscles demonstrated enhanced native Reinnervation and reduced foreign Reinnervation at 180 days in experimental animals. Fluorescent retrograde tracers true blue (TB) and fluorogold (FG) were injected into the PCA and TA, respectively. The identity and relative locations of labeled motoneurons in the nucleus ambiguus were analyzed for segregation and compared to normal animals. Results: PCA and TA muscles that appeared to become selectively reinnervated based on physiologic measurements retained the normal localization of motoneuron cell bodies in the nucleus ambiguus. Significant segregation was observed across the mediolateral axis. Animals with greater foreign Reinnervation based on physiologic measurements showed more random distribution of PCA and TA motoneurons, with variable double-labeling of some neurons. Conclusion: This study provides the first direct anatomic evidence that stimulation of a denervated laryngeal muscle promotes selective Reinnervation by native over foreign Reinnervation. The native Reinnervation appears to be from the original motoneuron projections to the PCA or TA located within the nucleus ambiguus of the brainstem. Significance: Laryngeal paralysis is a significant problem with decreased function and increased morbidity for affected individuals. This study demonstrates anatomically that stimulation of the larynx by an implantable device leads to improved Reinnervation. Thus, implantable devices may be useful in the rehabilitation of patients with laryngeal paralysis. Support: Supported by NIH grant R01-DC001149.
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The Effects of Chronic Electrical Stimulation on Laryngeal Muscle Reinnervation
ORL; journal for oto-rhino-laryngology and its related specialties, 2000Co-Authors: David L. Zealear, Cheryl R. Billante, Cheerasook Chongkolwatana, Garrett D. HerzonAbstract:The present study examined the effects of functional neuromuscular stimulation (FNS) on Reinnervation of the posterior cricoarytenoid (PCA) muscle. In 4 canines, the recurrent laryngeal nerve (RLN) was sectioned and anastomosed and a patch electrode array implanted for stimulation and recording at multiple PCA sites. Following implantation, FNS was applied to 2 canines for a period of 6 weeks. Two additional animals served as nonstimulated controls. In each animal, histomorphometric analysis of the RLN was used to assess the quality of nerve regeneration and the potential for muscle reconnection. The magnitude of Reinnervation was monitored by electromyographic (EMG) potentials evoked by RLN stimulation. The appropriateness of reconnection was determined by the pattern of spontaneous EMG activity and recovery of vocal fold abduction. Results of this preliminary study indicated that FNS caused an overall repression of Reinnervation. However, the repression preferentially inhibited reconnection by foreign nerve fibers, promoting selective Reinnervation and preventing synkinesis.
