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Hungchuan Pan - One of the best experts on this subject based on the ideXlab platform.
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down regulated expression of magnesium transporter genes following a high magnesium diet attenuates sciatic nerve Crush Injury
Neurosurgery, 2019Co-Authors: Yingju Chen, Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Jason P Sheehan, Hungchuan PanAbstract:Background Magnesium supplementation has potential for use in nerve regeneration. The expression of some magnesium transporter genes is reflective of the intracellular magnesium levels. Objective To assess the expression of various magnesium transporter genes as they relate to neurological alterations in a sciatic nerve Injury model. Methods Sciatic nerve Injury was induced in rats, which were then fed either basal or high magnesium diets. Magnesium concentrations and 5 magnesium transporter genes (SLC41A1, MAGT1, CNNM2, TRPM6, and TRPM7) were measured in the tissue samples. Results The high magnesium diet attenuated cytoskeletal loss in a dose-dependent manner in isolated nerve explants. The high magnesium diet augmented nerve regeneration and led to the restoration of nerve structure, increased S-100, and neurofilaments. This increased regeneration was consistent with the improvement of neurobehavioral and electrophysiological assessment. The denervated muscle morphology was restored with the high magnesium diet, and that was also highly correlated with the increased expression of desmin and acetylcholine receptors in denervated muscle. The plasma magnesium levels were significantly elevated after the animals consumed a high magnesium diet and were reciprocally related to the down-regulation of CNNM2, MagT1, and SCL41A1 in the blood monocytes, nerves, and muscle tissues of the nerve Crush Injury model. Conclusion The increased plasma magnesium levels after consuming a high magnesium diet were highly correlated with the down-regulation of magnesium transporter genes in monocytes, nerves, and muscle tissues after sciatic nerve Crush Injury. The study findings suggest that there are beneficial effects of administering magnesium after a nerve Injury.
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late administration of high frequency electrical stimulation increases nerve regeneration without aggravating neuropathic pain in a nerve Crush Injury
BMC Neuroscience, 2018Co-Authors: Chienyi Chiang, Meeiling Sheu, Chunjung Chen, Jason P Sheehan, Hungchuan PanAbstract:High-frequency transcutaneous neuromuscular electrical nerve stimulation (TENS) is currently used for the administration of electrical current in denervated muscle to alleviate muscle atrophy and enhance motor function; however, the time window (i.e. either immediate or delayed) for achieving benefit is still undetermined. In this study, we conducted an intervention of sciatic nerve Crush Injury using high-frequency TENS at different time points to assess the effect of motor and sensory functional recovery. Animals with left sciatic nerve Crush Injury received TENS treatment starting immediately after Injury or 1 week later at a high frequency(100 Hz) or at a low frequency (2 Hz) as a control. In SFI gait analysis, either immediate or late admission of high-frequency electrical stimulation exerted significant improvement compared to either immediate or late administration of low-frequency electrical stimulation. In an assessment of allodynia, immediate high frequency electrical stimulation caused a significantly decreased pain threshold compared to late high-frequency or low-frequency stimulation at immediate or late time points. Immunohistochemistry staining and western blot analysis of S-100 and NF-200 demonstrated that both immediate and late high frequency electrical stimulation showed a similar effect; however the effect was superior to that achieved with low frequency stimulation. Immediate high frequency electrical stimulation resulted in significant expression of TNF-α and synaptophysin in the dorsal root ganglion, somatosensory cortex, and hippocampus compared to late electrical stimulation, and this trend paralleled the observed effect on somatosensory evoked potential. The CatWalk gait analysis also showed that immediate electrical stimulation led to a significantly high regularity index. In primary dorsal root ganglion cells culture, high-frequency electrical stimulation also exerted a significant increase in expression of TNF-α, synaptophysin, and NGF in accordance with the in vivo results. Immediate or late transcutaneous high-frequency electrical stimulation exhibited the potential to stimulate the motor nerve regeneration. However, immediate electrical stimulation had a predilection to develop neuropathic pain. A delay in TENS initiation appears to be a reasonable approach for nerve repair and provides the appropriate time profile for its clinical application.
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retraction enhancement of regeneration with glia cell line derived neurotrophic factor transduced human amniotic fluid mesenchymal stem cells after sciatic nerve Crush Injury
Journal of Neurosurgery, 2015Co-Authors: Hungchuan PanAbstract:Object Human amniotic fluid–derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line–derived neurotrophic factor (GDNF)–modified human AFMSCs may enhance regeneration of sciatic nerve after a Crush Injury. Methods Peripheral nerve Injury was produced in Sprague-Dawley rats by Crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and ...
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enhancement of regeneration with glia cell line derived neurotrophic factor transduced human amniotic fluid mesenchymal stem cells after sciatic nerve Crush Injury
Journal of Neurosurgery, 2010Co-Authors: Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Minghong Tai, Daryu Yang, Shuzhen Lai, Hungchuan PanAbstract:Object Human amniotic fluid–derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line–derived neurotrophic factor (GDNF)–modified human AFMSCs may enhance regeneration of sciatic nerve after a Crush Injury. Methods Peripheral nerve Injury was produced in Sprague-Dawley rats by Crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and ...
Tom F. Lue - One of the best experts on this subject based on the ideXlab platform.
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Neurturin enhances the recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat.
Journal of brachial plexus and peripheral nerve injury, 2007Co-Authors: Anthony J Bella, Thomas M. Fandel, Kavirach Tantiwongse, William O. Brant, Robert D Klein, Carlos A Garcia, Tom F. LueAbstract:Background The molecular mechanisms responsible for the survival and preservation of function for adult parasympathetic ganglion neurons following Injury remain incompletely understood. However, advances in the neurobiology of growth factors, neural development, and prevention of cell death have led to a surge of clinical interest for protective and regenerative neuromodulatory strategies, as surgical therapies for prostate, bladder, and colorectal cancers often result in neuronal axotomy and debilitating loss of sexual function or continence. In vitro studies have identified neurturin, a glial cell line-derived neurotrophic factor, as a neuromodulator for pelvic cholinergic neurons. We present the first in vivo report of the effects of neurturin upon the recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat.
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fk1706 enhances the recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat
The Journal of Sexual Medicine, 2007Co-Authors: Anthony J Bella, Narihiko Hayashi, Rafael Carrion, Raymond D Price, Tom F. LueAbstract:ABSTRACT Introduction Advances in neurobiology have led to a surge of clinical interest in the development of protective and regenerative neuromodulatory strategies, as surgical therapies for prostate cancer often result in neuronal damage and debilitating loss of sexual function. Aim To investigate the dose-dependent efficacy of FK1706, a nonimmunosuppressant immunophilin ligand, for the recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat. Main Outcome Measures Recovery of erectile function was assessed by cavernous nerve electrostimulation and reported as maximal increase of intracavernous pressure (ICP) and area under the curve (AUC). Changes in animal weights, percentage completion of treatment course, and survival were compared between groups. Methods Thirty-five Sprague–Dawley male rats were randomly divided into five equal groups: seven animals received a sham operation, whereas 28 animals underwent bilateral cavernous nerve Crush Injury, followed by subcutaneous injection of vehicle alone (1.0 mL/kg), or low (0.1 mg/kg), medium (0.32 mg/kg), or high dose (1.0 mg/kg) FK1706 5 days per week for 8 weeks. Results Erectile dysfunction did not occur in the sham group (mean maximal ICP increase of 100.8 ± 6.3 cmH 2 O), whereas nerve Injury and vehicle treatment produced a significant reduction in ICP response to 34.4 ± 12.8 cmH 2 O. The mean ICP increase for high-dose FK106 treatment was 73.9 ± 6.3 cmH 2 O ( P 2 O and 56.9 ± 8.3 for low and medium doses ( P > 0.05). Similar stepwise findings were observed using AUC data. No significant maximal aortic blood pressure or weight differences occurred between groups and all animals completed treatment. Conclusion High-dose subcutaneous FK1706 therapy promoted recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat. No significant differences between groups were observed for changes in weight, and the 8-week treatment course was completed for all animals. Bella AJ, Hayashi N, Carrion RE, Price R, and Lue TF. FK1706 enhances the recovery of erectile function following bilateral cavernous nerve Crush Injury in the rat.
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the effect of fk1706 on erectile function following bilateral cavernous nerve Crush Injury in a rat model
The Journal of Urology, 2006Co-Authors: Narihiko Hayashi, Rafael Carrion, Raymond D Price, Thomas X Minor, Lora Nunes, Tom F. LueAbstract:Purpose: We investigated the neurotrophic effect of FK1706 on erectile recovery following bilateral cavernous nerve Crush Injury in a rat model.Materials and Methods: A total of 28 male Sprague-Dawley rats were randomly divided into 4 equal groups. Seven animals underwent sham operation and subcutaneous vehicle injection, whereas 21 underwent bilateral cavernous nerve Crush Injury followed by vehicle injection alone, or by low (0.1 mg/kg) or high (1.0 mg/kg) dose FK1706 treatment. Injections were continued 5 days weekly for 8 weeks. Erectile function was then assessed by cavernous nerve electrostimulation and penile tissue was evaluated immunohistochemically.Results: No erectile dysfunction was identified in the sham treated group (mean maximal intracavernous pressure ± SEM 106.8 ± 6.4 cm H2O), whereas nerve Injury significantly decreased ICP to 17.9 ± 7.0 cm H2O. FK1706 facilitated neural and erectile recovery in a concentration dependent manner with a mean ICP in the high dose FK treatment group of 80.1...
Chunjung Chen - One of the best experts on this subject based on the ideXlab platform.
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down regulated expression of magnesium transporter genes following a high magnesium diet attenuates sciatic nerve Crush Injury
Neurosurgery, 2019Co-Authors: Yingju Chen, Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Jason P Sheehan, Hungchuan PanAbstract:Background Magnesium supplementation has potential for use in nerve regeneration. The expression of some magnesium transporter genes is reflective of the intracellular magnesium levels. Objective To assess the expression of various magnesium transporter genes as they relate to neurological alterations in a sciatic nerve Injury model. Methods Sciatic nerve Injury was induced in rats, which were then fed either basal or high magnesium diets. Magnesium concentrations and 5 magnesium transporter genes (SLC41A1, MAGT1, CNNM2, TRPM6, and TRPM7) were measured in the tissue samples. Results The high magnesium diet attenuated cytoskeletal loss in a dose-dependent manner in isolated nerve explants. The high magnesium diet augmented nerve regeneration and led to the restoration of nerve structure, increased S-100, and neurofilaments. This increased regeneration was consistent with the improvement of neurobehavioral and electrophysiological assessment. The denervated muscle morphology was restored with the high magnesium diet, and that was also highly correlated with the increased expression of desmin and acetylcholine receptors in denervated muscle. The plasma magnesium levels were significantly elevated after the animals consumed a high magnesium diet and were reciprocally related to the down-regulation of CNNM2, MagT1, and SCL41A1 in the blood monocytes, nerves, and muscle tissues of the nerve Crush Injury model. Conclusion The increased plasma magnesium levels after consuming a high magnesium diet were highly correlated with the down-regulation of magnesium transporter genes in monocytes, nerves, and muscle tissues after sciatic nerve Crush Injury. The study findings suggest that there are beneficial effects of administering magnesium after a nerve Injury.
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late administration of high frequency electrical stimulation increases nerve regeneration without aggravating neuropathic pain in a nerve Crush Injury
BMC Neuroscience, 2018Co-Authors: Chienyi Chiang, Meeiling Sheu, Chunjung Chen, Jason P Sheehan, Hungchuan PanAbstract:High-frequency transcutaneous neuromuscular electrical nerve stimulation (TENS) is currently used for the administration of electrical current in denervated muscle to alleviate muscle atrophy and enhance motor function; however, the time window (i.e. either immediate or delayed) for achieving benefit is still undetermined. In this study, we conducted an intervention of sciatic nerve Crush Injury using high-frequency TENS at different time points to assess the effect of motor and sensory functional recovery. Animals with left sciatic nerve Crush Injury received TENS treatment starting immediately after Injury or 1 week later at a high frequency(100 Hz) or at a low frequency (2 Hz) as a control. In SFI gait analysis, either immediate or late admission of high-frequency electrical stimulation exerted significant improvement compared to either immediate or late administration of low-frequency electrical stimulation. In an assessment of allodynia, immediate high frequency electrical stimulation caused a significantly decreased pain threshold compared to late high-frequency or low-frequency stimulation at immediate or late time points. Immunohistochemistry staining and western blot analysis of S-100 and NF-200 demonstrated that both immediate and late high frequency electrical stimulation showed a similar effect; however the effect was superior to that achieved with low frequency stimulation. Immediate high frequency electrical stimulation resulted in significant expression of TNF-α and synaptophysin in the dorsal root ganglion, somatosensory cortex, and hippocampus compared to late electrical stimulation, and this trend paralleled the observed effect on somatosensory evoked potential. The CatWalk gait analysis also showed that immediate electrical stimulation led to a significantly high regularity index. In primary dorsal root ganglion cells culture, high-frequency electrical stimulation also exerted a significant increase in expression of TNF-α, synaptophysin, and NGF in accordance with the in vivo results. Immediate or late transcutaneous high-frequency electrical stimulation exhibited the potential to stimulate the motor nerve regeneration. However, immediate electrical stimulation had a predilection to develop neuropathic pain. A delay in TENS initiation appears to be a reasonable approach for nerve repair and provides the appropriate time profile for its clinical application.
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enhancement of regeneration with glia cell line derived neurotrophic factor transduced human amniotic fluid mesenchymal stem cells after sciatic nerve Crush Injury
Journal of Neurosurgery, 2010Co-Authors: Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Minghong Tai, Daryu Yang, Shuzhen Lai, Hungchuan PanAbstract:Object Human amniotic fluid–derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line–derived neurotrophic factor (GDNF)–modified human AFMSCs may enhance regeneration of sciatic nerve after a Crush Injury. Methods Peripheral nerve Injury was produced in Sprague-Dawley rats by Crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and ...
Meeiling Sheu - One of the best experts on this subject based on the ideXlab platform.
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down regulated expression of magnesium transporter genes following a high magnesium diet attenuates sciatic nerve Crush Injury
Neurosurgery, 2019Co-Authors: Yingju Chen, Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Jason P Sheehan, Hungchuan PanAbstract:Background Magnesium supplementation has potential for use in nerve regeneration. The expression of some magnesium transporter genes is reflective of the intracellular magnesium levels. Objective To assess the expression of various magnesium transporter genes as they relate to neurological alterations in a sciatic nerve Injury model. Methods Sciatic nerve Injury was induced in rats, which were then fed either basal or high magnesium diets. Magnesium concentrations and 5 magnesium transporter genes (SLC41A1, MAGT1, CNNM2, TRPM6, and TRPM7) were measured in the tissue samples. Results The high magnesium diet attenuated cytoskeletal loss in a dose-dependent manner in isolated nerve explants. The high magnesium diet augmented nerve regeneration and led to the restoration of nerve structure, increased S-100, and neurofilaments. This increased regeneration was consistent with the improvement of neurobehavioral and electrophysiological assessment. The denervated muscle morphology was restored with the high magnesium diet, and that was also highly correlated with the increased expression of desmin and acetylcholine receptors in denervated muscle. The plasma magnesium levels were significantly elevated after the animals consumed a high magnesium diet and were reciprocally related to the down-regulation of CNNM2, MagT1, and SCL41A1 in the blood monocytes, nerves, and muscle tissues of the nerve Crush Injury model. Conclusion The increased plasma magnesium levels after consuming a high magnesium diet were highly correlated with the down-regulation of magnesium transporter genes in monocytes, nerves, and muscle tissues after sciatic nerve Crush Injury. The study findings suggest that there are beneficial effects of administering magnesium after a nerve Injury.
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late administration of high frequency electrical stimulation increases nerve regeneration without aggravating neuropathic pain in a nerve Crush Injury
BMC Neuroscience, 2018Co-Authors: Chienyi Chiang, Meeiling Sheu, Chunjung Chen, Jason P Sheehan, Hungchuan PanAbstract:High-frequency transcutaneous neuromuscular electrical nerve stimulation (TENS) is currently used for the administration of electrical current in denervated muscle to alleviate muscle atrophy and enhance motor function; however, the time window (i.e. either immediate or delayed) for achieving benefit is still undetermined. In this study, we conducted an intervention of sciatic nerve Crush Injury using high-frequency TENS at different time points to assess the effect of motor and sensory functional recovery. Animals with left sciatic nerve Crush Injury received TENS treatment starting immediately after Injury or 1 week later at a high frequency(100 Hz) or at a low frequency (2 Hz) as a control. In SFI gait analysis, either immediate or late admission of high-frequency electrical stimulation exerted significant improvement compared to either immediate or late administration of low-frequency electrical stimulation. In an assessment of allodynia, immediate high frequency electrical stimulation caused a significantly decreased pain threshold compared to late high-frequency or low-frequency stimulation at immediate or late time points. Immunohistochemistry staining and western blot analysis of S-100 and NF-200 demonstrated that both immediate and late high frequency electrical stimulation showed a similar effect; however the effect was superior to that achieved with low frequency stimulation. Immediate high frequency electrical stimulation resulted in significant expression of TNF-α and synaptophysin in the dorsal root ganglion, somatosensory cortex, and hippocampus compared to late electrical stimulation, and this trend paralleled the observed effect on somatosensory evoked potential. The CatWalk gait analysis also showed that immediate electrical stimulation led to a significantly high regularity index. In primary dorsal root ganglion cells culture, high-frequency electrical stimulation also exerted a significant increase in expression of TNF-α, synaptophysin, and NGF in accordance with the in vivo results. Immediate or late transcutaneous high-frequency electrical stimulation exhibited the potential to stimulate the motor nerve regeneration. However, immediate electrical stimulation had a predilection to develop neuropathic pain. A delay in TENS initiation appears to be a reasonable approach for nerve repair and provides the appropriate time profile for its clinical application.
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enhancement of regeneration with glia cell line derived neurotrophic factor transduced human amniotic fluid mesenchymal stem cells after sciatic nerve Crush Injury
Journal of Neurosurgery, 2010Co-Authors: Fu-chou Cheng, Chunjung Chen, Meeiling Sheu, Minghong Tai, Daryu Yang, Shuzhen Lai, Hungchuan PanAbstract:Object Human amniotic fluid–derived mesenchymal stem cells (AFMSCs) have been shown to promote peripheral nerve regeneration, and the local delivery of neurotrophic factors may additionally enhance nerve regeneration capacity. The present study evaluates whether the transplantation of glia cell line–derived neurotrophic factor (GDNF)–modified human AFMSCs may enhance regeneration of sciatic nerve after a Crush Injury. Methods Peripheral nerve Injury was produced in Sprague-Dawley rats by Crushing the left sciatic nerve using a vessel clamp. Either GDNF-modified human AFMSCs or human AFMSCs were embedded in Matrigel and delivered to the injured nerve. Motor function and electrophysiological studies were conducted after 1 and 4 weeks. Early or later nerve regeneration markers were used to evaluate nerve regeneration. The expression of GDNF in the transplanted human AFMSCs and GDNF-modified human AFMSCs was monitored at 7-day intervals. Results Human AFMSCs were successfully transfected with adenovirus, and ...
Kathryn J. Jones - One of the best experts on this subject based on the ideXlab platform.
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single session of brief electrical stimulation immediately following Crush Injury enhances functional recovery of rat facial nerve
Journal of Rehabilitation Research and Development, 2012Co-Authors: Eileen M Foecking, Sam J Marzo, Keith N Fargo, Lisa M Coughlin, James T Kim, Kathryn J. JonesAbstract:Peripheral nerve injuries lead to a variety of pathological conditions, including paresis or paralysis when the Injury involves motor axons. We have been studying ways to enhance the regeneration of peripheral nerves using daily electrical stimulation (ES) following a facial nerve Crush Injury. In our previous studies, ES was not initiated until 24 h after Injury. The current experiment tested whether ES administered immediately following the Crush Injury would further decrease the time for complete recovery from facial paralysis. Rats received a unilateral facial nerve Crush Injury and an electrode was positioned on the nerve proximal to the Crush site. Animals received daily 30 min sessions of ES for 1 d (day of Injury only), 2 d, 4 d, 7 d, or daily until complete functional recovery. Untreated animals received no ES. Animals were observed daily for the return of facial function. Our findings demonstrated that one session of ES was as effective as daily stimulation at enhancing the recovery of most functional parameters. Therefore, the use of a single 30 min session of ES as a possible treatment strategy should be studied in human patients with paralysis as a result of acute nerve injuries.
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electrical stimulation facilitates rat facial nerve recovery from a Crush Injury
Otolaryngology-Head and Neck Surgery, 2008Co-Authors: Devyani Lal, Kathryn J. Jones, Laura Hetzler, Nijee Sharma, Robert D Wurster, Sam J Marzo, Eileen M FoeckingAbstract:ObjectiveTo study the effect of electrical stimulation on accelerating facial nerve functional recovery from a Crush Injury in the rat model.Study DesignExperimental.MethodThe main trunk of the right facial nerve was Crushed just distal to the stylomastoid foramen, causing right-sided facial paralysis in 17 Sprague-Dawley rats. An electrode apparatus was implanted in all rats. Nine rats underwent electrical stimulation and eight were sham stimulated until complete facial nerve recovery. Facial nerve function was assessed daily by grading eyeblink reflex, vibrissae orientation, and vibrissae movement.ResultsAn electrical stimulation model of the rat facial nerve following axotomy was established. The semi-eyeblink returned significantly earlier (3.71 + 0.97 vs 9.57 + 1.86 days post axotomy) in stimulated rats (P = 0.008). Stimulated rats also recovered all functions earlier, and showed less variability in recovery time.ConclusionElectrical stimulation initiates and accelerates facial nerve recovery in the ...