Дисертації з теми "Motor periphery"
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Zapletal, Ladislav. "Řídicí systém kamerového sceneru pro monitorování růstu rostlin." Master's thesis, Vysoké učení technické v Brně. Fakulta elektrotechniky a komunikačních technologií, 2017. http://www.nusl.cz/ntk/nusl-318195.
Повний текст джерелаEggers, Thomas Elliott. "Chronic Peripheral Nerve Recordings and Motor Recovery with the FINE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1516624330839376.
Повний текст джерелаSzlavik, Robert Bruce. "In vivo electrical stimulation of motor nerves." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0032/NQ66239.pdf.
Повний текст джерелаHigashimori, Haruki. "Systemic inductive mechanism of burn-induced peripheral motor and sensory neuropathy /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2004. http://uclibs.org/PID/11984.
Повний текст джерелаPashalis, Despina. "Central cortical processes or peripheral motor processes differentiate extraverts from introverts /." Title page, table of contents and abstract only, 2002. http://web4.library.adelaide.edu.au/theses/09ARPS/09arpsp2818.pdf.
Повний текст джерелаMcDowell, Sally-Ann. "The effects of peripheral vision on motor initiation in Parkinson's disease." Thesis, University of Reading, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.296634.
Повний текст джерелаDrew, Alexander Peter. "Genetics of distal hereditary motor neuropathies." Thesis, The University of Sydney, 2012. http://hdl.handle.net/2123/8652.
Повний текст джерелаWallquist, Wilhelm. "On laminins and laminin receptors and their role in regeneration and myelination of the peripheral nerve /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-781-9/.
Повний текст джерелаMaskill, David William. "Peripheral and central influences on the electromographic responses of muscle to transcranial magnetic stimulation in man." Thesis, Imperial College London, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.283732.
Повний текст джерелаBanks, Daniel John. "Modelling studies on peripheral nerve neural signal transduction using thin-film microelectrodes." Thesis, University of Surrey, 1994. http://epubs.surrey.ac.uk/842690/.
Повний текст джерелаCharlton, Shona. "The effect of prolonged peripheral stimulation on the excitability of human motor cortex /." Title page and abstract only, 1999. http://web4.library.adelaide.edu.au/theses/09SB/09sbc481.pdf.
Повний текст джерелаLee, Stella Joonmyung. "A Critical Period for Functional Motor Recovery After Peripheral Nerve Injury in the Mouse." Thesis, Harvard University, 2014. http://etds.lib.harvard.edu/hms/admin/view/64.
Повний текст джерелаNelson, Sandahl Hygeia. "Effects on motor neuron development of altering peripheral targets in embryonic leeches (Hirudo verbana)." Diss., [La Jolla] : University of California, San Diego, 2009. http://wwwlib.umi.com/cr/ucsd/fullcit?p1473082.
Повний текст джерелаTitle from first page of PDF file (viewed Feb. 1, 2010). Available via ProQuest Digital Dissertations. Includes bibliographical references (p. 31-32).
Parsons, Perez Maria Cristina. "HSV vectors for gene delivery to motor neurons following peripheral administration : function of Reg-2." Thesis, University College London (University of London), 2003. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398050.
Повний текст джерелаMiressi, Federica. "Hereditary Peripheral Neuropathies : from Molecular Genetics to a cellular model of hiPSC-derived motor neurons." Thesis, Limoges, 2020. http://aurore.unilim.fr/theses/nxfile/default/56675caf-59b3-4af2-ae86-c5e356784128/blobholder:0/2020LIMO0053.pdf.
Повний текст джерелаCharcot-Marie-Tooth (CMT) disease is the most common hereditary peripheral neuropathy. To date, more than 80 genes have been identified to be involved in CMT, but genetic diagnosis is achieved only in 30-40% of cases. This study presented two main objectives: first, we focused on CMT and associated peripheral neuropathies using molecular and bioinformatic approaches to optimize their genetic characterization ; secondly, we investigated impaired mechanisms in an axonal CMT form, by creating a human cellular model of human induced pluripotency stem cells (hiPSC) and their differentiation into motor neurons (MN).In the first part of the project, we developed a new bioinformatic tool, CovCopCan, to detect Copy Number Variations (CNV), starting from NGS data. Thanks to CovCopCan, two new CNV have been identified and we discuss their involvement in two complex cases of peripheral neuropathy. We also identified three genetic variations in a CMT patient highlighting that CMT can be a multilocus genetic pathology. In the second part of the project, we successfully generated a cellular model of MN for the study of GDAP1 gene and its associated CMT2H form. We reprogrammed dermal fibroblasts of five control subjects and two CMT patients, carrying two different homozygous codon-stop mutations in GDAP1, into human inducedpluripotent stem cells (hiPSC). Then, we established a differentiation protocol to generate MN from hiPSC.MN with the GDAP1 p.Ser194* mutation were analyzed by expression, morphological, and functional tests. We confirmed the neural expression of GDAP1, and we suggested that oxidative stress and mitochondrial impairment could be responsible for the pathological condition in CMT2H MN. Taken together, our results highlighted that both genetic and functional analyses are essential in the complete characterization of CMT disease
Andersen, Mark Bille. "Psychosocial factors and changes in peripheral vision, muscle tension, and fine motor skills during stress." Diss., The University of Arizona, 1988. http://hdl.handle.net/10150/184446.
Повний текст джерелаWagner, Justin. "Whole Exome Sequencing to Identify Disease-Causing Mutations in Lower Motor Neuron Disease and Peripheral Neuropathy." Thesis, Université d'Ottawa / University of Ottawa, 2016. http://hdl.handle.net/10393/34124.
Повний текст джерелаJohnson, Lise. "DECODING ELECTRIC FIELDS OF THE NERVOUS SYSTEM: INVESTIGATIONS OF INFORMATION STORAGE AND TRANSFER IN THE CENTRAL AND PERIPHERAL NERVOUS SYSTEM." Diss., The University of Arizona, 2010. http://hdl.handle.net/10150/193574.
Повний текст джерелаVan, Dyk A. P. "The effects of a sports vision training programme on selected visual-motor skills in a non-fatigued and fatigued cardiovascular condition." Thesis, University of the Western Cape, 2014. http://hdl.handle.net/11394/4284.
Повний текст джерелаThe aim of the study was to determine the effects of a sports vision training programme on peripheral awareness, eye-hand coordination, eye-body coordination, visual reaction time and visual-motor response time of physically active males when in a non-fatigued condition and when in an induced-fatigue condition that simulates levels experienced when playing field-based sports. Scheduling challenges made it necessary to use a sample of convenience rather than random sampling to divide the 49 participants into a treatment group (n=16) and a control group (n=33). A pre-test was administered according to assessment protocols for five selected visual skills performed in both a nonfatigued and fatigued condition. The treatment group participated in an eight-week visual training intervention programme. The purpose of this visual training programme was to train the five selected visual skills (peripheral awareness, eye-hand coordination, eyebody coordination, visual reaction time and visual-motor response time and to practice these skills during fatigued cardiovascular conditions. The post test was administered immediately after the intervention period. Interaction effects were found for three variables: peripheral awareness, eye-hand coordination and visual reaction time, so conclusions could be drawn only for eye-body coordination and visual-motor response time. No significant differences were found for visual-motor response time in the non-fatigued condition. It can be concluded that the sports vision training programme, as implemented in this study, resulted in a significant improvement in visual-motor response time of the treatment group as compared to the control group, when performing under fatigue conditions.
Howard, Heidi C. "Identification of the gene responsible for peripheral neuropathy associated with agenesis of the corpus callosum." Thesis, McGill University, 2003. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=84259.
Повний текст джерелаWe genotyped polymorphic markers in the ACCPN candidate region on chromosome 15 in over 67 patients and 200 control individuals. Observation of affected haplotypes confirmed the presence of a founder effect in the French Canadian population. Recombination analysis reduced the candidate interval to approximately 2 cM between markers D15S1040 and ACTC on chromosome 15. Linkage disequilibrium analysis suggested the gene resides nearest marker D15S1232. A physical map of the newly refined candidate region was constructed using YAC, BAC and PAC clones. These clones were used to confirm the position of candidate ESTs and genes as being either within or outside the ACCPN candidate region.
The connexin 36 gene, which was confirmed to reside within the region, was excluded as the gene responsible for ACCPN using SSCP analysis. The SLC12A6 gene was also confirmed to reside within the candidate interval and was tested for mutations using SSCP, dHPLC and sequence analyses. We found a total of four disease-specific mutations in SLC12A6, all of which are expected to truncate the KCC3 protein (the protein produced by the SLC12A6 gene). Two of the four mutations were identified in the French Canadian population; 80 French Canadian ACCPN patients are homozygous for the c.2436delG in exon 18 and one French Canadian patient is a compound heterozygote, having the c.2436delG mutation as well as the 1584_1585delCTinsG mutation in exon 11. Two additional mutations were identified in one Turkish and one Italian family in exons 22 and 15 respectively. The effects of the c.2436delG mutation on KCC3 function was studied in X. laevis oocytes and the truncated protein is not functional. Finally, collaborators at Vanderbilt University disrupted the slc12a6 gene in the mouse and found a phenotype similar to the human disease.
Identification of SLC12A6 as the gene mutated in ACCPN will allow for accurate molecular diagnosis as well as carrier testing in the French Canadian population. It is also the first step in understanding the molecular mechanism leading to the disease.
Peterson, Erik J. "INFRARED NEURAL STIMULATION AND FUNCTIONALRECRUITMENT OF THE PERIPHERAL NERVE." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1363640552.
Повний текст джерелаOulad, Ben Taib Nordeyn. "Effects of hemicerebellectomy on the excitability of the motor cortex." Doctoral thesis, Universite Libre de Bruxelles, 2011. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/209895.
Повний текст джерелаgauches; (3) la stimulation électrique par stimulation cérébelleuse profonde (stimulation des noyaux interposés) sur le côté gauche; et (4) la stimulation électrique des noyaux cérébelleux du côté controlatéral. Pour la stimulation périphérique, tous les animaux ont reçu 1 heure de stimulation électrique. Les trains de stimulation ont consisté en cinq stimuli (durée de 1 stimulus: 1 ms) à une fréquence de 10 Hz. Pendant la stimulation du cortex moteur, les amplitudes pic-à-pic des réponses du muscle gastrocnémien gauche ont été analysées. Le seuil moteur (motor threshold :MT) a été défini comme l'intensité la plus basse induisant au moins 5 réponses avec une amplitude >20 µV sur 10 réponses évoquées. L'intensité utilisée était à 130 % du seuil moteur (130 % de MT). Dans la condition basale (avant la stimulation répétitive), les amplitudes des réponses motrices sont similaires dans les six groupes de rats. Chez les rats sans intervention cérébelleuse, la stimulation électrique périphérique a été associée à une augmentation significative de l’amplitude des réponses corticomotrices par rapport à la condition basale. Chez les rats avec infusion de Ringer, les réponses motrices ont augmenté de manière similaire par rapport à la condition basale. L'administration d'éthanol dans le cervelet a empêché la majoration de la réponse ipsilatérale. La même observation a été faite après l'infusion de TTX et après la stimulation électrique des noyaux cérébelleux du côté gauche. Cependant, la stimulation électrique des noyaux cérébelleux du côté droit n'a pas détérioré la modulation des efférences corticomotrices associée à la stimulation répétitive du nerf sciatique. Nous avons ensuite analysé les effets de l’hémicérébellectomie sur la modulation des activités des efférences du cortex moteur associée à la stimulation électrique répétitive du nerf sciatique chez le rat. L’hémicérébellectomie constitue un modèle de lésion aigüe étendue du cervelet. L’hémicérébellectomie a bloqué la majoration de la réponse corticomotrice, confirmant que le cervelet est un acteur-clé de cette forme de plasticité à court terme. Nous avons examiné les réflexes cutanéomusculaires au niveau du muscle plantaire des rats (1) en réponse à la stimulation cutanée isolée, et (2) en réponse à une association de stimuli cutanés avec des trains de stimuli de haute fréquence appliqués sur le cortex moteur controlatéral, avant et après la stimulation répétitive périphérique. Après une période de stimulation répétitive périphérique, l’amplitude des réponses cutanéomusculaires augmente lorsque des trains de stimulation de haute fréquence sont appliqués au niveau du cortex moteur controlatéral. Les réponses cutanéomusculaires ont aussi été examinées avec le même paradigme après hémicérébellectomie. Nous avons observé que la majoration de l’amplitude des réponses cutanéomusculaires associée aux trains de stimulation de haute fréquence après la période de stimulation répétitive périphérique a été bloquée par l’hémicérébellectomie. Nos résultats suggèrent donc que les voies passant par le cervelet sont impliquées dans le calibrage des réponses cutanéomusculaires et qu’une lésion cérébelleuse aigüe étendue altère cette fonction cérébelleuse.
Dans un travail suivant, nous avons analysé les effets de la stimulation répétitive à basse fréquence du cortex moteur (LFRSM1) (1) sur l'inhibition interhémisphérique (IHI), et (2) sur la modulation des réponses cutanéomusculaires chez des rats présentant une ablation de l’hémicervelet gauche. L’IHI a été évaluée par la méthode des stimulations pairées (technique de conditionnement), en utilisant un stimulus de conditionnement (CS) à M1 suivi par un stimulus test (TS) controlatéral. Nous avons mis en évidence que les LFRSM1 ont réduit l’IHI. La combinaison de LFRSM1 avec une stimulation répétitive périphérique a augmenté significativement l’amplitude des réponses cutanéomusculaires évoquées ipsilatéralement à l’ablation de l'hémicervelet. L'augmentation de l'intensité de la réponse cutanéomusculaire était corrélée à la réduction de l’IHI. Cependant, l’excitabilité du pool des motoneurones de la corne antérieure, évaluée par l’onde F, est restée inchangée. La conjonction des LFRSM1 avec la stimulation répétitive périphérique peut donc être utilisée pour rétablir la capacité du cortex moteur de moduler l'intensité des réponses cutanéomusculaires en cas de vaste lésion cérébelleuse unilatérale. Cette étude souligne pour la première fois le rôle potentiel des voies transcalleuses dans les déficits de la modulation corticomotrice des réponses cutanéomusculaires controlatérales à la lésion cérébelleuse aiguë étendue. Nous avons ensuite étudié les effets des stimulations électriques prémotrices de basse et de haute fréquence sur les réponses corticomotrices conditionnées, sur la facilitation intra-corticale (ICF) et sur l’excitabilité spinale chez des rats hémicérébellectomisés du côté gauche. Des trains de stimulations ont été appliqués dans la région préfrontale rFR2 (équivalente des aires prémotrices et motrices supplémentaires chez les primates) à une fréquence de 1 Hz (stimulation de basse fréquence: LFS) ou de 20 Hz (stimulation de haute fréquence: HFS). Des stimuli tests sur le cortex moteur ont été précédés par des stimuli conditionnant sur le nerf sciatique controlatéral (2 intervalles inter-stimuli – ISI- ont été étudiés: 5 ms et 45 ms): (A) à un ISI de 5 ms, le conditionnement augmente les amplitudes des potentiels évoqués moteurs au niveau du cortex moteur gauche. Cette facilitation afférente est majorée si elle est précédée par des trains de stimulation appliqués sur l’aire rFR2 ipsilatérale, et la stimulation HFS a un effet plus important que la stimulation LFS. La facilitation est plus faible au niveau du cortex moteur droit, aussi bien pour la stimulation LFS que pour la stimulation HFS, (B) à un ISI de 45 ms, les potentiels moteurs conditionnés sont déprimés en comparaison aux réponses non conditionnées (mécanisme d’inhibition afférente). Après une stimulation LFS, le degré d’inhibition est inchangé. Au niveau basal, l’inhibition est majorée au niveau du cortex moteur droit. De manière intéressante, l’inhibition afférente diminue significativement à la suite de la stimulation HFS, (C) l’ICF est déprimée au niveau du cortex moteur droit, mais est sensible à la stimulation LFS et HFS. Ces résultats (1) confirment la majoration de l’inhibition au niveau du cortex moteur controlatéral à l’ablation de
l’hémicervelet, (2) démontrent pour la première fois que le cervelet est nécessaire pour la modulation fine des amplitudes des réponses corticomotrices consécutives à la stimulation nerveuse périphérique, (3) montrent que l’application de stimulation LFS ou HFS ne modifie pas les anomalies de l’excitabilité du cortex moteur pour des ISI courts, et (4) suggèrent que pour des ISI longs, la stimulation HFS pourrait avoir des propriétés intéressantes pour la modulation de l’inhibition afférente en cas de lésion cérébelleuse étendue. Etant donné que le cervelet apparaît comme un modulateur-clé de l'activité du cortex moteur, permettant la maintenance et la modulation fine des décharges du cortex moteur, et qu’un des défauts élémentaires associés aux lésions cérébelleuses aiguës est une excitabilité réduite du cortex moteur controlatéral, nous avons évalué les effets des trains de stimulation anodale transcraniale directe (tDCS), qui produisent des changements (polarité-dépendant) des potentiels de membrane, chez des rats hémicérébellectomisés. Les trains de tDCS ont contrecarré les altérations de l’excitabilité corticomotrice controlatérale à l'ablation de l’hémicervelet. Toutefois, tant la dépression du réflexe H, que la dépression de l’onde F, sont restées inchangées avec la tDCS. Les réflexes cutanéomusculaires sont aussi restés inchangés. Les trains de tDCS ont antagonisé l’hypoexcitabilité corticomotrice induite par la stimulation à haute fréquence du noyau interposé. Nos résultats montrent que les trains de tDCS ont la capacité de moduler l’excitabilité du cortex moteur après dysfonction aigüe du cervelet. En particulier, en plaçant le cortex moteur à un niveau approprié d’excitabilité, les trains de tDCS pourraient permettre au cortex moteur de devenir plus réactif aux procédures d’apprentissage ou d’entraînement. Ceci a un potentiel clinique direct pour nos patients présentant une lésion cérébelleuse aigüe étendue. Nos travaux soulignent l’importance jouée par le cervelet dans la modulation des réponses corticomotrices chez le rat Wistar, tant pour le maintien d’un niveau approprié d’excitabilité que pour une réponse adéquate à des stimuli périphériques ou centraux. Nos résultats montrent pour la première fois que la tDCS pourrait constituer une technique de thérapie pour des patients cérébelleux présentant une dépression de l’excitabilité du cortex moteur. L’hypothèse que la tDCS pourrait contrecarrer l’hypoexcitabilité corticale chez le patient ataxique mérite d’être testée. Cette technique est peu invasive et commence à être utilisée chez l’homme.
Doctorat en Sciences médicales
info:eu-repo/semantics/nonPublished
FALZONE, YURI MATTEO. "Peripheral Nervous System Involvement in Amyotrophic Lateral Sclerosis: from diagnosis to disease understanding and development of novel biomarkers." Doctoral thesis, Università Vita-Salute San Raffaele, 2022. http://hdl.handle.net/20.500.11768/128353.
Повний текст джерелаLa diagnosi della Sclerosi Laterale Amiotrofica (SLA) è principalmente basata sulla valutazione clinica e può essere talvolta problematica soprattutto quando le manifestazioni cliniche sono sovrapponibili a quelle di malattie neurologiche che possono mimare la SLA. L’assenza di test diagnostici specifici limitano la possibilità di formulare la diagnosi in fase precoce di malattia. La definizione della prognosi dei malati di SLA è limitata dall’eterogeneità fenotipica della malattia e dalla sua intrinseca variabilità inter-individuale. Alla luce di tali considerazioni, eventuali biomarcatori potrebbero essere utili nel guidare decisioni diagnostiche, terapeutiche e di valutazione prognostica. Recenti evidenze di letteratura hanno individuato i neurofilamenti a catena leggera e pesante (NfL e pNfH) come i due più promettenti biomarcatori per la SLA. Nella prima parte del nostro studio, abbiamo valutato la concentrazione sierica dei pNfH in una numerosa cohorte di pazienti affetti da SLA (n=219). I nostri risultati evidenziano che in analisi multivariata i pNfH sono risultati fattori indipendenti nel predizione della sopravvivenza dei pazienti. Inoltre, la concentrazione dei pNfH è risultata eterogenea nella popolazione SLA; i valori più elevati sono stati riscontrati nei pazienti con prevalente interessamento del I neurone di moto e concomitante elevata velocità di progressione di malattia. In seguito, abbiamo effettuato un’analisi di espressione genica e sequenziale analisi di pathways su 8 nervi motori ottenuti da pazienti SLA e 7 da pazienti con neuropatia motoria considerati come controlli. Da tale analisi abbiamo indentificato UCHL1 come una proteina potenzialmente promettente come biomarcatore per la SLA. Abbiamo analizzato i valori plasmatici di tale proteina esplorandone le potenzialità diagnostiche e prognostiche, in parallelo abbiamo misurato anche i valori plasmatici di NfL, GFAP e tTAU in coorte di pazienti SLA (n=143) e di controllo. Nel nostro studio UCHL1 non si è confermato un promettente biomarcatore per la diagnosti di SLA, tuttavia è risultato essere un fattore determinante per la definizione prognostica dei pazienti stratificando ulteriormente la prognosi dei pazienti SLA con bassi valori plasmatici di NfL. Dalle nostre analisi si conferma che NfL come i migliori biomarcatori diagnostici sia per discriminare i pazienti SLA dai controlli sani (HC) e da pazienti affetti da altre malattie neurodegenerative (DEG). Tuttavia, la performance diagnostica degli NfL nel distinguere le SLA dalle patologie SLA mimic è sensibilmente ridotta con una sensibilità del 78%. Come osservato per i pNfH, anche i livelli di NfL sono più elevati in pazienti con prevalente interessamento del I neurone di moto e concomitante elevata velocità di progressione di malattia. I livelli plasmatici di GFAP riflettono i diversi gradi di interessamento cognitivo nei pazienti affetti da SLA, infatti pazienti SLA con concomitante demenza fronto-temporale o interessamento cognitivo presentavano più elevati valori di GFAP rispetto a pazienti SLA con selettivo interessamento motorio. Alla luce di questi dati GFAP potrebbe essere un biomarcatore utile per tracciare il declino cognitivo dei pazienti con SLA.
Lindholm, Tomas. "On traumatic lesions to the spinal cord and dorsal spinal roots : factors influencing axonal regrowth across the border between the central and peripheral nervous system in rat and man /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-163-2.
Повний текст джерелаSmělý, Jiří. "Sací kanály Wankelova motoru." Master's thesis, Vysoké učení technické v Brně. Fakulta strojního inženýrství, 2017. http://www.nusl.cz/ntk/nusl-318690.
Повний текст джерелаWelin, Dag. "Neuroprotection and axonal regeneration after peripheral nerve injury." Doctoral thesis, Umeå : Umeå university, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-32819.
Повний текст джерелаAllodi, Ilary. "Changing the Intrinsic Growth Capacity of motor and sensory neurons to promote axonal growth after injury." Doctoral thesis, Universitat Autònoma de Barcelona, 2012. http://hdl.handle.net/10803/96355.
Повний текст джерелаPeripheral nerves injuries result in paralysis, anesthesia and lack of autonomic control of the affected body areas. After injury, axons distal to the lesion are disconnected from the neuronal body and degenerate, leading to denervation of the peripheral organs. Wallerian degeneration creates a microenvironment distal to the injury site that supports axonal regrowth, while the neuron body changes in phenotype to promote axonal regeneration. However, the lack of specificity of nerve regeneration, in terms of motor and sensory axons regrowth, pathfinding and target reinnervation, is one the main shortcomings for recovery. The molecular mechanisms implicated in axonal regeneration and pathfinding after injury are complex, and take into account the cross-talk between axons and glial cells, neurotrophic factors, extracellular matrix molecules and their receptors. For these reasons, we characterized a model that allows us to compare under the same conditions motor and sensory neuron regeneration. We set up an in vitro model, based on organotypic cultures of spinal cord slices and dorsal root ganglia explants from P7 rats, embedded in a collagen matrix. By adding different neurotrophic factors in the collagen matrix, we evaluated the reliability of DRG and spinal cord preparations. Moreover, we also set up a co-culture with dissociated Schwann cells to further mimic the permissive environment of the peripheral nerve. Later, we screened in vitro the different capabilities of trophic factors with promising effect on specific reinnervation of target organs after peripheral nerve regeneration. Trophic factors which promoted in vitro neuritogenesis of sensory and motor neurons were up-regulated in Schwann cells obtained from axotomized sensory and motor branches respectively. We found that FGF-2 (18 kDa) was the trophic factor that exerted the most selective effect in promoting neurite outgrowth of spinal motoneurons both in terms of elongation and arborization. The mechanism underling this effect in neuritogenesis seems related to FGF-2 enhancing the interaction between FGFR-1 and PSA-NCAM. The interaction of these two receptors is important during early stages of neuritogenesis and pathfinding, while integrin alpha7B subunit seems to play a role during neurite stabilization. With the aim to further explore the potential capacity of FGF-2 to selectiveley promote motor regeneration in vivo, we produced a lentiviral (LV) vector to overexpress FGF-2 and we characterized it in vitro and in vivo. Addition of cultured Schwann cells infected with FGF-2 into a collagen matrix embedding spinal cords or DRG significantly increased motor neurite growth but not sensory outgrowth when compared to co-cultures with LV-GFP, thus demonstrating that the LV construct was as effective as direct addition of the trophic factor to selectively promote motor neuron growth. By injecting the LV construct direclty into the sciatic nerve in vivo, we corroborated the localization of the secreted FGF-2 in the basal lamina of Schwann cells. Levels of FGF-2 from homogenated sciatic nerves one week after injection of 1μl LV-FGF-2 were higher than from nerves injected with vehicle or LV-GFP. Therefore, the LV vector can be used in vivo to verify our in vitro results and further study the capacity of FGF-2 to enhance motor nerve regeneration. In the last part of our work, we compare the abilities of Olfactory Enshealting cells and Schwann cells in sustaining in vitro motor and sensory neuritogenesis. Co-culture of cells with DRG explants and spinal cord organotypic slices was set up. SCs were promoting motoneuron growth, whereas OEC were significantly increasing neurite outgrowth in DRGs. In contrast, when OEC were added into motoneuron culture, we saw cell clusters and motoneuron outgrowth inhibition. This behaviour of OEC could be due to the maintained cytoarchitecture of the spinal cord in vitro where astrocytes and endogenous Schwann cells were also present. Interactions of SC, OEC and astrocytes through FGFR1-FGF2-HSPG complex can cause cell clustering. In fact, high levels of HSPG were found into the boundary formations, and this can explain the chemorepellent role of the cluster on neurite outgrowth.
Lloyd, Alex. "Neuromuscular fatigue, muscle temperature and hypoxia : an integrative approach." Thesis, Loughborough University, 2016. https://dspace.lboro.ac.uk/2134/21766.
Повний текст джерелаAnsari, Yekta. "The Effect of Thermal Stimulation on Corticospinal Excitability." Thesis, Université d'Ottawa / University of Ottawa, 2019. http://hdl.handle.net/10393/39328.
Повний текст джерелаGraciani, Zódja. "Caracterização motora e funcional da paraplegia espástica, atrofia óptica e neuropatia periférica (síndrome Spoan)." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/5/5138/tde-22032010-172509/.
Повний текст джерелаINTRODUCTION: Spoan syndrome is a complex form of spastic paraplegia of recessive inheritance recently identified in individuals from Southwest of Rio Grande do Norte state. Clinical features are characterized by congenital optic atrophy, progressive spastic paraplegia, and axonal neuropathy, resulting in severe handicap. Phenotypic description of this disease is nevertheless not complete; functional and quantitative studies, that would help planning a rehabilitation strategy, have not been undertaken. OBJECTIVES: To evaluate the motor performance and functional abilities of individual with Spoan syndrome. CASUISTIC AND METHODS: 61 individuals with confirmed diagnosis of Spoan, with ages ranging from 5 and 72 years were evaluated. Hand grip strength was measured with a Jamar hydraulic dynamometer and the sensitivity to deep pressure and protective hands and feet with Semmes-Weinstein nylon monofilaments. Functional abilities were verified by the Modified Barthel Index. For motor performance, the following procedures were performed: 1. Spasticity quantification, according to modified Ashworth scale; 2. Dysfunction level, according to the spastic paraplegia rating scale described by Schule and functional scale of hereditary spastic paraplegia described by Fink; 3. Gait ability, verified with deambulation index; 4.Sitting ability, using motor assessment scale. RESULTS: grip hand weakness was reduced in all patients, with a moderate inverse correlation between age and hand strength. Sensibility was abnormal in 100% of evaluated individuals in at least six points of hands and feet. Dependency level was minimum in 3.3%, moderate in 23.3%, severe in 46.6%, and total in 26.6% of individuals. According to Schule s scale , 60% of individuals scored between 40/52 and 52/52 points; in Fink s scale,71% achieved level 5 (maximum) of dysfunction. Spasticity level had a bimodal distribution, with 30,5% achieving level 1 and 37,7% level 4. Gait ability was reduced, with 83% of individuals being wheelchair bound and 11% bedridden. Sitting ability was preserved in all patients, but 53% were able to sit only with support. CONCLUSION: Spoan syndrome is a severe form of hereditary spastic paraplegia that is responsible for progressive and long lasting handicap.
Narayan, Sreenath. "REANIMATION OF A DENERVATED MUSCLE USING UPPER MOTONEURON INJURED LOWER MOTONEURONS IN SPINAL CORD INJURY PATIENTS: A RAT MODEL." online version, 2006. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1133754830.
Повний текст джерелаPereira, Gleber. "Co-ordination and fatigue of countermovement jump /." Rio Claro : [s.n.], 2007. http://hdl.handle.net/11449/100397.
Повний текст джерелаAbstract: This thesis explored the cause of fatigue in countermovement jump performed under different intensities and its influence upon movement pattern. These aims were tested using two experimental studies. The first one aimed to compare the causes of fatigue development during a short- (=10 min) and a long-term (=20 min) countermovement jump protocols through the manipulation of resting interval. The results indicated that after short-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by central and peripheral fatigue. On the other hand, after long-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by peripheral fatigue. The second study used similar exercise protocol to induce fatigue on neuromuscular system. It was aimed to investigate the movement pattern of countermovement jump throughout fatigue exercise protocols. The timing and sequencing of inter-segmental movement and of muscle activation remained relatively unaltered under fatigue. However, in order to sustain required jump height, few adjustments were performed on control and on coordination of fatigued jumps, such as increased joint flexion and earlier initiation of joint extension. This result was quite similar irrespective of fatigue-induced exercise intensities. Considering both experimental studies, the results of present thesis suggest that the cause of fatigue in countermovement jump is task-dependent in which depends on what fatigue protocol is used, thereby the cause of fatigue can move from one site to another. Even with the neuromuscular system impaired, there was not change on the movement pattern of countermovement jump, irrespective of exercise duration and cause of fatigue. However, adjustments on control and coordination of countermovement jump were performed in order to compensate the force loss and to maintain the targeted jump height.
Orientador: Eduardo Kokubun
Coorientador: José Angelo Barela
Banca: André Luiz Félix Rodacki
Banca: Ana Maria Forti Barela
Banca: Carlos Ugrinowistch
Doutor
Pereira, Gleber [UNESP]. "Co-ordination and fatigue of countermovement jump." Universidade Estadual Paulista (UNESP), 2007. http://hdl.handle.net/11449/100397.
Повний текст джерелаConselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq)
Coordenação de Aperfeiçoamento de Pessoal de Nível Superior (CAPES)
O objetivo principal desta tese foi investigar a causa e a conseqüência da fadiga em countermovement jumps realizados em diferentes razões de esforço e pausa. Esses objetivos foram testados utilizando dois estudos experimentais. O primeiro estudo comparou as causas da fadiga em protocolos de fadiga de curta (=10 min) e longa duração (=20 min), manipulando as durações da pausa entre countermovement jumps. Os resultados indicaram que, após a realização do protocolo de fadiga de curta duração, houve redução da contração isométrica voluntária máxima para extensão do joelho acompanhada por fadiga central e periférica. Por outro lado, após a realização do protocolo de fadiga de longa duração, a redução da contração isométrica voluntária máxima para extensão do joelho foi associada apenas à fadiga periférica. No segundo estudo foi utilizado um protocolo de fadiga para o sistema neuromuscular similar ao primeiro estudo, tendo como objetivo investigar o padrão de movimento sob fadiga. O tempo e a seqüência da relação inter-segmental do movimento e da ativação muscular permaneceram inalteradas sob a condição de fadiga. Entretanto, alguns ajustes no controle de countermovement jumps realizados sob a condição de fadiga foram observados, provavelmente na tentativa de manter a altura do salto vertical. Entre alguns ajustes, é possível destacar um aumento na flexão das articulações e na duração do salto vertical. Esses resultados foram similares independentemente da razão de esforço e pausa utilizada para induzir fadiga em countermovement jumps. Considerando ambos os estudos experimentais, os resultados da presente tese sugerem que a causa da fadiga em countermovement jumps é tarefa-dependente. Isso significa que dependendo do protocolo de indução de fadiga utilizado, a causa da fadiga pode ser alterada de central para periférica, por exemplo...
This thesis explored the cause of fatigue in countermovement jump performed under different intensities and its influence upon movement pattern. These aims were tested using two experimental studies. The first one aimed to compare the causes of fatigue development during a short- (=10 min) and a long-term (=20 min) countermovement jump protocols through the manipulation of resting interval. The results indicated that after short-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by central and peripheral fatigue. On the other hand, after long-term fatigue protocol, maximal voluntary isometric contraction reduction was accompanied by peripheral fatigue. The second study used similar exercise protocol to induce fatigue on neuromuscular system. It was aimed to investigate the movement pattern of countermovement jump throughout fatigue exercise protocols. The timing and sequencing of inter-segmental movement and of muscle activation remained relatively unaltered under fatigue. However, in order to sustain required jump height, few adjustments were performed on control and on coordination of fatigued jumps, such as increased joint flexion and earlier initiation of joint extension. This result was quite similar irrespective of fatigue-induced exercise intensities. Considering both experimental studies, the results of present thesis suggest that the cause of fatigue in countermovement jump is task-dependent in which depends on what fatigue protocol is used, thereby the cause of fatigue can move from one site to another. Even with the neuromuscular system impaired, there was not change on the movement pattern of countermovement jump, irrespective of exercise duration and cause of fatigue. However, adjustments on control and coordination of countermovement jump were performed in order to compensate the force loss and to maintain the targeted jump height.
Basu, Debaleena. "Neural Mechanisms underlying the planning of sequential saccades." Thesis, 2018. https://etd.iisc.ac.in/handle/2005/4076.
Повний текст джерелаRungta, Satya Prakash. "Central and Peripheral Correlates of Motor Planning." Thesis, 2017. http://etd.iisc.ac.in/handle/2005/3092.
Повний текст джерелаRungta, Satya Prakash. "Central and Peripheral Correlates of Motor Planning." Thesis, 2017. http://hdl.handle.net/2005/3092.
Повний текст джерела"Ultrasound Modulation of the Central and Peripheral Nervous System." Doctoral diss., 2015. http://hdl.handle.net/2286/R.I.34846.
Повний текст джерелаDissertation/Thesis
Doctoral Dissertation Bioengineering 2015
Hsieh, Hsiu-Min, and 謝秀敏. "fMRI Studies of Central Motor Plasticity on Patients With Upper Limb Peripheral Nerve Injury." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/96434762679953355733.
Повний текст джерела國立陽明大學
神經科學研究所
89
To examine the reorganization of human cortical area in motor system, it is important to establish the normal subjects activation pattern and then apply to clinical patients by using non-invasive functional MRI(fMRI). In this study, we start 1) to elucidate the motortotopy in the human primary sensorimotor cortex responds to specific single joint movement (simple task), 2) to investigate the effect of patients with brachial plexus injury after intercostal-musculocutaneous nerve crossing in the primary sensorimotor cortex, 3) to explore the transcallosal inhibition pattern in the human motor system while execute unilateral hand movement, 4) to dissect the effect of patients with one upper extremity paralysis influence the transcallosal inhibition pattern when their execute the same movement with unaffected hand. The data of this fMRI study demonstrated that motortotopy existed in human primary sensorimotor cortex and patients with brachial plexus injury showed plasticity in this area. Besides, normal transcallosal inhibition also was established in ipsilateral primary sensorimotor area and patients with one upper extremity paralysis exhibited a relative deactivation in supplementary motor area, cingulated motor area, and caudate. This could result from loss of transcallosal inhibition which hypotheses that unilateral hand movements are associated with contralateral cerebral activation and ipsilateral cerebral deactivation and reorganization of the motor system. Our results offer the opportunity to look into the phenomenon of plasticity in adult human brain and to exploit the functional neuroimage technique for clinical study.
Candeias, Rui Dinis Teodoro. "Evaluation of motor neuron excitability by CMAP scanning with modulated current." Master's thesis, 2014. http://hdl.handle.net/10362/14288.
Повний текст джерелаTsai, Min-Ru, and 蔡旻儒. "Changes of Intracortical Inhibition and Facilitation at Primary Motor Cortex in Patients with Peripheral Neuropathy." Thesis, 2018. http://ndltd.ncl.edu.tw/handle/2zu422.
Повний текст джерелаTu, Hui-Chin, and 涂惠靖. "The Effects of EGCG on Motor Neurons in the Lower Brain Stem Following Peripheral Nerve Injury." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/42307122688728246344.
Повний текст джерела國立臺灣大學
解剖學研究所
92
Peripheral nerve injury would alter nitric oxide synthase activity to cause neuronal degeneration or cell death via the overproduction of nitric oxide and impingement on metabolic pathways of related neurochemicals. Recent studies have shown that (-)-epigallocatechin gallate (EGCG), one of the green tea polyphenols, has a strong antioxidant property. It could attenuate hypoxia-induced nerve injuries by decreasing the production of free radicals and lipid peroxidation. The present study, by using histochemical and immunohistochemical methods, aimed to explore whether EGCG treatment might affect the diversion or provide neuroprotection of motor neurons and neuroglia cells of the hypoglossal nucleus (HN) and of the dorsal motor nucleus (DMN) in the lower brainstem of young albino rats following crush injury (CI). Thus, experimental animals were divided into 4 groups with 12 in each. Unilateral (left-sided) hypoglossal and vagus nerve at the level of mid-digastric muscle and of bifurcation of common carotid artery, respectively, was crushed for 30 seconds. They were received an injection of 10, 25, 50 mg/kg EGCG or saline 30 min prior to CI. One to 6 days after CI, same dosages of EGCG or saline were applied to experimental animals. They were then allowed to survive for 3, 7, 14, and 28 days, respectively. The present results showed that the percentage and optical density of nNOS expression in motor neurons increased to peak at 7 days after CI in HN then tend to decrease; but progressively lean to increase in DMN. The expression of ChAT in HN reaching its nadir at 3 days after CI then progressively to increase; but incline to decrease in DMN at 7 days, then followed by the decrease with time points and reached its nadir at 28 days. The expression of CGRP in HN peaked at 3 days after CI, then progressively decreased at 7 days but tended to increase at 14 days after that return to normal condition. As regards to the neuroglial cells, the expression of OX42 and GFAP in the microglia and astrocyte peaked at 7 days and then tended to decrease with various time points. The percentage and optical density of nNOS expression in motor neurons decreased following high dosages (25, 50mg/kg) of EGCG treatment, followed by the increase of the expression of ChAT and decrease of CGRP following CI. In addition, the expression of immunoreactivity in the neuroglial cells also decreased. In conclusion, motor neurons in the HN tended to respond to the high dosages (25, 50 mg/kg) of EGCG treatment following CI; this result is comparable to the effect of acute hypoxia on the nodose ganglion of rats in our previous study. However, the dosage effect was found only in DMN following ceiling dosage (50 mg/kg) of EGCG treatment. Although we do not know the detailed mechanism for the recovery potentiality of motor neurons in these two nuclei, the discrepancy might be due to both nuclei endorse with different functional components. The current study provides the first morphological evidence that EGCG might have protective effect on motor neurons and neuroglial cells in the lower brainstem of rats following CI.
Creff, Natalie Eliane. "Time course of trophic factor expression in the proximal and distal stumps of transected peripheral motor nerve /." 2005. http://bvbr.bib-bvb.de:8991/F?func=service&doc_library=BVB01&doc_number=014720453&line_number=0001&func_code=DB_RECORDS&service_type=MEDIA.
Повний текст джерелаHwang, Chiao-wen, and 黃巧雯. "Electrophysiological Studies on Peripheral Neuropathy in Rats:Comparison of Conventional Nerve Conduction Studies and Magnetic Motor Root Stimulation." Thesis, 2006. http://ndltd.ncl.edu.tw/handle/24541285606245943567.
Повний текст джерела國立中山大學
生物科學系研究所
94
Numerous mechanisms contribute to peripheral nerve injuries such as chemical intoxication, compression, stretching and avulsion, which usually result in severe damage to the sensory and motor functions. The current approaches for evaluating nerve regeneration include expression analysis of molecular markers, histological analysis, behavior testing and electrophysiological studies. The aim of this study is to compare the diagnostic efficacy using the recently developed magnetic stimulation approach with that of conventional electrical stimulation method in different models of peripheral neuropathy and to compare in terms of latency and amplitude of the evoked response by electrical and magnetic stimulation. Adult male Sprague Dawley rats (250-300 g, n = 24) were divided into three groups: (1) control group, (2) sciatic nerve ligation group and (3) acrylamide intoxication group. The electrophysiological studies were carried out 3 days before ligation and every 7 days after ligation for 4 weeks. The measurements included amplitude and onset latency of maximal compound nerve action potential (CMAP) in branches of sciatic nerve (nerves to the gastrocnemius, tibialis anterior), motor nerve conduction velocity, H-reflex, F-wave, amplitude and onset latency of motor evoked potential by lumbosacral motor root magnetic stimulation, and denervation by electromyography (gastrocnemius, tibialis anterior). The results from studies using magnetic and electrical stimulation showed prominent reduction of CMAP amplitude in rats of sciatic nerve ligation and acrylamide intoxication group. The CMAP amplitude measured by magnetic stimulation was 76~85% of that by electrical stimulation. By either magnetic stimulation or electrical stimulation, there was no significant difference in the mean onset latency of CMAP between control and neuropathy groups. Volume conduction accounts for the interference of waveform and error is inevitable. Because of the short distance of hind limb of the rat, the nerve conduction velocity (NCV), H-reflex and F-wave could not be determined using magnetic stimulation. In contrast, electrophysiological analysis by electrical stimulation revealed slowed NCV, prolonged or absent H-reflex and F-wave in animals of neuropathy groups. Electromyography showed prominent denervation potentials over the sampling muscles in both models. In conclusion, magnetic stimulation of lumbosacral motor root is non-invasive and convenient. However, further improvement and establishment of basic parameters are required to facilitate a reliable tool in evaluation of peripheral nerve injury.
張宏名. "Effects of peripheral nerve injury along with hypoxia on the motor neurons,sensory neurons and glia cells in rats." Thesis, 2001. http://ndltd.ncl.edu.tw/handle/02431824437303005545.
Повний текст джерела國立臺灣大學
解剖學暨細胞生物學研究所
89
Either peripheral nerve injury or hypoxia will alter the NMDA receptor activity and result to neuronal degeneration or cell death via the over production of nitric oxide and affecting the metabolic pathways of related neurochemicals. By using the histochemical and immunohistochemical methods, the present study was aimed to determine the relationship between the neurochemical expression and neuronal degeneration of motor neurons, sensory neurons and glia cells under peripheral nerve injury along with hypoxia treatment. This study was also thought to explore whether the extra-administration of anti-oxidant (i.e. melatonin) will exert its neuroprotective effect on the lesioned neurons. Firstly, the acute high altitude (10000 m) hypoxic exposure was selected as the experimental paradigm to determine the effect of hypoxia on the expression patterns of related neurochemicals of sensory and motor neurons. The results revealed that after acute hypoxia treatment, the nitric oxide synthase (NOS), NMDA receptor as well as the calcitonin gene-related peptide immunoreactivities in the nodose ganglion were up-regulated, while the cytochrome oxidase (an endogenous metabolic marker) and the acetylcholinesterase histochemical staining were down-regulated. Significant neuronal loss was detected in the nodose ganglion 2 weeks following acute hypoxic exposure. On the contrary, acute hypoxia did not cause any noticeable changes in lower brainstem motor neurons bearing different functional component. Based on these results, we suggest that acute hypoxia will induce NMDA receptor mediated NOS activation in the sensory neuron, by excessive generation of free radicals and disturbing the energy metabolic pathway and neurotransmitter function, directly lead to neuronal damage or cell death. Furthermore, the peripheral nerve injury coupled with hypoxia was adopted as the double injury model to determine and compare the related neurochemical expression among the lower brainstem motor neurons bearing different functional component. The results indicated that following unilateral transection of the vagal and hypoglossal nerves, the NOS immunoreactivities were drastically increased in the lesioned nuclei. The extent of NOS up-regulation was positively correlated with the severity of neuronal damage. Besides, with the over production of nitric oxide, peripheral nerve injury and hypoxia will also suppress the reactivities of cytochrome oxidase, choline acetyltransferase as well as the Mn-superoxide dismutase (an anti-oxidant enzyme). On the other hand, axotomy along with hypoxia will cause the microglia and astrocyte activation within the lesioned nuclei as revealed by the GSA-IB4 lectin binding method and the glia fibrillary acidic protein immunohistochemistry, respectively. The expression patterns of related neurochemicals, activated status of glia cells and the numbers of neuronal loss were all more significant in the double injury treated rats as compared with those of normoxic ones. Based on these results, we suggest that peripheral nerve injury along with hypoxia will contribute to the severer neuronal damage via the over activation of NOS, which could subsequently broke the metabolic pathway, neurotransmitter function as well as the balanced status of the free radical/ anti-oxidative defense system. Results of the effects of melatonin on the acute hypoxia or peripheral nerve injury were indicated that melatonin would indeed suppress the NOS expression and reduce the neuronal demage in the lesioned neurons. The suppressive effect of melatonin on the NOS expression was dose dependent. The present study not only provides the first morphological evidence concerning the neuroprotective effect of melatonin but also increases the current knowledge for the therapeutic use of melatonin as a clinical trial to forestall the related neuropathies induced by hypoxia or peripheral nerve injury. In summary, by the use of acute hypoxia or peripheral nerve injury along with hypoxia as experimental models, the present study was clearly demonstrated the relationship between the related neurochemical expression and neuronal damage in the sensory neurons, motor neurons and glia cells. The results obtained from the present study will not only help us to better understand the physiological significance of hypoxia on the peripheral nerve injury, but also document the possible functional roles of related neurochemicals during the process of neuronal degeneration.
Tsung-Hsun, Hsieh, and 謝宗勳. "Modulation of Motor Evoked Potentials (MEPs) and H-reflexes after Peripheral Nerve Stimulation in Individuals with Sensory Impairment following SCI." Thesis, 2004. http://ndltd.ncl.edu.tw/handle/38207643581477853655.
Повний текст джерела長庚大學
復健科學研究所
92
Somatosensory input was required for accurate motor performance and for new motor skill learning. In humans, above motor threshold peripheral nerve stimulation resulted in an increased excitability of the motor pathway to the stimulated body parts. The purpose of this study was to investigate whether peripheral sensory afferents was essential in facilitation of motor pathway by electrical stimulation. Eight subjects with sensory impairment following SCI and nine healthy subjects were recruited. Motor evoked potentials (MEP), silent period(SP) elicited by 120% motor threshold transcranial magnetic stimulation (TMS), and H-reflex elicited by median nerve stimulation were recorded on flexor carpi radialis (FCR) muscle before, during, immediately and 30 minutes after repetitive electrical stimulation (25 Hz, on/off=800ms/ 800 ms) on median nerve. In healthy subjects, the averaged amplitude of MEP increased to 154±29% of initial (P=0.01) after repetitive electrical stimulation. This increment became statically non-significant 30 min after the stimulation stopped. In subjects with SCI, the MEP did not change. The H-reflex and low frequency depression ratio did not change in both subjects. We concluded that the sensory afferent input was essential to facilitate the corticomotoneuronal excitability during peripheral nerve stimulation.
Wang, Chao-Ting, and 王昭鼎. "A Study of Automobile Businesses Customer Relationship Management (CRM) with its Peripheral Businesses development ─A Case of Taiwan Yulon Motor Corporation." Thesis, 2003. http://ndltd.ncl.edu.tw/handle/55980980420341774286.
Повний текст джерела中原大學
企業管理研究所
91
The purpose of this research in understanding the competence of Taiwan automobile business environments, and the strategy planning of Taiwan car companies and their peripheral companies in Customer Relationship Management (CRM). By using the CRM strategies of mother company and information system, in order to satisfy the customers “Moving with Convenience,” also provide full range service, products difference, market segmentation, ensure the advantage of competence. In year 2000, Yulon Motor Group base on the 50% of automobile market share, starting the company Third stage (III) reengineering program. The peripheral business, being the stretch policy of Group’s Moving Value Chain (MVC) strategy, included: auto clinic, used car sales, car leasing, travel agent, insurance, financial loan, publisher, call center, high-tech products and integration information system. Above all focus on satisfies the customers, while they are driving & moving. Due to the complexity and variety of automobile industry, we need a systemize analysis and information platform, in order for manager integrate relative strategies efficiently. By common sharing resources, dual communicate with headquarter system, integrate down-stream business and peripheral value chain, create enterprise re-engineering process. Service all customers, by using electrical analytic data; improve customer’s royalty and satisfaction, finding potential business opportunities. According to customer’s requirements, develop differential products from the competitors; ensure the long-term competing advantage of company. Above mentioned automobile business characteristics, we can realize they have certain level of interactions among with social communities, enterprises and individuals. So how to enhance the competence and development of Taiwan local automobile business, the schools, enterprises and government, should concern this subject.
Roy, Francois D. "Associative plasticity and afferent regulation of corticospinal excitability in uninjured individuals and after incomplete spinal cord injury." Phd thesis, 2009. http://hdl.handle.net/10048/632.
Повний текст джерелаBořilová, Karolína. "Elektromyografické a klinické hodnocení vinkristinem indukované periferní neuropatie u pediatrických pacientů po dokončení léčby akutní lymfoblastické leukemie a korelace s Bruinkins-Oseretsky Test of Motor Proficiency - second edition." Master's thesis, 2020. http://www.nusl.cz/ntk/nusl-435228.
Повний текст джерелаMa, Xiya. "La formation de synapses par les neurones périphériques sur des surfaces synthétiques." Thèse, 2018. http://hdl.handle.net/1866/22316.
Повний текст джерела