Thèses sur le sujet « Nervous system – wounds and injuries – fiction »
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Moore, Leah Kathryn. « Neuronal viability and biochemical alterations after mechanical stretch injury : ban in vitro model of traumatic brain injury-induced neourodegeneration ». Thesis, Georgia Institute of Technology, 2003. http://hdl.handle.net/1853/5362.
Texte intégralMargand, Paul Marcus Buchanan. « Ultrastructural changes in electrically damaged x-enopus laevis sciatic nerve ». Scholarly Commons, 1991. https://scholarlycommons.pacific.edu/uop_etds/2217.
Texte intégralBastos, Lopes Alves João Nuno. « Strategies to block inhibition and restore plasticity in the central nervous system after injury ». Thesis, University of Cambridge, 2015. https://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.708968.
Texte intégralYuan, Qiuju, et 袁秋菊. « The plasticity of hypothalamic magnocellular system following axonal damage by hypophysectomy in developing and adult rats ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2004. http://hub.hku.hk/bib/B30301117.
Texte intégralShi, Ri Yi. « Neuronal Survival After Dendrite Amputation : Investigation of Injury Current Blockage ». Thesis, University of North Texas, 1988. https://digital.library.unt.edu/ark:/67531/metadc501278/.
Texte intégralHobbs, Catherine E., et n/a. « Perinatal hypoxia-ischaemia : neuroprotective strategies ». University of Otago. Department of Anatomy & ; Structural Biology, 2005. http://adt.otago.ac.nz./public/adt-NZDU20070221.145910.
Texte intégral袁秋菊 et Qiuju Yuan. « Effects of neurotrophic factors on motoneuron survival following axonal injury in developing rats ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2001. http://hub.hku.hk/bib/B42128705.
Texte intégralMillner, Mary Angela. « Modulation of CSPG sulfation patterns through siRNA silencing of sulfotransferase expression to promote CNS regeneration ». Thesis, Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/24647.
Texte intégralNiu, Chenchen, et 牛晨晨. « The neuroprotective signaling mechanisms of telomerase via the induction by brain-derived neurotrophic factor (BDNF) in nervoussystem injury ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2010. http://hub.hku.hk/bib/B45152883.
Texte intégralHu, Ying. « Optic nerve regeneration in adult rat ». University of Western Australia. School of Anatomy and Human Biology, 2007. http://theses.library.uwa.edu.au/adt-WU2007.0080.
Texte intégralJin, Ying, et 金瑩. « Neuronal survival and axonal regeneration of the lateral vestibular nucleus in rats after spinal cord injury ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31237113.
Texte intégralBell, Heather C., et University of Lethbridge Faculty of Arts and Science. « Playful feedback and the developing brain ». Thesis, Lethbridge, Alta. : University of Lethbridge, Faculty of Arts and Science, 2008, 2008. http://hdl.handle.net/10133/747.
Texte intégralx, 93 leaves : ill. ; 29 cm.
易亮華 et Leung-wah Yick. « Promotion of neuronal survival and axonal regeneration in Clarke's nucleus after spinal cord injury in adult rats ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1999. http://hub.hku.hk/bib/B31239651.
Texte intégral陳博文。 et Pok-man Chan. « Cloning of hamster GAP-43 to study the expression and regulation of GAP-43 mRNA in the retina during degeneration and regeneration ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1998. http://hub.hku.hk/bib/B31220423.
Texte intégralAllbutt, Haydn. « The rat spinal cord following traumatic injury : An anatomical and behavioural study examining NADPH-d and fos ». Thesis, The University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Texte intégralAllbutt, Haydn. « The rat spinal cord following traumatic injury : An anatomical and behavioural study examining NADPH-d and fos ». University of Sydney, 2004. http://hdl.handle.net/2123/1335.
Texte intégralThe general aim of this current work was to examine spinal cord injury (SCI), and in particular to examine the pathology of injury as it relates to changes in sensory transmission. Due to the limited possibilities for experimentation in humans, a range of animal models of SCI have been developed and are reviewed here. The weight drop SCI model is the most similar to the clinical presentation of SCI in humans and has been widely used in the rat. It was selected for the series of experiments reported in this thesis. Many of the functional deficits produced by SCI result from a cascade of biochemical events set into motion by the injury. Included amongst these is the activation of the enzyme nitric oxide synthase which produces the gaseous neuromodulator, nitric oxide (NO). NO is amongst the most widely distributed and widely utilised molecule in virtually all living organisms, and it is an important signalling molecule in the nervous system. One of the major functions performed by NO appears to relate to sensory transmission, and thus alterations in sensory transmission observed as a result of SCI may involve alterations to NO synthesis. One of the principal aims of this thesis was to examine the effect of SCI on the NO producing cells of the spinal cord and to consider what any changes in NO synthesis may suggest in regards to sensation. NO producing cells were examined using NADPH diaphorase (NADPH-d) histochemistry. As the symptoms of SCI such as motor loss and changes in sensory processing are functional changes, it was also useful to examine changes in neuronal function as a result of SCI. Widespread neuronal function was examined via immunohistochemical detection of the gene product of the immediate early gene, c-fos. It is not known how extensive the biochemical changes resulting from SCI may be, thus another of the aims of the present thesis was to examine the effects of SCI on NO synthesis not only at the level of injury, but also distant to the injury. Findings of the present thesis indicated that traumatic SCI resulted in a decrease in the number of NADPH-d positive cells from the superficial dorsal horn (SDH) of the spinal cord, while the number of these cells are increased in the ventral horn. These changes were restricted to spinal segments adjacent to the injury. Fos expression was also altered by injury and was found to decrease. The most profound changes were found to occur in lamina III, although the other laminae also demonstrated similar changes. Changes in fos expression however were notably more widespread than those for NADPH-d and were not restricted to the level of the injury, occurring at all levels of the spinal cord examined. It was interpreted that alterations in NO synthesis appear to be modulated by the local injury-induced environment while fos expression may be altered by widespread changes to the global level of activity within the central nervous system. Having observed that the number of NADPH-d positive cells of the SDH is reduced following injury, it was of interest to determine whether these cells were in fact killed, or whether they were still present but with reduced NADPH-d activity. Cell counts suggested that the NADPH-d positive cells, which were likely to represent a population of inhibitory interneurons, were not killed following injury, but rather are disrupted such that their normal biochemistry is altered. Since these cells were likely to be inhibitory and were located in laminae involved in sensory transmission, the question arose how disruption of these cells may relate to the neuropathic pain observed to develop following SCI. Thus both NADPH-d and fos expression were again examined, but this time in conjunction with the sensory function of the rats. Sensory thresholds to pain-like behaviour were determined prior to and after injury using Von Frey filaments. Rats that demonstrated a decrease in sensory threshold of at least two Von Frey filament gradations (>70%) were classed as allodynic, while those with a less than a 70% decrease in threshold were classed as non-allodynic. A subpopulation of each of the groups of rats (uninjured, non-allodynic and allodynic) underwent a somatic stimulation paradigm. It was found that stimulation resulted in an increase in the number of NO producing cells but only in the allodynic group of animals. Since this group of animals by definition would perceive this stimulation as noxious, it is likely that the noxious nature of the stimulation resulted in the increased number of NO producing cells observed. This effect occurred only in segments adjacent to the injury. When fos expression was examined in the uninjured animals it was noted that somatic stimulation resulted in a decrease in fos expression, almost exclusively in lamina III. Following injury, there was no change in fos expression in lamina III observed. Instead the only change observed was an increase in fos expression in the deep dorsal horn (DDH, lamina IV and V). This occurred most profoundly in the allodynic group. These results suggested that SCI may lead to misprocessing of sensory signals such that non-noxious somatic stimuli are processed in the DDH rather than lamina III following SCI. It is proposed here that this change in laminae processing may be responsible for the perception of pain towards a non-noxious stimulus, and that the reported injury-induced loss of NO producing inhibitory interneurons in the SDH may be responsible for this alteration in sensory processing following SCI. Sensation is also processed by a number of supraspinal structures and a number of these have been implicated in the development of neuropathic pain states. The effects of SCI on neuronal activity as well as NO synthesis were examined in the periaqueductal grey region of the mid brain (PAG). SCI was shown to result in reduced neuronal activity in the PAG. This reduction in activity did not follow the somatotopy of the lateral column of the PAG (lPAG). It was suggested the reduced activity may not be solely caused by reduced spinal input as a result of SCI. Reduced neuronal activity in the PAG may indicate reduced PAG function, which includes descending modulation of spinal sensory transmission. Injury was not found to alter NADPH-d expression in the PAG. The effect of traumatic lumbar SCI on the parietal (sensorimotor) cortex of the rat was also examined, as loss of inputs following SCI have been shown to result in a profound reorganisation of the cortex. Results indicated that SCI results in a virtual cessation of neuronal activity in areas 1 and 2 of the parietal cortex, likely as a result of lost afferent drive. Theories of cortical plasticity suggest that while the primary inputs via the lumbar spinal cord may be lost following SCI, other less dominants input will remain and become more dominant. It has been proposed previously that cortical reorganisation involves a rapid reorganisation of the entire sensory system. It was interpreted that a similar process may explain the system-wide reduction in neuronal activity observed in the present series of studies.
Stabenfeldt, Sarah Elizabeth. « Bioactive thermoresponsive hydrogels for neural tissue engineering ». Diss., Atlanta, Ga. : Georgia Institute of Technology, 2007. http://hdl.handle.net/1853/26680.
Texte intégralCommittee Chair: LaPlaca, Michelle; Committee Member: Bellamkonda, Ravi; Committee Member: Garcia, Andres; Committee Member: Hochman, Shawn; Committee Member: Wang, Yadong. Part of the SMARTech Electronic Thesis and Dissertation Collection.
Khong, Pek-Lan, et 孔碧蘭. « Diffusion tensor MR imaging in the evaluation of treatment-induced white matter injury in childhood cancer survivors ». Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B38320666.
Texte intégralEsteves, Luiz Adriano 1972. « Avaliação do tratamento das lesões traumáticas da junção craniocervical ». [s.n.], 2015. http://repositorio.unicamp.br/jspui/handle/REPOSIP/312694.
Texte intégralDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
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Resumo: INTRODUÇÃO: As lesões traumáticas da junção craniocervical constituem um grupo heterogêneo de afecções que acometem os ossos da base do crânio, o atlas, o áxis e as estruturas ligamentares que os estabilizam. OBJETIVOS: Avaliar a correlação entre o tratamento empregado, as características das lesões e o resultado clínico em pacientes com diagnóstico de lesões traumáticas na junção craniocervical. MÉTODO: Realizou-se estudo retrospectivo de pacientes maiores de 18 anos com diagnóstico de trauma na junção craniocervical tratados em um hospital terciário. RESULTADOS: Foram analisados 37 pacientes, sendo a maioria do sexo masculino (73%), com idade média de 41,7 anos. Doze pacientes (32%) foram submetidos à cirurgia precoce quando do diagnóstico das lesões e 24 (68%) a tratamento conservador com órtese cervical rígida. Sete pacientes (29%) do grupo conservador foram submetidos posteriormente à cirurgia devido à falha no tratamento. No grupo cirúrgico, houve sete casos de fratura de odontóide tipo II, dois casos de fratura de elementos posteriores do áxis, um caso de luxação C1-C2, um caso de deslocamento occipito-cervical e um caso de fraturas de C1 e C2 e luxação facetária. Apenas um paciente apresentava déficit neurológico incompleto que melhorou após o tratamento. Houve dois casos de complicações pós-cirúrgicas, uma fístula liquórica e uma infecção de ferida operatória, sendo que a infecção requereu reabordagem para debridamento. No grupo conservador predominaram as fraturas do odontóide (oito casos) e a dos elementos posteriores de C2 (cinco casos). Em dois casos, além das lesões da junção craniocervical, havia fraturas em outros segmentos da coluna. Nenhum dos pacientes do grupo de tratamento conservador, inclusive aqueles submetidos à cirurgia posteriormente, apresentou deterioração neurológica. CONCLUSÃO: As lesões da junção craniocervical são raras, sendo as mais frequentes as fraturas do odontóide e dos elementos posteriores do áxis. Os resultados obtidos nos levam a sugerir o tratamento cirúrgico precoce para as fraturas do odontóide tipo II (mesmo na ausência de fatores de risco) e para os pacientes com lesões ligamentares. Para as demais lesões, o tratamento conservador, com órtese cervical rígida, mostrou-se adequado
Abstract: Abstract INTRODUCTION: Traumatic injuries of the craniocervical junction are a heterogeneous group of injuries, affecting the bones of the skull base, the atlas and the axis and their stabilizing ligaments. OBJECTIVES: Evaluate the correlation between the treatment used, the characteristics of the lesions and the clinical outcome of patients with traumatic injuries in the craniocervical junction. METHOD: A retrospective study of patients older than 18 years of age with traumatic injury in the craniocervical junction treated at a tertiary hospital. RESULTS: We analyzed 37 patients, mostly male (73%), with a mean age of 41.7 years. Twelve patients (32%) were submitted to surgical treatment at the time of diagnosis and 24 received conservative treatment (24%). Of these, seven (29%) were posteriorly submitted to surgery due to failure of the conservative treatment. In the surgical group, there were seven cases of odontoid type II fractures, two cases of fracture of the posterior elements of the axis, one case of C1-2 dislocation (with associated fracture of C2), one case of occipitocervical dislocation, and one case of fractures of C1, C2 and facet dislocation. Only one patient had an incomplete neurological deficit which improved after treatment. In the group treated conservatively, odontoid fractures (eight cases) and the fracture of the posterior elements of C2 (five cases) predominated. In two cases, in addition to the injuries of the craniocervical junction, there were fractures in other segments of the spine. None of the patients who underwent conservative treatment, including those undergoing surgery later presented neurological deterioration. CONCLUSION: Injuries of the craniocervical junction are rare, and frequently present as fractures of the odontoid and the posterior elements of the axis. Our results recommend early surgical treatment for type II odontoid fractures, even in the absence of risk factors and for patients with ligament injuries. For other injuries, conservative treatment, with rigid cervical collar, was adequate
Mestrado
Neurologia
Mestre em Ciências Médicas
Wolf, Amy. « In Vitro Studies of Nuclear Changes in Mammalian CNS Neurons Subjected to Rapid Acceleration Impact Injury ». Thesis, University of North Texas, 1995. https://digital.library.unt.edu/ark:/67531/metadc278044/.
Texte intégralSimon, Crystal Michelle. « Investigation of plasma membrane compromise and citicoline-mediated repair after spinal cord injury repair ». Diss., Atlanta, Ga. : Georgia Institute of Technology, 2008. http://hdl.handle.net/1853/28276.
Texte intégralCommittee Chair: LaPlaca, Michelle; Committee Member: Backus, Deborah; Committee Member: Bellamkonda, Ravi; Committee Member: Lee, Robert; Committee Member: Prausnitz, Mark.
Colley, Jennifer Margaret. « The psycho-social impact of pain on spinal cord injured patients ». Thesis, 2012. http://hdl.handle.net/10210/6557.
Texte intégralSpinal cord trauma resulting in paraplegia or quadriplegia is one of the most devastating injuries. A frequent complication of spinal cord injury is intractible pain. It compounds a host of personal and social consequences: disruption of personal roles, dysfunctional marital and family relationships, unemployment, financial hardship, depression, anxiety, lowered self-esteem and hopelessness. There is an abundance of research on pain in general, but a dearth of literature on chronic pain in the spinal cord injured population - especially in the South African context. This study examined the psychosocial impact of pain on spinal cord injured patients in a hospital setting. Specifically, it addressed six core research questions, concerned with the physiological components of pain, and the social, affective and rehabilitation consequences of pain for spinal cord injured patients. The effects of etiology and level of lesion, age, gender and culture on the general pain experience were investigated. The purpose of this study was to accurately describe the phenomenon of pain as experienced by spinal cord injured (SCI) patients. The evidence showed that pain was a serious problem for SCI patients. A variety of physical and social modifiers of the pain experience were identified, as were several important temporal features of pain. SCI patients reported high frequencies of social, affective (depression, low selfesteem, suicidal responses and partner relationship problems), and rehabilitation consequences. The etiology of spinal cord injury was found to be related to pain intensity, while the level of the lesion was not associated with pain intensity or frequency. Some effect was found for age, however, gender did not contribute to the variance of any of the dependent variables. The culture of SCI patients plays an important role in both pain perception and the psychosocial and rehabilitation consequences of chronic pain. The results suggest that pain in SCI patients, as in other pain populations, needs to be recognized as a complex, multidimensional phenomena. Successful treatment requires an understanding of the SCI patient's emotional and psychological, as well as his physical requirements. The role of pain assessment is fundamental to any pain management programme.
« Insulin-like growth factor-1 to improve neurological recovery after acute spinal cord injury : a porcine study ». 2012. http://library.cuhk.edu.hk/record=b5549520.
Texte intégral研究方法:以運動誘發電位為指導,通過直接壓迫和牽拉造成脊髓損傷。18頭猪只隨機分為3組:胰島素樣生長因子-1治療組、生長激素治療組及生理鹽水對照組。脊髓損傷后1小時、24小時及48小時經鞘內注射給藥。于術後第1天、第3天及第21天收集腦脊液檢測胰島素樣生長因子-1和生長激素濃度。連續21天使用修正的 Tarlov 評分標準對動物的運動功能進行評估。第21天處死動物並取材,檢測脊髓中NeuN, GFAP, caspase-3 的活性,并通過TUNEL染色觀察細胞凋亡情況,比較各組之間有無差別。
研究結果:通過這種方法建立的脊髓損傷動物模型穩定可靠,各組之間無明顯差異。鞘內給藥24小時及48小時后,腦脊液中胰島素樣生長因子-1和生長激素濃度明顯升高,術後21天檢測,其濃度恢復至基礎值。胰島素樣生長因子-1治療組的運動功能的恢復優於其它各組。與生理鹽水對照組比較,胰島素樣生長因子-1治療組可以明顯提高脊髓損傷后神經元的存活數量,抑制星形膠質細胞增生,減少細胞凋亡。而生長激素治療組僅抑制星形膠質細胞增生,其它方面與生理鹽水對照組無明顯差別。
結論:胰島素樣生長因子-1通過提高神經元存活數量,抑制星形膠質細胞增生,以及減少細胞凋亡促進脊髓損傷的恢復。
Objective: Spinal cord injury is a devastating condition that leads to long-term disabilities. Currently, there is no effective treatment that minimizes spinal cord damage or enhances neurological recovery. Recent studies in rats or rabbits suggested that neurologic recovery after spinal cord injury could be improved with the administration of neurotropic hormones, such as insulin-like growth factor-1 (IGF-1). In order to apply such bench-side discovery to clinical practice, we conducted a study in a higher animal model, akin to human physiology, to evaluate the effectiveness of intrathecal injections of IGF-1to improve neurological recovery in a porcine model of acute traumatic spinal cord injury.
Methods: Traumatic spinal cord injury model was produced by controlled compression and distraction of the exposed T12 segment of the spinal cord. Eighteen pigs were randomly assigned to receive intrathecal injections of either IGF-1, growth hormone or saline at 1, 24 and 48 hours after spinal cord injury. Locomotor function was assessed daily using the validated modified Tarlov’s scale for 21 days. Spinal cord segments were then harvested and the survival of neurons, reactive astrogliosis and apoptosis were determined using neuronal-specific nuclear protein (NeuN), glial fibrillary acidic protein (GFAP), cleaved caspase-3 and terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL) assays.
Results: Intrathecal injections of IGF-1 and growth hormone significantly increase the concentrations of the neurotropic hormones in the cerebrospinal fluid after injury (p < 0.01). These concentrations returned to baseline by 21 days after drug delivery. Motor deficits on the first day after injury were comparable between animals in the treatment and control groups. By the end of the third week, neurologic recovery was better in animals receiving IGF-1 treatment (p < 0.05). Immunohistological and western blot studies of the injured segments of spinal cord showed that treatment with both IGF-1 and growth hormone prevented reactive astrogliosis (p < 0.05) while only IGF-1 improved the survival of mature neurons (p < 0.05). IGF-1 also inhibited apoptosis after spinal cord injury (p < 0.05).
Conclusions: In our clinically relevant model of traumatic spinal cord injury in pigs, intrathecal injection of IGF-1 demonstrated beneficial effects on neurological and histological recovery.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Detailed summary in vernacular field only.
Wang, Qinzhou.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2012.
Includes bibliographical references (leaves 105-122).
Abstract also in Chinese.
Declaration of origination --- p.I
Abstract --- p.II
Acknowledgements --- p.VI
Table of Contents --- p.VIII
List of Tables --- p.XII
List of Figures --- p.XIII
Abbreviations --- p.XVIII
Chapter Part 1 --- Spinal Cord Injury: A Review --- p.1
Chapter Chapter 1-1 --- Acute Spinal Cord Injury: Epidemiology, Socioeconomic Impact --- p.2
Chapter 1.1.1 --- Epidemiology of Spinal Cord Injury --- p.2
Chapter 1.1.2 --- Socioeconomic Impact of Acute Spinal Cord Injury --- p.5
Chapter Chapter 1-2 --- Mechanisms of Spinal Cord Injury --- p.6
Chapter Chapter 1-3 --- Putative Treatments for Spinal Cord Injury --- p.8
Chapter 1.3.1 --- Methylprednisolone --- p.8
Chapter 1.3.2 --- Stem Cell Therapy --- p.11
Chapter 1.3.3 --- Riluzole --- p.11
Chapter 1.3.4 --- Other Pharmacological Therapies for Spinal Cord Injury --- p.12
Chapter Chapter 1-4 --- Insulin-like Growth Factor-1 for the Treatment of Spinal Cord Injury --- p.13
Chapter Chapter 1-5 --- Summary --- p.17
Chapter Part 2 --- Insulin-like Growth Factor-1 and Growth Hormone for Spinal Cord Injury --- p.18
Chapter Chapter 2-1 --- Hypothesis and Objectives --- p.19
Chapter Chapter 2-2 --- Establishment of Animal Models for Acute Spinal Cord Injury --- p.22
Chapter 2.2.1 --- Introduction --- p.22
Chapter 2.2.2 --- Experimental Animals --- p.22
Chapter 2.2.3 --- Anesthesia --- p.23
Chapter 2.2.4 --- Transcranial Electrical Motor Evoked Potential --- p.26
Chapter 2.2.5 --- Surgery --- p.28
Chapter 2.2.6 --- Statistics --- p.34
Chapter 2.2.7 --- Results --- p.34
Chapter 2.2.8 --- Discussion --- p.38
Chapter Chapter 2-3 --- Optimal Stimulation Protocols for Transcranial Electrical Motor Evoked Potential. --- p.42
Chapter 2.3.1 --- Introduction --- p.42
Chapter 2.3.2 --- Methods --- p.42
Chapter 2.3.2.1 --- Experimental Animals and Anesthesia --- p.42
Chapter 2.3.2.2 --- Transcranial Electrical Motor Evoked Potential Recording --- p.44
Chapter 2.3.2.3 --- Stimulation Protocol --- p.44
Chapter 2.3.3 --- Analyses --- p.44
Chapter 2.3.4 --- Results --- p.45
Chapter 2.3.5 --- Discussion --- p.52
Chapter Chapter 2-4 --- Evaluation of the Efficacy of Insulin-like Growth Factor-1 and Growth Hormone in a Porcine Model --- p.54
Chapter 2.4.1 --- Introduction --- p.54
Chapter 2.4.2 --- Materials and Methods --- p.54
Chapter 2.4.2.1 --- Study Design --- p.54
Chapter 2.4.2.2 --- Intrathecal Injection and Collection of Cerebrospinal Fluid --- p.58
Chapter 2.4.2.3 --- Measurements --- p.58
Chapter 2.4.2.3.1 --- Clinical Evaluation --- p.58
Chapter 2.4.2.3.2 --- Biochemical Assessments --- p.58
Chapter 2.4.2.3.3 --- Spinal Cord Section, Histological and Immunochemical Staining --- p.63
Chapter 2.4.2.3.4 --- Western Blot --- p.69
Chapter 2.4.3 --- Statistical Analysis and Sample Size Calculation --- p.72
Chapter 2.4.3.1 --- General Analysis --- p.72
Chapter 2.4.3.2 --- Sample Size --- p.72
Chapter 2.4.4 --- Results --- p.73
Chapter 2.4.4.1 --- Changes of TceMEP --- p.73
Chapter 2.4.4.2 --- Motor Deficit after Spinal Cord Injury at Baseline --- p.75
Chapter 2.4.4.3 --- Insulin-like Growth Factor-1 and Growth Hormone in Cerebrospinal Fluid --- p.77
Chapter 2.4.4.4 --- Clinical Assessment --- p.80
Chapter 2.4.4.5 --- Demyelination, Neuron Survival and Astrocyte Reaction --- p.85
Chapter 2.4.4.6 --- Apoptosis --- p.89
Chapter 2.4.5 --- Discussion --- p.93
Chapter 2.4.5.1 --- Principal Findings --- p.93
Chapter 2.4.5.2 --- Insulin-like Growth Factor-1 and Neuroprotection after Spinal Cord Injury --- p.93
Chapter 2.4.5.3 --- Growth Hormone and Neuroprotection after Spinal Cord Injury --- p.95
Chapter 2.4.5.4 --- Strengths and Limitations of Our Study --- p.96
Chapter 2.4.5.5 --- Summary --- p.97
Chapter Part 3 --- Summary and Future Directions --- p.99
Chapter Chapter 3-1 --- Summary --- p.100
Chapter Chapter 3-2 --- Future Directions --- p.103
Chapter Part 4 --- References and appendixes --- p.104
References --- p.105
Appendixes --- p.123
Mureriwa, Joachim F. L. « Traumatic brain injury and attention : postconcussion symptoms and indices of reaction time ». Thesis, 1997. http://hdl.handle.net/10500/17545.
Texte intégralPsychology
Ph. D. (Psychology)
Clark, Jillian Mary. « The relationship of mineral and bone metabolism in the systematic response to neurotrauma of adult males with spinal cord injury ». 2008. http://hdl.handle.net/2440/57507.
Texte intégralhttp://proxy.library.adelaide.edu.au/login?url= http://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1345019
Thesis (Ph.D.) - University of Adelaide, School of Medicine, Discipline of Orthopaedics and Trauma, 2008
Deng, Lingxiao. « Regeneration and plasticity of descending propriospinal neurons after transplantation of Schwann cells overexpressing glial cell line-derived neurotrophic factor following thoracic spinal cord injury in adult rats ». 2015. http://hdl.handle.net/1805/7347.
Texte intégralAfter spinal cord injury (SCI), poor axonal regeneration of the central nervous system, which mainly attributed to glial scar and low intrinsic regenerating capacity of severely injured neurons, causes limited functional recovery. Combinatory strategy has been applied to target multiple mechanisms. Schwann cells (SCs) have been explored as promising donors for transplantation to promote axonal regeneration. Among the central neurons, descending propriospinal neurons (DPSN) displayed the impressive regeneration response to SCs graft. Glial cell line-derived neurotrophic factor (GDNF), which receptor is widely expressed in nervous system, possesses the ability to promote neuronal survival, axonal regeneration/sprouting, remyelination, synaptic formation and modulate the glial response. We constructed a novel axonal permissive pathway in rat model of thoracic complete transection injury by grafting SCs over-expressing GDNF (SCs-GDNF) both inside and caudal to the lesion gap. Behavior evaluation and histological analyses have been applied to this study. Our results indicated that tremendous DPSN axons as well as brain stem axons regenerated across the lesion gap back to the caudal spinal cord. In addition to direct promotion on axonal regeneration, GDNF also significantly improved the astroglial environment around the lesion. These regenerations caused motor functional recovery. The dendritic plasticity of axotomized DPSN also contributed to the functional recovery. We applied a G-mutated rabies virus (G-Rabies) co-expressing green fluorescence protein (GFP) to reveal Golgi-like dendritic morphology of DPSNs and its response to axotomy injury and GDNF treatment. We also investigated the neurotransmitters phenotype of FluoroGold (FG) labeled DPSNs. Our results indicated that over 90 percent of FG-labeled DPSNs were glutamatergic neurons. DPSNs in sham animals had a predominantly dorsal-ventral distribution of dendrites. Transection injury resulted in alterations in the dendritic distribution, with dorsal-ventral retraction and lateral-medial extension of dendrites. Treatment with GDNF significantly increased the terminal dendritic length of DPSNs. The density of spine-like structures was increased after injury and treatment with GDNF enhanced this effect.
Kirk, Maia P. « The role of retinoids in the regeneration of the axolotl spinal cord ». Thesis, 2015. http://hdl.handle.net/1805/7965.
Texte intégralRetinoids play an important role in tissue patterning during development as well as in epithelial formation and health. In the mammalian central nervous system, the meninges are a source of retinoids for brain tissue. Retinoid production has been described in juvenile Axolotl ependymal cells. Retinoid effects may possess a significant role in the regeneration-permissive interaction of the meninges and ependyma of the Axolotl spinal cord after penetrating injury. During spinal cord regeneration in urodele amphibians, the pattern of retinoid production changes as the meninges interact with the injury-reactive ependymal cells reconstructing the injured spinal cord. In order to determine which components of the retinoid metabolism and intracellular signaling pathway act in Urodele spinal cord regeneration, we employed antibody/horseradish peroxidase staining of both intact and regenerating Axolotl spinal cord tissues obtained from adult animals as well as cell culture techniques to determine expression of three retinoid pathway components: Cellular Retinoic Acid Binding Protein II (CRABP 2), Cellular Retinol Binding Protein I (CRBP 1), and Retinaldehyde Dehydrogenase II (RALDH 2). Current results demonstrate the following in the intact cord: 1) CRBP 1 is expressed in the pia and dura mater meningeal layers, in gray matter neurons (including their axonal processes), and the ependymal cell radial processes that produce the glia limitans, 2) CRABP 2 is expressed in the arachnoid and/or dura mater meningeal layers surrounding the spinal cord, and 3) RALDH 2 is expressed in the meninges as well as cytoplasm of grey matter neurons and some ependymal/sub-ependymal cells. In the regenerating cord, CRBP 1 is expressed in ependymal cells that are undergoing epithelial-to-mesenchymal transition (EMT), as is CRABP 2. RALDH 2 staining is very strong in the reactive meninges; in addition, expression is also upregulated in the cytoplasmic and perinuclear regions of reactive grey matter neurons, including motor neurons and in the apical region of ependymal. Preliminary studies culturing reactive meninges and ependymal cells together suggested that the meninges could drive re-epithelialization of the reactive ependymal cells. Experiments to characterize this interaction show an unusual proliferation pattern: Proliferating Cell Nuclear Antigen (PCNA) labeling is present in intact and regenerating cord ependymal cells. However, in culture, the presence of meninges results in no proliferation proximal to the explant, but extensive proliferation in leading cell outgrowth; also, the cultured meninges is positive for RALDH2. In summary, the intact adult cord shows meningeal production of RA, which is upregulated following injury; in addition, during this time, RA production is upregulated in the adult ependymal cells as well. In culture, the reactive meninges appears to modulate the behavior of reactive ependymal cells.
Meadows, Rena Marie. « Effects of electrical stimulation and testosterone on regeneration-associated gene expression and functional recovery in a rat model of sciatic nerve crush injury ». Thesis, 2014. http://hdl.handle.net/1805/5504.
Texte intégralAlthough peripheral motoneurons are phenotypically endowed with robust regenerative capacity, functional recovery is often suboptimal following peripheral nerve injury (PNI). Research to date indicates that the greatest success in achieving full functional recovery will require the use of a combinatorial approach that can simultaneously target different aspects of the post-injury response. In general, the concept of a combinatorial approach to neural repair has been established in the scientific literature but has yet to be successfully applied in the clinical situation. Emerging evidence from animal studies supports the use of electrical stimulation (ES) and testosterone as one type of combinatorial treatment after crush injury to the facial nerve (CN VII). With the facial nerve injury model, we have previously demonstrated that ES and testosterone target different stages of the regeneration process and enhance functional recovery after facial nerve crush injury. What is currently unknown, but critical to determine, is the impact of a combinatorial treatment strategy of ES and testosterone on functional recovery after crush injury to the sciatic nerve, a mixed sensory and motor spinal nerve which is one of the most serious PNI clinical problems. The results of the present study indicate that either treatment alone or in combination positively impact motor recovery. With regard to molecular effects,single and combinatorial treatments differentially alter the expression of regeneration-associated genes following sciatic nerve crush injury relative to facial nerve injury. Thus, our data indicate that not all injuries equally respond to treatment. Furthermore, the results support the importance of treatment strategy development in an injury-dependent manner and based upon the functional characteristics of spinal vs. cranial nerves.
« In vivo and in vitro studies of the anti-oxidative, anti-inflammatory and anti-apoptotic effects of Gastrodiae Rhizoma water extract on ischemic stroke ». 2013. http://library.cuhk.edu.hk/record=b5884430.
Texte intégralThesis (M.Phil.)--Chinese University of Hong Kong, 2013.
Includes bibliographical references (leaves 186-192).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts also in Chinese.
Walker, Chandler L. « Targeting acute phosphatase PTEN inhibition and investigation of a novel combination treatment with Schwann cell transplantation to promote spinal cord injury repair in rats ». Thesis, 2014. http://hdl.handle.net/1805/4210.
Texte intégralHuman traumatic spinal cord injuries (SCI) are primarily incomplete contusion or compression injuries at the cervical spinal level, causing immediate local tissue damage and a range of potential functional deficits. Secondary damage exacerbates initial mechanical trauma and contributes to function loss through delayed cell death mechanisms such as apoptosis and autophagy. As such, understanding the dynamics of cervical SCI and related intracellular signaling and death mechanisms is essential. Through behavior, Western blot, and histological analyses, alterations in phosphatase and tensin homolog (PTEN)/phosphatidylinositol-3-kinase (PI3K) signaling and the neuroprotective, functional, and mechanistic effects of administering the protein tyrosine phosphatase (PTP) inhibitor, potassium bisperoxo (picolinato) vanadium ([bpV[pic]) were analyzed following cervical spinal cord injury in rats. Furthermore, these studies investigated the combination of subacute Schwann cell transplantation with acute bpV(pic) treatment to identify any potential additive or synergistic benefits. Although spinal SC transplantation is well-studied, its use in combination with other therapies is necessary to complement its known protective and growth promoting characteristics. v The results showed 400 μg/kg/day bpV(pic) promoted significant tissue sparing, lesion reduction, and recovery of forelimb function post-SCI. To further clarify the mechanism of action of bpV(pic) on spinal neurons, we treated injured spinal neurons in vitro with 100 nM bpV(pic) and confirmed its neurprotection and action through inhibition of PTEN and promotion of PI3K/Akt/mammalian target of rapamycin (mTOR) signaling. Following bpV(pic) treatment and green fluorescent protein (GFP)-SC transplantation, similar results in neuroprotective benefits were observed. GFP-SCs alone exhibited less robust effects in this regard, but promoted significant ingrowth of axons, as well as vasculature, over 10 weeks post-transplantation. All treatments showed similar effects in forelimb function recovery, although the bpV and combination treatments were the only to show statistical significance over non-treated injury. In the following chapters, the research presented contributes further understanding of cellular responses following cervical hemi-contusion SCI, and the beneficial effects of bpV(pic) and SC transplantation therapies alone and in combination. In conclusion, this work provides a thorough overview of pathology and cell- and signal-specific mechanisms of survival and repair in a clinically relevant rodent SCI model.
Wilson, Sarah Marie. « Involvement of Collapsin Response Mediator Protein 2 in Posttraumatic Sprouting in Acquired Epilepsy ». Thesis, 2014. http://hdl.handle.net/1805/5604.
Texte intégralPosttraumatic epilepsy, the development of temporal lobe epilepsy (TLE) following traumatic brain injury, accounts for 20% of symptomatic epilepsy. Reorganization of mossy fibers within the hippocampus is a common pathological finding of TLE. Normal mossy fibers project into the CA3 region of the hippocampus where they form synapses with pyramidal cells. During TLE, mossy fibers are observed to innervate the inner molecular layer where they synapse onto the dendrites of other dentate granule cells, leading to the formation of recurrent excitatory circuits. To date, the molecular mechanisms contributing to mossy fiber sprouting are relatively unknown. Recent focus has centered on the involvement of tropomycin-related kinase receptor B (TrkB), which culminates in glycogen synthase kinase 3β (GSK3β) inactivation. As the neurite outgrowth promoting collapsin response mediator protein 2 (CRMP2) is rendered inactive by GSK3β phosphorylation, events leading to inactivation of GSK3β should therefore increase CRMP2 activity. To determine the involvement of CRMP2 in mossy fiber sprouting, I developed a novel tool ((S)-LCM) for selectively targeting the ability of CRMP2 to enhance tubulin polymerization. Using (S)-LCM, it was demonstrated that increased neurite outgrowth following GSK3β inactivation is CRMP2 dependent. Importantly, TBI led to a decrease in GSK3β-phosphorylated CRMP2 within 24 hours which was secondary to the inactivation of GSK3β. The loss of GSK3β-phosphorylated CRMP2 was maintained even at 4 weeks post-injury, despite the transience of GSK3β-inactivation. Based on previous work, it was hypothesized that activity-dependent mechanisms may be responsible for the sustained loss of CRMP2 phosphorylation. Activity-dependent regulation of GSK3β-phosphorylated CRMP2 levels was observed that was attributed to a loss of priming by cyclin dependent kinase 5 (CDK5), which is required for subsequent phosphorylation by GSK3β. It was confirmed that the loss of GSK3β-phosphorylated CRMP2 at 4 weeks post-injury was likely due to decreased phosphorylation by CDK5. As TBI resulted in a sustained increase in CRMP2 activity, I attempted to prevent mossy fiber sprouting by targeting CRMP2 in vivo following TBI. While (S)-LCM treatment dramatically reduced mossy fiber sprouting following TBI, it did not differ significantly from vehicle-treated animals. Therefore, the necessity of CRMP2 in mossy fiber sprouting following TBI remains unknown.