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Developing an in vivo reporter system for the monitoring of therapeutic effects on neuroblastomaTam, Pui-see, Patricia., 談沛詩. January 2009 (has links)
published_or_final_version / Surgery / Master / Master of Medical Sciences
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Excitotoxic model of posttraumatic syringomyelia in the ratYang, Liqun. January 1999 (has links) (PDF)
Bibliography: leaves 112-127. Study using an animal model (Sprague-Dawley rats) to elucidate the role of EAAs and spinal subarachnoid blockade in posttraumatic syringomelia. Results support the proposal that in posttraumatic spinal cord injury, primary injury and exitotoxic cell death, occuring secondary to elevated levels of EAAs, contribute to a pathologic process leading to the formation of spinal cavities, and a subarachnoid block by arachnoiditis is one of the pathogenic factors most responsible for initiating extension of the cavity.
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Investigation on the correlation between redox changes and oxidative stress in diabetes, and their role in transcription factors activation in vitro and in vivoChung, Wai Shing 01 January 2002 (has links)
No description available.
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Investigating the potential significance of tau protein in corticosterone-induced depression and neurodegeneration : implication in Alzheimer's diseaseTsang, Wing-ting, Andrea, 曾詠婷 January 2014 (has links)
Alzheimer’s disease (AD) is a devastating neurodegenerative disease with growing prevalence in our society. Patients suffering from this debilitating disorder also develop neuropsychiatric symptoms. Depression is one of the most frequently conveyed comorbidity; moreover, depression is also a risk factor associated with AD development. There is a complex interplay between the neurobiology of depression and AD, but their concomitant disease mechanisms remain largely unknown. Retraction of axons and dendrites has been reported to be a common occurrence in both illnesses, proposing the involvement of cytoskeletal dysfunction.
Tau is a microtubule-associated protein that undergoes aberrant processing to form neurofibrillary tangles in neurodegenerative diseases such as AD. However, the role of tau in depression has not been well studied. The elucidation of pathophysiological mechanisms in depression is important to provide a more holistic understanding of AD pathogenesis. This study proposes the potential participation of tau phosphorylation in the pathogenesis of depression. In addition, this study will also investigate tau modifications under concomitant models of depression and AD.
Primary cultures of hippocampal neurons were exposed to independent and cotreatments of corticosterone and β-amyloid (Aβ), to induce in vitro models of depression and AD, respectively. Sprague Dawley rats were subcutaneously injected with corticosterone for 14 days to induce an in vivo model of depression. Tau phosphorylation, aggregation and interaction with microtubules were examined.
Results demonstrated that in both in vitro and in vivo models of corticosterone-induce depression, tau underwent increased phosphorylation at residues S396 and S404. Phosphorylated tau showed decreased interactions with microtubules and increased vulnerability to aggregate. Furthermore, the in vivo model of depression illustrated an altered localization of tau in the CA3 region of the hippocampus. Co-treatment of corticosterone and Aβ exacerbated aberrant tau phosphorylation and aggregation.
In conclusion, this study provides evidence for the role of tau in depression, suggesting the occurrence of abnormal tau phosphorylation as an early event in the pathogenesis. Additionally, the pathophysiology of depression and AD may involve similar mechanisms in tau phosphorylation and aggregation. This study provides insight into the neurobiological linkages between depression and AD, and emphasizes the importance of tau-targeted interventions in neuropsychiatric disorders. / published_or_final_version / Anatomy / Master / Master of Philosophy
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Reverse cholesterol transport in type 2 diabetes mellitusZhou, Huali., 周華麗. January 2008 (has links)
published_or_final_version / Medicine / Doctoral / Doctor of Philosophy
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Ultrastructural basis of steroid-induced ocular hypertensionLee, Yan-yee, Jacinta., 李茵怡. January 2010 (has links)
published_or_final_version / Anatomy / Master / Master of Philosophy
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Functional neuroimaging of auditory hallucinationsMcguire, Philip Kevin January 1998 (has links)
No description available.
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Brain structural and functional changes during the course of schizophreniaGuo, Yu January 2014 (has links)
No description available.
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Bladder and brain function in children with severe nocturnal enuresis. / CUHK electronic theses & dissertations collectionJanuary 2005 (has links)
Conclusion. Impairment in bladder and brain functions was identified in children with severe NE. Post-treatment studies indicated that brain function normalized in parallel with amelioration of bladder dysfunction. Interaction between brain and bladder dysfunction is likely to have an important implication in the pathophysiology and resolution of NE. / Objective. To (1) investigate sleep pattern and cortical arousals in enuretic children; (2) assess brain and bladder function in enuretic children; (3) evaluate post-treatment brain and bladder functional changes in enuretic children and correlate these with the treatment outcomes. / Part II. Fifty-two patients with severe PNE and 15 normal controls were recruited. Bladder and brain functions (sleep arousal threshold, P300 ERPs latency and PPI of startle amplitude) in enuretic children were evaluated, and brain function was compared with normal controls. / Part II. Markedly reduced nocturnal FBC and impaired brain function were found in enuretic patients. Higher sleep arousal threshold was negatively correlated to lower FBC. Prolonged P300 ERPs and higher PPI of startle amplitude were positively correlated to a higher sleep arousal threshold. / Part III. NE episodes and bladder function were re-evaluated in 52 severely enuretic children (Part II) at 3 and 6 months on treatment. Brain function was re-evaluated in 41/52 enuretic children at 6 months on treatment. / Part III. Post-treatment FBC significantly increased, and sleep arousal threshold, number of awakenings, P300 ERPs latency and PPI of startle amplitude normalized in treatment responders. NE episodes reduction was significantly correlated to the improvement in FBC and brain function. Greater decrease in sleep arousal threshold was positively correlated to higher FBC increase. Higher P300 ERPs latency and PPI of startle amplitude reduction were positively correlated to greater decrease in sleep arousal threshold. / Patients and methods. Part I. Thirty-five children with refractory PNE and 21 normal controls were recruited. Overactive bladder contractions, NE episodes and volume in enuretic children, sleep stages and cortical arousals in all children were recorded. / Results. Part I. Underlying bladder dysfunction, abnormal sleep architecture and increased cortical arousal index were found in enuretic children. Cortical arousal index was positively correlated to the frequency of overactive bladder contractions. / Diao Mei. / "May 2005." / Adviser: Chung-Kwong Yeung. / Source: Dissertation Abstracts International, Volume: 67-07, Section: B, page: 3693. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (p. 135-159). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Electronic reproduction. [Ann Arbor, MI] : ProQuest Information and Learning, [200-] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Abstract in English and Chinese. / School code: 1307.
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Implication des vésicules extracellulaires d'érythrocytes dans la dysfonction vasculaire drépanocytaireSadoudi, Sihem 28 November 2017 (has links)
L'hémolyse intravasculaire est la destruction prématurée et chronique des globules rouges. Elle est caractérisée par une libération accrue d’hème et de microvésicules (MV) membranaires dans la circulation sanguine. L'hémolyse chronique est une des caractéristiques de la drépanocytose. Elle joue un rôle très important dans la physiopathologie de la drépanocytose. La drépanocytose est associée à une agrégation des globules rouges dans la circulation, menant à des occlusions vasculaires et des crises vaso-occlusives extrêmement douloureuses. Les travaux précédents de l’équipe dans la drépanocytose, ont montré que les MV de globules rouges transfèrent de l’hème aux cellules endothéliales, participent à la dysfonction vasculaire et induisent des vaso-occlusions rénales dans un modèle de souris drépanocytaire. Ces résultats nous ont incités à poursuivre l’étude des effets des MV de globules rouges, chargées en hème. Nous avons émis l’hypothèse que les MV chargées en hème stimulent également l’inflammation dans la drépanocytose au de-là de la dysfonction endothéliale. Ce travail regroupe trois parties. Dans une première partie, nous nous sommes intéressés à l’effet pro-inflammatoire des MV de globules rouges, chargées en hème. Nous avons démontré que les MV stimulent les neutrophiles qui libèrent leur ADN. Les taux plasmatiques d’ADN extracellulaire sont élevés dans la drépanocytose, comparés aux taux plasmatiques chez les individus sains, et augmentent encore durant les crises vaso-occlusives. Cet ADN, qui pourrait provenir en partie des pièges extracellulaires d’ADN (dits NETs), affecte l’hémorhéologie drépanocytaire en modifiant les propriétés d’agrégation et d’adhésion des globules rouges. Par ailleurs, nous avons constaté que le plasma des patients drépanocytaires était incapable de dégrader l’ADN in vitro, et présentait une activité DNase plasmatique réduite. La baisse de l’activité DNase dans la drépanocytose crée un déséquilibre entre les taux d’ADN circulant et son inhibiteur endogène. En contre partie, une supplémentation en DNase-I humaine recombinante par perfusion intraveineuse a libèré les vaso-occlusions rénales dans le modèle de souris drépanocytaire et a réduit l’excès d’agrégation et d’adhésion des globules rouges drépanocytaires. Ces résultats démontrent un déséquilibre entre les taux d’ADN circulant et l’activité DNase chez les patients drépanocytaires conduisant à une inflammation chronique, une forte agrégation des globules rouges et la survenue des vaso-occlusions. Dans une deuxième partie, nous nous sommes intéressés aux effets du remodelage et du remaniement membranaire des globules rouges dans la drépanocytose. Nous avons identifié que les globules rouges et leurs MV sont associés à une externalisation accrue de la phosphatidylsérine et que cette externalisation accrue ne résulte pas d’une composition lipidique modifiée de la membrane des globules rouges, mais, il s’agit principalement d'une externalisation exagérée de la phosphatidylsérine. L’externalisation de la phosphatidylsérine contribue aux occlusions vasculaires in vivo. La neutralisation de la phosphatidylsérine des MV et des globules rouges avec de l’annexine-A5 recombinante permet la libération des vaso-occlusions rénales induites par les MV de globules rouges dans le modèle de souris drépanocytaire. Ces résultats démontrent le rôle de la phosphatidylsérine externalisée par les globules rouges et les MV dans les occlusions vasculaires in vivo et le potentiel thérapeutique de l’annexine-A5 pour restaurer l’hémorhéologie et la perfusion tissulaire durant les vaso-occlusions drépanocytaires. Dans une troisième partie, nous nous sommes intéressés aux annexines en tant qu’inhibiteurs endogènes de la phosphatidylsérine des membranes de globules rouges et de MV. Nous avons mis au point un nouveau test qui permet de quantifier la fonctionnalité de l’annexine-A5 et –A7. (...) / Pas de résumé
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