Tesis sobre el tema "Cerebral ischemia – Treatment"
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Yang, Di y 楊荻. "Neuroprotective effects of lycium barbarum extracts in cerebral and retinal ischemia/reperfusion injury". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2014. http://hdl.handle.net/10722/206738.
Texto completopublished_or_final_version
Ophthalmology
Doctoral
Doctor of Philosophy
Chan, Chu-fung y 陳柱峰. "Neuroprotective effects of granulocyte-colony stimulating factor in a mice stroke model". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B40687284.
Texto completoXu, Mingjing y 徐明婧. "Baicalin protects neural cells from cerebral ischemia reperfusion injury by scavenging peroxynitrite". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2011. http://hub.hku.hk/bib/B47753110.
Texto completopublished_or_final_version
Chinese Medicine
Master
Master of Philosophy
Khanasari, Parto S. "An investigation of the neuroprotective properties of fenamate NSAIDs, against experimental model of ischemic stroke". Scholarly Commons, 2007. https://scholarlycommons.pacific.edu/uop_etds/671.
Texto completoWeiss, Miriam [Verfasser], Gerrit Alexander [Akademischer Betreuer] Schubert y Martin [Akademischer Betreuer] Wiesmann. "Endovascular rescue treatment for delayed cerebral ischemia after subarachnoid hemorrhage is safe and effective / Miriam Weiss ; Gerrit Alexander Schubert, Martin Wiesmann". Aachen : Universitätsbibliothek der RWTH Aachen, 2019. http://d-nb.info/1215927614/34.
Texto completoBoulos, Sherif. "Identification and characterisation of potential neuroprotective proteins induced by erythropoietin (EPO) preconditioning of cortical neuronal cultures". University of Western Australia. School of Biomedical and Chemical Sciences, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0128.
Texto completoRahman, Rosanna y n/a. "Potential causes of the delayed neural damage observed post-stroke & the effects of epigallocatechin gallate administration". University of Otago. Department of Pharmacology & Toxicology, 2006. http://adt.otago.ac.nz./public/adt-NZDU20070508.122246.
Texto completoPütz, Volker, Matthias Weise, Rüdiger von Kummer y Georg Gahn. "Effective Treatment with Abciximab for Consecutive Bilateral Middle Cerebral Artery Occlusion". Saechsische Landesbibliothek- Staats- und Universitaetsbibliothek Dresden, 2014. http://nbn-resolving.de/urn:nbn:de:bsz:14-qucosa-135290.
Texto completoPütz, Volker, Matthias Weise, Rüdiger von Kummer y Georg Gahn. "Effective Treatment with Abciximab for Consecutive Bilateral Middle Cerebral Artery Occlusion". Karger, 2006. https://tud.qucosa.de/id/qucosa%3A27636.
Texto completoBrodin, Camille. "De la paillasse au lit du patient, surmonter les problèmes de translation dans le domaine de l'AVC ischémique Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Single- and two- chain tissue plasminogen activator treatment differentially influence cerebral recovery after stroke Cerebral blood flow correlates with ischemic brain lesion only when Stroke occurs awake: a preclinical model to bypass the translational roadblocks to clinic". Thesis, Normandie, 2019. http://www.theses.fr/2019NORMC427.
Texto completoThe lack of translation between preclinical studies and clinical trials in the field of ischemic stroke and the failure of therapeutic developments could be explained by three aspects: (1) the lack of understanding the mechanism of the two forms of tPA, the pharmacological treatment in stroke; (2) the lack of optimized perfusion imaging tools for small animal and (3) the influence of anesthesia on treatment tested in animal models.tPA used in the clinical setting (Actilyse®) is a mix of two forms of tPA: single chain form (sc-rtPA) and two chains form (tc-rtPA). Despite similar fibrinolytic activities, these two forms exert distinct brain functions therefore influencing differentially the outcome patients. We then decided to further investigate in a relevant model of thromboembolic stroke in rodents, the mechanisms that can explain these differential effects. Here, we have confirmed differential outcomes of the two forms: whereas sc-rtPA is clearly beneficial when infused shortly after stroke onset, tc-rtPA is deleterious due to an increased alteration of the blood brain barrier integrity.Live imaging of cerebral perfusion of the whole brain is an asset for both clinical and preclinical studies. The emergence of ultrafast ultrasound led to the development of ultrafast Doppler (fUS) and Ultrasound Localization Microscopy (ULM), two methods with different sets of spatio-temporal resolutions and excellent sensitivity to small blood flows. We combined these two methods to provide a longitudinal monitoring of whole brain perfusion using the thromboembolic stroke model in mice with rtPA-induced reperfusion. Our data show that fUS and ULM are of major interest for early prognosis of ischemic stroke and response to treatment, with a tight correlation between early reperfusion at 2h and tissue recovery at 24h. Finally, we develop a relevant awake ischemic stroke model to test new therapies, avoiding interferences due to anesthesia commonly used during in vivo studies mice. The patern of the MCA was followed using Laser Doppler monitoring before, during and 45 min after the stroke onset. Although rtPA treatment is beneficial in both awake and anesthetized stroke models, anesthesia is associated with a lack of correlation between recanalization and stroke outcome. We are now testing a neuroprotective molecule, which was promising before failing in clinical trials (NXY-059), to assess the relevance of this innovative stroke model for future pharmacological studies. Altogether, we provide here a set of innovative pre-clinical data to improve our chance of translation to clinic, including a relevant model of thromboembolic stroke in awake animals and an early prognosis imaging method of response to vascular treatments
Poignet, Hervé. "Activites pharmacologiques des antagonistes du calcium sur differents modeles physiopathologiques utilises dans l'ischemie cerebrale experimentale : effets sur les atteintes fonctionnelles et neuronales". Clermont-Ferrand 2, 1988. http://www.theses.fr/1988CLF21111.
Texto completoHuang, Chien-Chih y 黃千芝. "Delayed Treatment with Cinnamophilin Improves Electrophysiological and Neurobehavioral Outcomes in Rats Subjected to Transient Focal Cerebral Ischemia". Thesis, 2006. http://ndltd.ncl.edu.tw/handle/51816525239392927642.
Texto completo國立成功大學
醫學工程研究所碩博士班
94
The neuroprotective properties of cinnamophilin, a strong natural antioxidant and free radical scavenger which may enhance cerebral hemodynamics, decrease platelet aggregation and lipid peroxidation, and prevent energy depletion during ischemia, will be evaluated in Sprague-Dawley rats subjected to 1-hour transient middle cerebral artery (MCA) occlusion. A series of experiments with delayed treatment of CINN was employed to examine whether CINN is neuroprotective following a short period of recovery using a model of reversible MCA occlusion which includes ischemic brain damage not only caused by grey matter but also by white matter damages. Postmortem infarct volumes will be determined by quantitative image analysis of Nissl-stained brain sections and by immunohistochemical methods. In addition, postischemic electrophysiological recovery will be evaluated. The possible mechanisms of action relevant to short-term neuroprotective efficacy by which CINN may exhibit the neuroprotective effects was evaluated in the model. The data not only extend our original findings to the ischemic-reperfusion injury but also look at prolonged outcomes, thus, may provide a potential outlook to treat patients against ischemic stroke. Delayed intravenous administration with CINN at 120 minutes after ischemia both enhances electrophysiological and neurobehavioral outcomes and reduces cortical and striatal infarction after cerebral ischemia-reperfusion. Since CINN is noted to be lack of toxicity and has persistent neuroprotection, it is worthwhile further investigating for potential benefits for those patients who will undergo planned cerebrovascular occlusion during neurosurgical surgery and for possible applications for ischemic stroke patients.
Chen, Li-Hsuan y 陳俐璇. "Delayed Treatment with Magnesium Improves Electrophysiological and Neurobehavioral Outcomes in Rats Subjected to Transient Focal Cerebral Ischemia". Thesis, 2005. http://ndltd.ncl.edu.tw/handle/90184549099176769182.
Texto completo國立成功大學
醫學工程研究所
93
In the current study, magnesium sulfate (750μmol/kg) was given via intracarotid infusion at the beginning of reperfusion in a rat model of transient focal cerebral ischemia. Much evidence implicated neuroprotective mechanisms of Mg2+ to include inhibition of excitatory neurotransmitter release, blockade of voltage-dependent NMDA channels, and blockade of L- and N-type voltage-operated calcium channels. In addition to reduced brain infarction, this study emphasized the importance of electrophysiological and neurobehavioral outcomes. Improvement of functional outcome is more important than reduced brain damage with regard to stroke patients through treatment. The results showed that the P1-N1 amplitude of somatosensory evoked potentials (SSEP) recorded from ischemic fore- and hindpaw cortical fields decreased to 18% and 26% of baselines in vehicle-injected rats at 72 hr after the onset of reperfusion. Respectively, the P1-N1 amplitude of SSEP recorded from cerebral ischemia rats treated with MgSO4 improved to 24% and 40% of baselines. Additionally, MgSO4 also improved the neurobehavioral outcomes.
Tsai, Yi-Yin y 蔡宜殷. "Delayed Treatment with Melatonin Improves Electrophysiological and Neurobehavioral Outcomes in Rats Subjected to Transient Focal Cerebral Ischemia". Thesis, 2003. http://ndltd.ncl.edu.tw/handle/43528059838035888218.
Texto completo國立成功大學
醫學工程研究所
91
In general, cerebral ischemia elicits calcium accumulation and production of free radicals leading to irreversible cell damage and neurobehavioral dysfunction. Thus an effective neuroprotective agent is needed to protect ischemic brain after thrombolytic therapies. Melatonin is well known a direct free radical scavenger and an indirect antioxidant, and was reported to reduce infarct volume recently. In the current study, we investigate weather delayed treatment with melatonin (5mg/kg iv) could improve electrophysiology and neurobehavioral function in the transient cerebral ischemia model. Because for stroke patients through treatment, the improvement of functional outcome is more important than reduced brain damage In controls, the amplitude of somatosensory evoked potentials (SSEPs) recorded from fore- and hindpaw cortical fields decreased to 39% and 36% of baselines. Respectively, the amplitude of SSEPs recorded from cerebral ischemia rats treat with melatonin improved to 65% and 74% of baselines. Additionally, melatonin also reduced cerebral infarction volume. In conclusion, delayed treatment with melatonin could improve the electrophysiology and neurobehavioral outcomes and reduce brain damage induced by brain ischemia and reperfusion.
"Diagnosis, microemboli detection and hemodynamic monitoring of intracranial atherosclerosis by transcranial Doppler in the ischemic stroke". Thesis, 2008. http://library.cuhk.edu.hk/record=b6074600.
Texto completoFinally, one study was performed to assess the changes of hemodynamic parameters after stenting of severe stenosis in the MCA. We aimed to investigate whether TCD can reflect the lumen changes after revascularization and detect hyperperfusion. The findings showed that the velocity of stented MCA in most patients normalized within 24 hours after procedure, but the role of TCD in detecting restenosis in long run needed to be verified; no one suffered from hyperperfusion during the period of our study. The long-term outcomes of patients with normalized velocity versus those with persistently high velocity needed to be further studied. Apart from the velocity changes, changes of the collateral flow after intervention may also be an important part of hemodynamic changes. (Abstract shortened by UMI.)
It was suggested that anti-platelet therapy can reduce the MES, but little was known about the efficacy of low molecular weight heparin (LMWH) although in theory LMWH can reduce the red fibrin-dependent thromboemboli. As a sub-analysis of Fraxiparine in Ischemic Stroke (FISS)-tris study, our study did not show advantages of LMWH in eliminating MES compared with aspirin.
Previous studies showed the accuracy of TCD in diagnosis of middle cerebral artery (MCA) stenosis was variable and the positive predictive value (PPV) was less than 50% in a recent report. One of the important reasons was that most criteria were based on the velocity-only method, ignoring other non-velocity information. Thus, we tried to establish new diagnostic criteria by means of designing an assessment form which integrated more characteristics apart from the velocity acceleration. A composite score for each MCA was calculated according to following parameters in the form: Velocity Scale (score 0-6 for peak systolic velocities<140 to ≥300cm/s), Hemodynamic Scale (score 0-5 for focal or diffuse velocity increase; score 0-6 for differences between bilateral MCA; score 17 for damping velocity), Spectrum Scale (score 0-2 for normal spectrum, turbulence and musical murmurs). Our results showed that compared with the previously reported criteria, the score calculated from the assessment form yielded much more balanced accuracy against magnetic resonance angiography (MRA) and digital subtraction angiography (DSA). However, the composition of the assessment form was only based on personal experience and need to be further modified. Multicenter studies with large sample size are also needed to confirm the advantages of this new method.
Second, we performed three studies to investigate the relationship between the progression of MES and the short or long-term outcome and the relationship between MES and different treatments.
Hao, Qing.
Adviser: Ka Sing Wong.
Source: Dissertation Abstracts International, Volume: 70-06, Section: B, page: 3419.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2008.
Includes bibliographical references (leaves 155-181).
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.
Abstracts in English and Chinese.
School code: 1307.
Hsieh, Fu-Shun y 謝復順. "Transplantation of low-energy laser stimulation on adipose tissue-derived stem cells treatment of focal cerebral ischemia in rats". Thesis, 2012. http://ndltd.ncl.edu.tw/handle/38450605186460127492.
Texto completo中臺科技大學
醫學影像暨放射科學系暨研究所
100
This study investigated the influence of a large-area irradiation of low-level laser on the proliferation and differentiation of inductions of adipose-derived stem cells (i-ADSCs) into nerve cells. We then applied this approach to treat ischemic stroke in rats in the evaluation of various treatment mechanisms. DAPI staining showed that the number of cells did not increase as a result of irradiation; MTT assays indicated no significant difference between the number of laser-treated and non-laser-treated cells. Our results demonstrate that wide-area irradiation using a low power laser did not have a significant impact on the differentiation of i-ADSCs. Immunofluorescent staining indicated a significant increase in the neural stem cell marker Nestin following exposure to low power laser irradiation. No significant difference was observed between the glial cell marker GFAP and neuronal precursor cell protein DCX because the differentiation agent used in this study induced differentiation into nerve cells, rather than glial cells. Moreover, DCX can only be detected after neural stem cells form neurons in later stages; therefore, we conclude that the irradiation had no influence on the expression of this protein. Western blotting also showed that following irradiation, the expression of Nestin was significantly increased. The experiment results indicate that a large-area irradiation of low-level laser had no particular influence on the proliferation of i-ADSCs but still facilitated the differentiation of i-ADSCs considerably. This study employed stem cell implantation to treat rats following stroke. In the recovery of motor functions, the rats implanted with i-ADSCs (LS+) began regaining running and gripping functions on the 14th day following treatment. In comparison, stroke rats implanted with i-ADSCs (LS-) presented symptoms of dysfunction. At 28 days post treatment, the motor functions of the rats treated with i-ADSCs (LS+) did not differ greatly from those in the sham group, while the motor functions of the rats treated with i-ADSCs (LS-) remained somewhat dysfunctional. H&E-stained brain tissue samples from the rats treated with i-ADSCs (LS+) exhibited near-complete recovery with almost no brain tissue damage, whereas tissue from the rats treated with i-ADSCs (LS-) displayed necrotic scarring and voids. Western blotting revealed a significant expression of Oligo-2, a protein produced by the myelin-forming oligodendrocytes of the central nervous system, in the rats treated with i-ADSCs (LS+) as well as the sham group. From this, we can determine that treatment involving the implantation of i-ADSCs (LS+) is capable of repairing brain tissue damaged by ischemia. The results of this experiment also demonstrate that a large-area irradiation of low-level laser has a positive influence on the differentiation of i-ADSCs and can be employed to treat rats suffering from ischemic stroke to regain motor functions.
"External counterpulsation (ECP): a new, non-invasive method to enhance cerebral blood flow and its application in ischemic stroke". Thesis, 2007. http://library.cuhk.edu.hk/record=b6074448.
Texto completoThesis (Ph.D.)--Chinese University of Hong Kong, 2007.
Includes bibliographical references (p. 182-204).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstracts in English and Chinese.
Turner, Renée Jade. "Characterising the role of substance P in acute ischaemic stroke". 2007. http://hdl.handle.net/2440/56839.
Texto completohttp://library.adelaide.edu.au/cgi-bin/Pwebrecon.cgi?BBID=1298280
Thesis (Ph.D.) -- The University of Adelaide, School of Medical Sciences, 2007
Turner, Renée Jade. "Characterising the role of substance P in acute ischaemic stroke". Thesis, 2007. http://hdl.handle.net/2440/56839.
Texto completoThesis (Ph.D.) -- The University of Adelaide, School of Medical Sciences, 2007
"The hemodynamic effects of external counterpulsation in patients with recent stroke". Thesis, 2011. http://library.cuhk.edu.hk/record=b6075504.
Texto completoThesis (Ph.D.)--Chinese University of Hong Kong, 2011.
Includes bibliographical references (leaves 162-190).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Chang, Chia-Yu y 張嘉祐. "Therapeutic Treatment with Ascorbate Rescues Mice from Heat Stroke-induced Death and Reduces Focal Cerebral Ischemia-induced Brain Infarction in Rats". Thesis, 2016. http://ndltd.ncl.edu.tw/handle/aj93gy.
Texto completo國立中興大學
食品暨應用生物科技學系所
105
The impact of ascorbate (vitamin C, ascorbic acid) on oxidative stress-related diseases is moderate because of its limited oral bioavailability and rapid clearance. However, parenteral administration can increase the benefit of ascorbate supplementation as is evident in critically ill patients. Heatstroke is defined as a form of excessive hyperthermia associated with a systemic inflammatory response that results in multiple organ dysfunctions in which central nervous system disorders such as delirium, convulsions, and coma are predominant. The thermoregulatory, immune, coagulation and tissue injury responses of heatstroke closely resemble those observed during sepsis and are likely mediated by similar cellular mechanisms. This study was performed by using the characteristic high lethality rate and sepsis-mimic systemic inflammatory response of a murine model of heat stroke to test our hypothesis that supra-physiological doses of ascorbate may have therapeutic use in critical care. We demonstrated that parenteral administration of ascorbate abrogated the lethality and thermoregulatory dysfunction in murine model of heat stroke by attenuating heat stroke-induced accelerated systemic inflammatory, coagulation responses and the resultant multiple organ injury, especially in hypothalamus. Stroke is a major public health problem and ranks third most common cause of death in adults worldwide. Focal ischemic stroke can cause permanent disability and lead to severe neurological sequelae. In this study, we hypothesized that high- dose ascorbate may exert its therapeutic effects through attenuating oxidative stress driven cerebral ischemia-reperfusion injury in a rat model of transient focal cerebral ischemia. Indeed, we did demonstrate that administration of supra-physiological doses of ascorbate significantly improved neurological deficits, the sequelae of brain infarction and edema, in a rat model of transient focal cerebral ischemia by attenuating cerebral neuronal apoptosis and blood brain barrier disruption. Overall, our findings support the hypothesis and notion that supra-physiological doses of ascorbate may have therapeutic use in critical care. Parenteral administration of high-dose ascorbate provides an inexpensive, strong and multifaceted antioxidant therapy, especially robust for resuscitation of the circulation. In critically ill patients, future research should focus on the use of short-term high-dose intravenous ascorbate as a resuscitation drug, or combined with other antioxidants to intervene as early as possible in the oxidant cascade in order to optimize macrocirculation and microcirculation and to limit cellular injury.
Liao, Wen-Yen y 廖文彥. "Evaluating the role of Toll-like receptors 2 and 4 in treatment of Moutan Cortex Radicis and Paeonol on cerebral ischemia-reperfusion injured rat". Thesis, 2015. http://ndltd.ncl.edu.tw/handle/j2e3mr.
Texto completo"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.
Texto completoThesis (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.
"Potential of serotonin in stem cell technology and therapy in a mouse ischemic stroke model". 2012. http://library.cuhk.edu.hk/record=b5549580.
Texto completoLi, Jin.
"November 2011."
Thesis (Ph.D.)--Chinese University of Hong Kong, 2012.
Includes bibliographical references (leaves 195-241).
Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
Abstracts in English.
ACKNOWLEDGEMENTS --- p.i
LIST OF PUBLICATIONS --- p.ii
ABSTRACT --- p.iii
ABSTRACT [in Chinese] --- p.v
TABLE OF CONTENT --- p.vi
LISTS OF FLOWCHARTS --- p.xii
LISTS OF FIGURES --- p.xiii
LIST OF TABLES --- p.xvi
LIST OF EQUIPMENTS --- p.xvii
LIST OF ABBREVATIONS --- p.xvii
Chapter Chapter1 --- Introduction --- p.1
Chapter 1.1 --- Central nervous system disorder --- p.1
Chapter 1.1.1 --- Stroke --- p.1
Chapter 1.1.2 --- Spinal cord injuries --- p.4
Chapter 1.1.3 --- Parkinson's disease --- p.6
Chapter 1.1.4 --- Amyotrophic Lateral Sclerosis --- p.8
Chapter 1.2 --- Stem cell therapy --- p.10
Chapter 1.2.1 --- General considerations in stem cell therapy --- p.11
Chapter 1.2.2 --- Stem cell therapy for stroke --- p.11
Chapter 1.2.3 --- Stem cell therapy for spinal cord injury --- p.15
Chapter 1.2.4 --- Stem cell therapy for Parkinson's disease --- p.16
Chapter 1.2.5 --- Stem cell therapy for ALS --- p.18
Chapter 1.3 --- Stem cells --- p.20
Chapter 1.3.1 --- Embryonic stem cells --- p.21
Chapter 1.3.1.1 --- Derivation and characterization --- p.21
Chapter 1.3.1.2 --- Biology of ES cells --- p.21
Chapter 1.3.1.2.1 --- Pluripotency of ES cells --- p.21
Chapter 1.3.1.2.2 --- Differentiation of ES cells to multiple lineages --- p.24
Chapter 1.3.1.2.2.1 --- Ectodermal differentiation --- p.25
Chapter 1.3.1.2.2.2 --- Mesodermal differentiation --- p.27
Chapter 1.3.1.2.2.3 --- Endodermal differentiation --- p.28
Chapter 1.3.2 --- Neural stem cells --- p.30
Chapter 1.3.2.1 --- Derivation and characterization --- p.30
Chapter 1.3.2.2 --- Biology of NS cells --- p.32
Chapter 1.3.3 --- Induced pluripotent stem cells --- p.34
Chapter 1.3.4 --- Mesenchymal stem cells --- p.35
Chapter 1.4 --- Serotonin (5-HT) --- p.36
Chapter 1.4.1 --- Distribution --- p.37
Chapter 1.4.2 --- Metabolism --- p.37
Chapter 1.4.3 --- Biological effects of 5-HT --- p.38
Chapter 1.4.4 --- Serotonin receptor subtypes and receptor signal transduction pathways --- p.40
Chapter Chapter2 --- Aim --- p.43
Chapter 2.1 --- Hypothesis and study objectives --- p.43
Chapter Chapter3 --- Materials and Methods --- p.49
Chapter 3.1 --- Chemicals and Reagents --- p.49
Chapter 3.1.1 --- Cell culture --- p.49
Chapter 3.1.2 --- Serotonin, serotonin receptor subtypes specific agonists/antagonists and drugs that regulate serotonin metabolism --- p.51
Chapter 3.1.3 --- Cell proliferation assay --- p.52
Chapter 3.1.4 --- Cell apoptosis assay --- p.52
Chapter 3.1.5 --- Immunohistochemistry and staining --- p.52
Chapter 3.1.6 --- Western blotting --- p.55
Chapter 3.1.7 --- Molecular biology --- p.56
Chapter 3.1.8 --- Whole genome cDNA micro array --- p.58
Chapter 3.1.9 --- MAO activity assay --- p.58
Chapter 3.1.10 --- Endogenous ROS production assay --- p.58
Chapter 3.2 --- Consumable --- p.58
Chapter 3.3 --- Cells --- p.60
Chapter 3.3.1 --- Feeder cell --- p.60
Chapter 3.3.1.1 --- Mouse embryonic fibroblasts --- p.60
Chapter 3.3.2 --- ES cells --- p.61
Chapter 3.3.2.1 --- ES cell D3 --- p.61
Chapter 3.3.2.2 --- ES cell-E14TG2a --- p.61
Chapter 3.3.3 --- NS cells --- p.61
Chapter 3.3.3.1 --- Neural progenitor cells line C172 --- p.61
Chapter 3.3.3.2 --- Mouse embryonic neural stem cells --- p.61
Chapter 3.4 --- In-house prepared solutions --- p.62
Chapter 3.4.1 --- Stock solution ofInsulin, Transferrin, Selentine (ITS) Supplement --- p.63
Chapter 3.4.2 --- Gelatin solution 01% --- p.62
Chapter 3.4.3 --- Paraformaldehyde solution 4% (PFA) --- p.62
Chapter 3.4.4 --- Tritox X-lOO solution 03% --- p.63
Chapter 3.4.5 --- Popidium iodide solution 1 ug/ml (PI) --- p.63
Chapter 3.4.6 --- Poly-L-ornithine solution --- p.63
Chapter 3.4.7 --- Laminin solution --- p.64
Chapter 3.4.7 --- MEF Maintenance medium --- p.64
Chapter 3.4.9 --- Cryopreservation Media for MEF and C172 (2X) --- p.64
Chapter 3.4.10 --- Cryopreservation Media for mouse ES cell (2X) --- p.65
Chapter 3.4.11 --- Cryopreservation Media for mouse NS cell (2X) --- p.65
Chapter 3.4.12 --- Serum based maintenance medium for C172 --- p.65
Chapter 3.4.13 --- Serum free maintenance medium for C172 --- p.66
Chapter 3.4.14 --- Serum-based propagation medium for ES cells --- p.66
Chapter 3.4.15 --- Serum-free propagation medium forES cells --- p.67
Chapter 3.4.16 --- Serum-free induction medium for ES cells --- p.67
Chapter 3.4.16.1 --- Serum-free induction medium I --- p.67
Chapter 3.4.16.2 --- Serum-free induction medium II --- p.68
Chapter 3.4.16.3 --- Serum-free induction medium III --- p.68
Chapter 3.4.17 --- Tris-HCl (1 M), pH 74 --- p.68
Chapter 3.4.18 --- Tris-HCl (1 M), pH 87 --- p.69
Chapter 3.4.19 --- Tris-HCI (1 M), pH 69 --- p.69
Chapter 3.4.20 --- APS 10% (wt/vol) --- p.69
Chapter 3.4.21 --- Protease inhibitor (10X) --- p.70
Chapter 3.4.22 --- RIPA --- p.70
Chapter 3.4.23 --- Resolving buffer (8X) --- p.70
Chapter 3.4.24 --- Stacking buffer (4X) --- p.71
Chapter 3.4.25 --- Protein running buffer (lOX) --- p.71
Chapter 3.4.26 --- Transfer buffer (10X) --- p.72
Chapter 3.4.27 --- Transfer buffer (IX) --- p.72
Chapter 3.4.28 --- Blocking buffer (lOX) --- p.72
Chapter 3.4.29 --- TBS (10X) --- p.73
Chapter 3.4.30 --- TBS-T (IX) --- p.73
Chapter 3.4.31 --- Stacking gel --- p.73
Chapter 3.4.32 --- Resolving gel --- p.74
Chapter 3.5 --- Methods --- p.75
Chapter 3.5.1 --- Cell culture --- p.75
Chapter 3.5.1.1 --- Preparation of acid washed cover slips --- p.75
Chapter 3.5.1.2 --- Preparation of gelatinized culture wares --- p.75
Chapter 3.5.1.3 --- Poly-L-omithine and laminin coating --- p.76
Chapter 3.5.1.4 --- Thawing cryopreserved cells --- p.76
Chapter 3.5.1.5 --- Passage of culture --- p.77
Chapter 3.5.1.5 --- 6 Cell count --- p.78
Chapter 3.5.1.7 --- Cytospin --- p.78
Chapter 3.5.1.8 --- Trypan blue dye exclusion test --- p.78
Chapter 3.5.1.9 --- Cryopreservation --- p.79
Chapter 3.5.1.10 --- Derivation and culture of mouse embryonic fibroblasts (MEF) --- p.79
Chapter 3.5.1.11 --- Propagation of ES cells in serum-based/free medium --- p.81
Chapter 3.5.1.12 --- Neural differentiation ofES cells --- p.83
Chapter 3.5.1.13 --- Propagation ofNP cell C172 in serum-based or serum-free medium --- p.84
Chapter 3.5.1.14 --- Neural differentiation ofC172 --- p.85
Chapter 3.5.1.15 --- Derivation and propagation of embryonic NS cells --- p.85
Chapter 3.5.1.13 --- Neural differentiation of embryonic NS cells --- p.86
Chapter 3.5.1.17 --- BrdU labeling of the ES cells derived products --- p.87
Chapter 3.5.2 --- Cell proliferation assay --- p.87
Chapter 3.5.2.1 --- Cell morphology --- p.87
Chapter 3.5.2.2 --- WST-1 assay --- p.88
Chapter 3.5.2.3 --- BrdU incorporation assay --- p.88
Chapter 3.5.2.4 --- NCFC assay --- p.89
Chapter 3.5.3 --- Conventional and quantitative RT-PCR --- p.89
Chapter 3.5.3.1 --- RNA extraction --- p.89
Chapter 3.5.3.2 --- RNA quantitation --- p.90
Chapter 3.5.3.3 --- Reverse Transcription ofthe First Strand complementary DNA --- p.90
Chapter 3.5.3.4 --- Polymerase chain reaction --- p.91
Chapter 3.5.3.5 --- RNA Integrity Check --- p.91
Chapter 3.5.3.6 --- Electrophoresis and visualization of gene products --- p.91
Chapter 3.5.3.7 --- Real-time quantitative PCR --- p.92
Chapter 3.5.4 --- Microarray --- p.94
Chapter 3.5.5 --- Immunofluoresent staining --- p.94
Chapter 3.5.6 --- Western blot --- p.95
Chapter 3.5.6.1 --- Harvesting samples --- p.95
Chapter 3.5.6.2 --- Protein extraction --- p.96
Chapter 3.5.6.3 --- Protein quantification --- p.96
Chapter 3.5.6.4 --- SDS-PAGE --- p.97
Chapter 3.5.6.5 --- Wet transfer of protein to PVDF membrane --- p.97
Chapter 3.5.6.6 --- Blocking the membrane --- p.97
Chapter 3.5.6.7 --- Immunoblotting --- p.97
Chapter 3.5.6.8 --- Signal detection --- p.98
Chapter 3.5.7 --- Cell apoptosis assay --- p.98
Chapter 3.5.7.1 --- ANNEXINV-FITC apoptosis detection --- p.98
Chapter 3.5.7.2 --- TUNEL --- p.99
Chapter 3.5.8 --- Endogenous ROS assay --- p.100
Chapter 3.5.9 --- In vivo studies --- p.101
Chapter 3.5.9.1 --- Induction of cerebral ischemia in mice --- p.101
Chapter 3.5.9.2 --- Transplantation --- p.101
Chapter 3.5.9.3 --- Assessment of learning ability and memory --- p.102
Chapter 3.5.10 --- Histological analysis --- p.103
Chapter 3.5.10.1 --- Animal sacrifice for brain harvest --- p.103
Chapter 3.5.10.2 --- Cryosectioning --- p.103
Chapter 3.5.10.3 --- Haematoxylin and eosin staining --- p.104
Chapter 3.6 --- Data analysis --- p.104
Chapter Chapter4 --- Results --- p.113
Chapter 4.1 --- Expression profile of 5-HT receptors and metablism of endogenous 5-HT --- p.113
Chapter 4.1.1 --- Expression profiles of 5-HT receptors in stem cells --- p.113
Chapter 4.1.2 --- Biosynthesis of endogenous 5-HT --- p.115
Chapter 4.2 --- Effects of 5-HT on proliferation of mouse ES cells and NS cells --- p.115
Chapter 4.2.1 --- Effects of 5-HT on proliferation ofES cells --- p.115
Chapter 4.2.2 --- Effects of 5-HT on proliferation ofNP and NS cells --- p.117
Chapter 4.3 --- Effects of 5-HT on differentiation of mouse ES cells and NS cells --- p.119
Chapter 4.3.1 --- Neural differentiation ofES cells --- p.119
Chapter 4.3.2 --- Effects of 5-HT on differentiation ofES cells --- p.119
Chapter 4.3.3 --- Neural differentiation ofNP and NS cells --- p.120
Chapter 4.3.4 --- Effects of 5-HT on differentiation ofNP and NS cells --- p.121
Chapter 4.4 --- 5-HT metabolism in mouse ES cells and NS cells --- p.122
Chapter 4.4.1 --- Expression of key 5-HT metablic genes in stem cells --- p.122
Chapter 4.4.2 --- Detection ofROS generation in mouse NS cells --- p.123
Chapter 4.4.3 --- Effects of 5-HT on expression level of MAO-A, MAO-B and SERT --- p.123
Chapter 4.5 --- Anti-apoptotic effect of 5-HT on NP and NS cells in neural induction --- p.127
Chapter 4.6 --- Potential signaling pathways mediated by 5-HT --- p.130
Chapter 4.7 --- Therapeutic effects of 5-HT treated mouse ES cell-derived cells in a stoke model --- p.130
Chapter 4.7.1 --- Induction of global ischemia by transient BCCAO --- p.130
Chapter 4.7.1.1 --- HE staining of post ischemic brain --- p.131
Chapter 4.7.1.2 --- TUNEL analysis of cell apoptosis at post ischemia day 3 --- p.132
Chapter 4.7.2 --- Cell labelling --- p.132
Chapter 4.7.3 --- Cognition monitoring post transplantation --- p.133
Chapter 4.7.4 --- Survival, migration and differentiation of transplanted neural cells --- p.135
Chapter Chapter5 --- Discussion --- p.180
Chapter Chapter6 --- Conclusions --- p.192
References --- p.195
"Baicalin-mediated neuronal induction of neural stem cells and improvement of cognitive function in a mouse stroke model". Thesis, 2009. http://library.cuhk.edu.hk/record=b6074973.
Texto completoNature provides a vast pool of natural compounds with neuroprotection and neurotrophism. A few of these compounds can induce the differentiation of neural stem cells (NSC). There are ample opportunities to discover more natural compounds with differentiation inducing effect on NSC. One of the objectives of this project is to look for novel natural compounds showing neurogenic effect on NSC. This project has established a platform for screening medicinal materials and natural compounds with neural differentiation promoting effect on C17.2 mouse neural stem cell line. Screening results identified total Sanqi saponins, total Renshen saponins, Huangqin extracts and baicalin as potent candidates for inducing this differentiation of NSC.
This project also aims at characterizing the mechanisms involved in the neuronal differentiation effect of baicalin on NSC. Annotation from microarray analysis indicated that baicalin treatment on C17.2 NSC is related to development of tissue and nervous system. qPCR study attested the increased gene expression of nerve growth factor-beta, neurotrophin-3, pro-neural transcriptional factors Ngn1, Ngn2 and NeuroD2. Western blotting showed that baicalin activated ERK1/2 MAP kinase but not JNK and p38 MAP kinases.
This project demonstrated the neurogenic potential of natural resources on NSC. A novel neuronal induction effect of baicalin on NSC was also demonstrated with its mechanisms characterized. This project also revealed that baicalin can be used for promoting functional recovery of post-ischemia animals.
This study showed for the first time that baicalin exerts neuronal differentiation inducing effect on NSC. Another objective of this project is to study whether baicalin can promote functional recovery of animals with ischemia brain injury. Mice having undergone transient occlusion of the bilateral common carotid arteries with blood-reperfusion to induce global cerebral ischemia were treated with baicalin and/or EGFP-NSC. Ischemia animals received implantation of EGFP-NSC into the caudate putamen and/or intravenous injection of baicalin on alternate days for two-week on day seven post-ischemia displayed significant improvement of the cognitive function in terms of the incident of error and escape time in the water T-maze task compared to the control arm of ischemia mice. Data of the study suggested that the therapeutic effect of baicalin would be comparable to that of neural stem cell transplant in improving the cognitive function in a mouse ischemic stroke model.
Li, Ming.
Adviser: P. C. Shaw.
Source: Dissertation Abstracts International, Volume: 73-01, Section: B, page: .
Thesis (Ph.D.)--Chinese University of Hong Kong, 2009.
Includes bibliographical references (leaves 199-232).
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, [201-] System requirements: Adobe Acrobat Reader. Available via World Wide Web.
Abstract also in Chinese.
"The effects of hematopoietic growth factors and tanshinone IIA on neuro-protection". Thesis, 2005. http://library.cuhk.edu.hk/record=b6073980.
Texto completoOur observation provided the first evidence showing the expression of functional TPO receptor c-mpl in central nervous system. It revealed that novel agents TPO, EPO and tanshinone IIA have neuroprotection effects against brain injury induced by hypoxia-ischemia in neonatal rats, and these agents could be developed for clinical applications.
To investigate the effect of TPO, EPO and tanshinone IIA on in-vivo neural protection, a neonatal rat model of hypoxic-ischemic brain damage was established. Our results demonstrated significant and sustained brain injury in the hypoxic-ischemic and vehicle-treated group, measured by the reduction in relative weights of the ipsilateral (right) to the contralateral (left) brain at 1 and 3 weeks post-surgery, compared with those of sham-operated animals. At 3 weeks post-surgery, the hypoxic-ischemic animals had decreased cortical neuron density quantified by neuron-specific enolase (NSE) staining, and compromised sensorimotor functions in response to the postural reflex test. Treatment with TPO, EPO and tanshinone IIA significantly reduced the severity of brain injury, as indicated by the significantly increased ipsilateral brain weight and neuron density. Recoveries of sensorimotor functions (p < 0.05) and histopathology were also observed in animals that received TPO, EPO and tanshinone IIA. The plasma of tanshinone IIA-treated animals exhibited higher antioxidant activities (oxygen radical absorbance capacity assay) than those from vehicle-treated rats.
TPO and TPO receptor (c-mpl) mRNA was identified in human cerebral hemispheres, cerebellum, mouse neural progenitor cell line C17.2 and four neuroblastoma cell lines (SK-N-MC, MHH-NB-11, SK-N-AS and SH-SY-5Y) using RT-PCR methods. TPO proteins were detected in human cerebrospinal fluid (CSF) and plasma by ELISA. Furthermore, TPO receptor c-mpl was confirmed in human cerebral hemispheres, hippocampus, cerebellum, brainstem and spinal cord using immunohistostaining. TPO had a stimulating effect on the growth of neural progenitor cell C17.2 in culture via the phosphoinositide 3-kinase (PI3K)/Akt signaling pathway as demonstrated by Western blot. The anti-apoptotic effects of TPO, EPO on C17.2 cells were demonstrated by staining with Annexin-V and PI. EPO exerted a protective effect against SHSY-5Y cell damage induced by NMDA (N-methyl-d-aspartate), as demonstrated by the MTT and LDH assay. The anti-oxidative property of tanshinone IIA was studied in the C17.2 cell line. Tanshinone IIA increased the viability of these cells subjected to 2,2'-azobis (2-amidino propane hydrochloride) (AAPH)-induced oxidative stress.
by Xia Wen-Jie.
"May 2005."
Advisers: Kwok-Pui Fung, Tai-Fai Fok.
Source: Dissertation Abstracts International, Volume: 67-01, Section: B, page: 0126.
Thesis (Ph.D.)--Chinese University of Hong Kong, 2005.
Includes bibliographical references (p. 126-146).
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.
Abstracts in English and Chinese.
School code: 1307.
Chen, Chun-Hao y 陳君豪. "Antioxidant Defenses of Astrocytes Activation after Hyperbaric Oxygen Treatment in Transient Focal Cerebral Ischemic Rats". Thesis, 2007. http://ndltd.ncl.edu.tw/handle/78103140084657078491.
Texto completo國立陽明大學
物理治療學系暨研究所
95
Background and Purpose: Brain following transient focal cerebral ischemia develops a complex series of pathophysiological events. As a consequence of ischemia and subsequent reperfusion, the reactive free radicals react with cellular components (carbohydrates, amino acids, DNA, and phospholipids) and damage them. Hyperbaric oxygenation (HBO) has a characteristic in dramatically increasing the oxygen content of blood by physically dissolving oxygen and theoretically penetrates to deeper and poorly perfused ischemic areas. Thus, HBO appears to be a neuroprotective procedure for treating the cerebral ischemia. However, the neurophysiological mechanisms underlying such neuroprotective effects are still uncertain. It is suggested that some of the effects of HBO on neuronal survival are mediated indirectly by astrocyte. Moreover, astrocytes are believed to play a crucial part in the antioxidant defense of the brain, due to containing the high concentrations of antioxidants as well as providing the neurons with substrates for important antioxidants such as glutathione (GSH). The purpose of this study was to investigate whether HBO can promote the neuronal antioxidant defenses by activation the astrocytes in transient focal cerebral ischemic rats. Methods: 48 male Spraque-Dawley rats were subjected to 60 minutes middle cerebral artery occlusion (MCAO). Animals were randomly assigned to the HBO group or the control group (n=24 in each group). HBO was administered at a pressure of 3 atm absolute (3 ATA) for 1 hour with 100% oxygen, starting at 3 hours after MCAO in the HBO group. For the control group, animals were placed in the chamber and exposed to normobaric room air. All rats were sacrificed 24 hours after the MCAO procedure. The infarct volume, activation of astrocyte, glutathione, and the degree of lipid peroxidation were assessed for both groups. Comparisons of infarct volume, level of activated astrocyte, glutathione and lipid peroxidation between groups were carried out by independent t-test. Statistical comparisons of the glutathione and lipid peroxidation among the four cerebral areas were analyzed by one-way analysis of variance (ANOVA) and the post hoc Bonferroni test for pairwise comparisons if a significant difference was found. A probability value <0.05 was considered significant. Results: Total infarct volume was reduced by 35% (control group: 21.69±4.27% versus HBO group: 13.96±2.33%; P<0.01). Furthermore, HBO treatment enhanced the activation of astrocytes in the affected brain area compared with that of the control group, especially in the cerebral cortex. The GSH levels of right cortex (mean±SD, 2.5061±0.6470 nmol/mg tissue) and right striatum (mean±SD, 1.7419±0.5526 nmol/mg tissue) were increased after HBO treatment, especially in right cortex (P<0.05) compared with that of control group. Additionally, oxidative injuries due to cerebral ischemia were also significantly attenuated in the HBO-treated rats compared to those of the control rats. Conclusions: In the present investigation, we demonstrated a single HBO treatment after a transient ischemic insult in rats resulted in a significant reduction of the infarct volume. Our study also revealed astrocyte activation and decrease in oxidative injury in HBO rats. According to our findings, we suggest that HBO can promote the antioxidant defenses by activation the astrocytes and results in decreasing infarct volume in transient focal cerebral ischemic rats. Clinical Relevance: The present results provide evidence for possible neuroprotective mechanisms of the hyperbaric oxygen treatment, which is a clinical treatment for ischemic stroke patients.