Diss. (sammanfattning) Stockholm : Karol. inst. / Härtill 6 uppsatser.

Thesis (Ph.D.) - University of Glasgow, 2007. / Ph.D. theses submitted to the Faculty of Medicine, Division of Clinical Neuroscience, University of Glasgow, 2007. Includes bibliographical references. Print version also available.

by Lam Ying Wan. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1991. / Includes bibliographical references. / Acknowledgement --- p.5 / List of Abbreviations --- p.7 / Abstract --- p.10 / Chapter Chapter 1: --- Introduction --- p.13 / Chapter 1.1 --- Distribution and Biosynthesis of Taurine --- p.14 / Chapter 1.2 --- Physiological Functions of Taurine --- p.17 / Chapter 1.2.1 --- Interaction of Taurine and Calcium --- p.17 / Chapter 1.2.2 --- Neuroinhibitory action of Taurine --- p.18 / Chapter 1.2.3 --- Taurine as an Osmoeffector --- p.20 / Chapter 1.2.4 --- Integrative Model of Taurine Action --- p.22 / Chapter 1.3 --- Taurine and Volume Regulation in Astrocytes --- p.22 / Chapter 1.3.1 --- Response of Cells to Anisosmotic Media --- p.22 / Chapter 1.3.2 --- Mechanism of Regulatory Cell Volume Decrease --- p.23 / Chapter 1.3.3 --- Regulatory Volume Decrease (RVD) in Astrocytes --- p.25 / Chapter 1.3.4 --- Taurine and Volume Regulation in Astrocytes --- p.25 / Chapter 1.4 --- Ion Channels and Transporters in Astrocytes --- p.26 / Chapter 1.4.1 --- Potassium Channels --- p.26 / Chapter 1.4.2 --- Sodium Channels --- p.27 / Chapter 1.4.3 --- Chloride Channels --- p.27 / Chapter 1.4.4 --- Stretch-activated Ion Channels --- p.27 / Chapter 1.4.5 --- (KC1 + NaCl) Carrier --- p.27 / Chapter 1.4.6 --- Na+/H+ exchange --- p.28 / Chapter 1.4.7 --- C1-/HCO3- exchange --- p.28 / Chapter Chapter 2: --- Materials and Methods --- p.30 / Chapter 2.1 --- Cell Culture --- p.30 / Chapter 2.1.1 --- Preparation of Culture Medium --- p.30 / Chapter 2.1.2 --- Preparation of Phosphate Buffered Saline --- p.30 / Chapter 2.1.3 --- Cell Counting Method --- p.31 / Chapter 2.1.4 --- Culture of U373MG Human Astrocytoma Cells --- p.31 / Chapter 2.1.5 --- Culture of Primary Astrocytes --- p.32 / Chapter 2.2 --- Taurine Release Experiment --- p.32 / Chapter 2.2.1 --- Preparation of Physiological Salt Solution (PSS) --- p.32 / Chapter 2.2.2 --- Preparation of Hyposmotic Solution --- p.33 / Chapter 2.2.3 --- Preparation of Chloride Free Solution --- p.33 / Chapter 2.2.4 --- Preparation of Sodium Free Solution --- p.33 / Chapter 2.2.5 --- Preparation of Calcium Free Solution --- p.34 / Chapter 2.2.6 --- Preparation of High Potassium Solution --- p.34 / Chapter 2.2.7 --- Preparation of Urea containing PSS --- p.34 / Chapter 2.2.8 --- Assay of [3H]-Taurine Release --- p.34 / Chapter 2.2.9 --- Drug pretreatment --- p.35 / Chapter 2.2.10 --- Data Calculation --- p.35 / Chapter 2.3 --- Volume Determination --- p.36 / Chapter 2.3.1 --- Experimental procedure --- p.36 / Chapter 2.3.2 --- Drug pretreatment --- p.37 / Chapter 2.3.3 --- Data calculation --- p.40 / Chapter 2.4 --- Taurine Influx Experiment --- p.41 / Chapter 2.4.1 --- Experimental Procedure --- p.41 / Chapter 2.5 --- Drug Preparation --- p.42 / Results / Chapter Chapter 3: --- Hyposmolarity-Induced [3H]-Taurine Release --- p.45 / Chapter 3.1 --- Responses of Astrocytes to Hyposmotic Conditions --- p.45 / Chapter 3.1.1 --- Effect of Hyposmotic Medium on the Release of Preloaded [3H]-taurine in U373MG astrocytoma cell --- p.45 / Chapter 3.1.2 --- Time Course of the Hyposmolarity-induced [3H]-taurine Release --- p.49 / Chapter 3.1.3 --- Response of Primary Astrocytes to Hyposmotic Medium --- p.49 / Chapter 3.2 --- Effect of MK196 on Hyposmolarity-Induce Taurine Release --- p.52 / Chapter 3.3 --- Effects of Inhibitors of (NaCl+KCl) Cotransporter and C1- /HCO3- Anion Exchanger on Hyposmolarity-induced [3H]- taurine Release --- p.56 / Chapter 3.3.1 --- Effect of (NaCl + KC1) Cotransporter Inhibitors on Hyposmolarity-induced [3H]-taurine Release --- p.56 / Chapter 3.3.2 --- "Effects of two stilbene derivatives, SITS and DIDS,on hyposmolarity-induced [3H]-taurine release" --- p.56 / Chapter 3.3.3 --- "Effect of a Chloride Channel Blocker, Antracene-9- Carboxylate on Hyposmolarity-induced [3H]-taurine Release" --- p.57 / Chapter 3.3.4 --- Effect of MK473 on Hyposmolarity-induced [3H]-taurine Release --- p.58 / Chapter 3.4 --- Effect of Chloride Depletion on Hyposmolarity-induced [3H]- taurine Release --- p.58 / Chapter 3.4.1 --- Effect of Replacing Chloride with Nitrate --- p.58 / Chapter 3.4.2 --- Effect of Replacing Sodium Chloride with Sucrose --- p.59 / Chapter 3.4.3 --- Effect of Replacing Chloride with Gluconate --- p.59 / Chapter 3.5 --- Investigation of the Transduction Mechanism of Hyposmolarity- induced [3H]-taurine Release --- p.71 / Chapter 3.5.1 --- Effect of Depleting Extracellular Ca2+ --- p.71 / Chapter 3.5.2 --- Effect of Staurosporine on Hyposmolarity-induced [3H]- taurine Release --- p.71 / Chapter 3.6 --- Effect of SITS on the Swelling Process of U373 MG cells --- p.74 / Chapter 3.6.1 --- Regulatory Volume Decrease (RVD) in U373 MG Cells --- p.74 / Chapter 3.6.2 --- Effect of SITS on RVD in U373 MG Cells --- p.74 / Chapter 3.7 --- Effect of Hyposmotic Medium on Sodium-Independent Taurine Uptake in U373 MG Cells --- p.77 / Chapter Chapter 4 : --- Urea-Induced [3H]-Taurine Release --- p.80 / Chapter 4.1 --- Concentration Dependency of Urea-Induced Efflux of [3H]-taurine from U373 MG Cells --- p.80 / Chapter 4.2 --- Effect of MK 196 on the Urea-Induced [3H]-taurine Release from U373 MG Cells --- p.82 / Chapter 4.3 --- Effect of SITS on the Urea-induced [3H]-taurine Release from U373 MG Cells --- p.82 / Chapter Chapter 5: --- High Potassium-Induced Efflux of [3H]-taurine --- p.86 / Chapter 5.1 --- High Potassium Concentration Induced Release of [3H]-taurine from U373 MG Cells --- p.86 / Chapter 5.1.1 --- High Potassium Concentration Induced Release of [3H]- taurine --- p.86 / Chapter 5.1.2 --- Effect of the Concentration of HCO3- on High Potassium Induced Release [3H]-taurine Release --- p.87 / Chapter 5.2 --- Effect of MK 196 on High Potassium Induced [3H]-taurine Release in U373 MG --- p.87 / Chapter 5.3 --- Effect of (NaCl + KC1) Cotransporter Inhibitors on High Potassium Induced Taurine Release from U373 MG Cells --- p.91 / Chapter 5.3.1 --- Effect of Furosemide on High Potassium Induced [3H]- taurine Release --- p.91 / Chapter 5.3.2 --- Effect of Bumetanide on High Potassium Induced [3H]- taurine Release --- p.91 / Chapter 5.4 --- Effect of C1-/HCO3- Anion Exchanger Inhibitors on High Potassium Induced Release of [3H]-taurine from U373 MG Cells --- p.91 / Chapter 5.4.1 --- Effect of SITS on High Potassium Induced [3H]-taurine Release --- p.91 / Chapter 5.4.2 --- Effect of Antracene-9-Carboxylate on High Potassium Induced [3H]-taurine Release --- p.96 / Chapter 5.4.3 --- Effect of MK 473 on High Potassium Induced [3H]- taurine Release --- p.96 / Chapter 5.5 --- Effect of Chloride Depletion on High Potassium-Induced [3H]- taurine Release --- p.96 / Chapter 5.5.1 --- Effect of Replacing C1- by NO3- --- p.96 / Chapter 5.5.2 --- Effect of Replacing C1- by Gluconate --- p.96 / Chapter Chapter 6: --- Discussion --- p.102 / Chapter 6.1 --- Hyposmolarity Induced [3H]-taurine Release --- p.103 / Chapter 6.1.1 --- Hyposmolarity is the Key Stimulation for [3H]-taurine Release --- p.103 / Chapter 6.1.2 --- Hyposmolarity Induced [3H]-taurine Release and the C1- /HCO3- anion exchanger --- p.104 / Chapter 6.1.3 --- Comparision of the Hyposmolarity-induced Release of [3H]-taurine in U373 MG cells and primary astrocytes --- p.106 / Chapter 6.1.4 --- Comparision between the Hyposmolarity-induced Taurine Release and the Na+-independent Uptake for Taurine --- p.106 / Chapter 6.1.5 --- Transduction Mechanisms of Hyposmolarity-induced [3H]-taurine Release --- p.107 / Chapter 6.2 --- Urea-Induced Release of [3H]-taurine --- p.107 / Chapter 6.3 --- High Potassium-Induced [3H]-taurine Release --- p.108 / Chapter 6.3.1 --- Pharmacological Properties of High Potassium-induced [3H]-taurine Release --- p.108 / Chapter 6.3.2 --- Effect of Ionic Environment on High Potassium-Induced [3H]-taurine Release --- p.108 / Chapter 6.4 --- Mechanism of Swelling-Induced Taurine Release --- p.109 / Chapter 6.4.1 --- Involvement Stretched Activated Channel (SACs) in Swelling-Induced Taurine Release --- p.109 / Chapter 6.4.2 --- Involvement of the C1-/HCO3- Anion Exchanger in Swelling-Induced Taurine Release --- p.110 / Chapter 6.4.3 --- Possibility of Taurine as a Substrate of the C1-/HCO3- Anion Exchanger --- p.111 / Chapter 6.4.4 --- Conclusion --- p.114 / Chapter Chapter 7: --- Conclusion --- p.116 / References --- p.119

Kwong Man Kwong. / "June 2000." / Thesis (Ph.D.)--Chinese University of Hong Kong, 2000. / Includes bibliographical references (p. 114-141). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

No description available.

Central nervous system injuries often lead to devastating consequences due to an unfavourable environment created after the injury. Current treatments have yet to address the environment for improved prospects of functional recovery. Transplantation of Schwann cells into the lesion site could in part address the issue, promoting nerve regeneration and enhancing functional recovery. Bone marrow stromal cells (BMSCs) promise to be a viable, autologous source for Schwann cell derivation. Fate-committed Schwann cells derived from BMSCs through co-culture with purified dorsal root ganglia (DRG) neurons suggest that the DRG neurons present juxtacrine cues that direct commitment to the Schwann cell fate. We hypothesize that Neuregulin 1 type III (NRG1(III)) is one such juxtacrine cue to which BMSC-derived Schwann cell-like cells (SCLC) respond in the switch to fate commitment. In this study, NRG1(III) was found to be expressed on freshly isolated DRG neurons and that SCLCs expressed both the ErbB2 and 3 receptors. Western blot analysis for phosphorylated Akt and MAPK provided indicators of downstream signalling of NRG1/ErbB complexes. We then tested if both the soluble and membrane bound forms of NRG1 mediate SCLC differentiation towards fate commitment. In contrast to the membrane-bound form on DRG neurons, soluble NRG1 failed to direct the SCLCs towards the Schwann cell fate. HEK293T cells that stably overexpress NRG1(III) were generated and tested as a neuronal surrogate that presents NRG1(III) on the cell surface. In a 5-day co-culture system with HEK293TNrg1(III) cells, SCLCs were found to develop elongated processes, acquiring either unipolar or bipolar morphology that resembles that of Schwann cells. Screening for marker expression by RT-PCR suggested that at this stage of morphological transition, SCLCs were not yet committed to the Schwann cell fate. The co-culture system will be pursued to find ex vivo conditions that direct differentiation of BMSC-derived SCLCs to fate-committed Schwann cells. / published_or_final_version / Biochemistry / Master / Master of Philosophy

published_or_final_version / Medicine / Master / Doctor of Medicine

No description available.

Thesis (Ph. D.)--University of Washington, 2004. / Vita. Includes bibliographical references (leaves 93-112).

Thesis (M.D.)--University of Hong Kong, 1997. / Includes bibliographical references (leaf 246-315).