Thesis (Ph.D.). / Written for the Dept. of Anatomy and Cell Biology. Title from title page of PDF (viewed 2008/05/12). Includes bibliographical references.

Thesis (Ph. D.)--University of Virginia, 1998. / Includes bibliographical references (157-170). Also available online through Digital Dissertations.

Thesis (Ph. D.)--University of Washington, 1998. / Vita. Includes bibliographical references (leaves [121]-138).

Thesis (Ph. D.)--Cornell University, 1989. / Vita. Includes bibliographical references.

No description available.

Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.

Diss. (sammanfattning) Umeå : Univ., 2009. / Härtill 4 uppsatser.

Diss. (sammanfattning) Linköping : Univ., 2003. / Härtill 4 uppsatser.

As pesquisas em lesão medular tiveram um avanço significativo nas últimas duas décadas. Várias substâncias têm sido testadas, dentre elas, os fatores neurotróficos que são proteínas que auxiliam na maturação e desenvolvimento do sistema nervoso. O objetivo deste estudo foi conduzir testes que propiciem a análise dos efeitos da recuperação funcional locomotora e regeneração axonal em ratos submetidos a testes experimentais com a utilização da substância neurotropina-4. O estudo consistiu de 30 ratos adultos jovens, da raça Wistar, que foram submetidos à lesão medular ao nível de TX, provocado por um aparelho denominado NYU impactor. Os ratos foram divididos em dois grupos de 15 ratos cada, denominados de grupo controle e grupo tratamento, que receberam aplicação de água destilada e 1g de neurotropina-4, respectivamente. Estes foram avaliados funcionalmente pela escala BBB e submetidos à análise histológica. Concluiu-se que a neurotropina-4 promove a recuperação locomotora funcional e diminui os efeitos secundários da lesão medular, comparativamente ao grupo controle / Research into spinal cord injury has advanced significantly over the past two decades. Many substances have been tested, including the neurotrophics factors, which are proteins that aid in the maturation and development of the nervous system. The objective of this study was to conduct tests that provide the analysis of the effects of the locomotor functional recovery and axonal regeneration in rats subjected to experimental tests with the use of the substance neurotrophin-4. The study consisted of thirty young adult rats, Wistar race, which received TX level of spinal cord injury through a device called NYU impactor. The rats were divided into two groups of fifteen rats each, called the control group and treatment group, which received application of distilled water and 1 g Neurotrophin-4, respectively. They were evaluated functionally by the BBB scale and submitted to the histological analysis. It was concluded that the Nt-4 promotes the recuperation of the locomotor function and reduces the side effects of spinal cord injury, compared to the control group

Lai, Ching Janice. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 148-168). / Abstracts in English and Chinese. / Abstract --- p.i / Abstract in Chinese --- p.iii / Acknowledgements --- p.v / Table of Content --- p.vi / List of Tables --- p.x / List of Figures --- p.xi / Abbreviations --- p.xii / Chapter Chapter 1 --- Introduction --- p.1 / Chapter 1.1 --- General Introduction --- p.1 / Chapter 1.2 --- Nervous System and the Blood-Brain-Barrier --- p.3 / Chapter 1.3 --- Glial cells --- p.3 / Chapter 1.4 --- Studying Astrocyte Responses As a New Direction in Neuroscience --- p.4 / Chapter 1.5 --- The Roles of Astrocyte in the CNS --- p.5 / Chapter 1.5.1 --- Energy-Dependent Communication Between Neurons and Astrocytes --- p.7 / Chapter 1.5.2 --- Strategies for Metabolic Exchange Between Astrocytes and Neurons --- p.8 / Chapter 1.5.2.1 --- Provision of Energy Metabolites to Neurons by Astrocytes --- p.9 / Chapter 1.5.2.2 --- Glucose Transporters in the CNS --- p.10 / Chapter 1.5.2.3 --- The Lactate Shuttle Hypothesis --- p.12 / Chapter 1.5.2.4 --- The Regulation of Glucose Uptake at the Blood-Brain-Barrier (BBB) by the Activity of Neurons --- p.14 / Chapter 1.5.3 --- Alternation of Energy Metabolism in Neuropathy --- p.15 / Chapter 1.5.3.1 --- Ketone Body Shuttle Hypothesis --- p.15 / Chapter 1.5.3.2 --- The Utilization of Free Fatty Acids by the Brain --- p.17 / Chapter 1.5.4 --- The Provision of Neurotrophic Factors to Neurons by Astrocytes --- p.17 / Chapter 1.5.4.1 --- Neurotrophins --- p.18 / Chapter 1.5.4.1.1 --- Relationship Between Neurotrophins and Glucose --- p.20 / Chapter 1.5.4.2 --- S100B --- p.21 / Chapter 1.5.5 --- Astrocytic Cholesterol in Astrocytes as a Neurotrophic Factor --- p.22 / Chapter 1.6 --- Neuroprotective Effect of Glucose vi - --- p.23 / Chapter 1.7 --- Diseases Associated with Decreased Glucose Transport at the BBB --- p.24 / Chapter 1.7.1 --- Glucose Transporter Type 1 Deficiency Syndrome (GlutlDS) --- p.24 / Chapter 1.7.2 --- Hypoglycemia with Insulin Therapy for Diabetes Patients --- p.24 / Chapter 1.8 --- Aims and Hypothesis of Study --- p.26 / Chapter Chapter 2. --- 2 Materials and Methods --- p.27 / Chapter 2.1 --- Materials --- p.27 / Chapter 2.1.1 --- Cell Culture --- p.27 / Chapter 2.1.1.1 --- Cells --- p.27 / Chapter 2.1.1.1.1 --- C6 cells --- p.27 / Chapter 2.1.1.1.2 --- Primary Astrocytes --- p.27 / Chapter 2.1.1.2 --- Cell Culture Reagent --- p.27 / Chapter 2.1.2 --- Study of Growth Properties --- p.31 / Chapter 2.1.2.1 --- Equipment for Growth Curve Construction --- p.31 / Chapter 2.1.2.2 --- Reagents for Flow Cytometry --- p.32 / Chapter 2.1.2.3 --- Reagents for 3H-thymidine Incorporation Assay --- p.32 / Chapter 2.1.3 --- Study of Neurotrophic Properties --- p.33 / Chapter 2.1.3.1 --- Determination of Neurotrophic Factor Productions --- p.33 / Chapter 2.1.3.1.1 --- Reagents and Buffers for Northern Blot Analysis --- p.33 / Chapter 2.1.3.2 --- Reagents and Buffers for Western Blot Analysis --- p.43 / Chapter 2.1.3.2.1 --- Protein Assay --- p.43 / Chapter 2.1.3.2.2 --- Reagents for SDS Polyacrylamide Electrophoresis of Proteins --- p.44 / Chapter 2.1.3.2.3 --- Reagents for the Transfer of Protein to Membrane and Signal Detection --- p.47 / Chapter 2.1.4 --- Study of Lipid in Glial cells --- p.50 / Chapter 2.1.4.1 --- Determination of Genes Expression in Lipid Metabolism --- p.50 / Chapter 2.1.4.2 --- Reagents for Determination of Cholesterol and Fatty Acid Levels by Gas Chromatography --- p.50 / Chapter 2.2 --- Methods --- p.54 / Chapter 2.2.1 --- Cell culture --- p.54 / Chapter 2.2.1.1 --- Maintenance of C6 cells --- p.54 / Chapter 2.2.1.2 --- Primary Culture of Rat Astrocytes --- p.54 / Chapter 2.2.2 --- Study of Growth Properties of Glial Cells vii - --- p.56 / Chapter 2.2.2.1 --- Construction of cell growth curve --- p.56 / Chapter 2.2.2.2 --- Flow Cytometric Analysis of Cell Cycle Profile --- p.56 / Chapter 2.2.2.3 --- Measurement of DNA Synthesis --- p.57 / Chapter 2.2.3 --- Study of Neurotrophic Properties --- p.58 / Chapter 2.2.3.1 --- Determination of Neurotrophic Facotor Production --- p.58 / Chapter 2.2.3.1.1 --- Northern Blot Analysis --- p.58 / Chapter 2.2.3.1.2 --- Western Blot Analysis --- p.67 / Chapter 2.2.3.2 --- Determination of Gene Expression in Lipid Metabolism --- p.72 / Chapter 2.2.3.2.1 --- Northern Blot Analysis --- p.72 / Chapter 2.2.3.2.2 --- RT-PCR --- p.72 / Chapter 2.2.3.3 --- Study of Lipid Profiles in Glial Cells --- p.73 / Chapter 2.2.3.3.1 --- Sample preparation --- p.73 / Chapter 2.2.3.3.2 --- Total Cholesterol Determination --- p.73 / Chapter 2.2.3.3.3 --- Total Fatty Acid Determination --- p.75 / Chapter 2.2.3.3.4 --- Quantification of Proteins --- p.76 / Chapter 2.2.4 --- Statistical Analysis --- p.77 / Chapter Chapter 3 --- Results --- p.78 / Chapter 3.1 --- The effects of glucose deficiency on cell proliferation --- p.78 / Chapter 3.1.1 --- Direct Cell Count Assay --- p.78 / Chapter 3.1.2 --- Flow Cytometry Assay --- p.83 / Chapter 3.1.3 --- 3H-Thymidine Uptake Assay --- p.85 / Chapter 3.2 --- The Effects of Glucose Deficiency on Neurotrophic Properties of Glial Cells --- p.87 / Chapter 3.2.1 --- The Effects of Glucose Deficiency on mRNA and Protein Expressions of Neurotrophins --- p.88 / Chapter 3.2.1.1 --- Northern Blot Assays --- p.88 / Chapter 3.2.1.2 --- Western Blot Assays --- p.93 / Chapter 3.2.2 --- The Effects of Glucose Deficiency on Lipid Homeostasis --- p.96 / Chapter 3.2.2.1 --- Northern Blot Assays --- p.96 / Chapter 3.2.2.2 --- Gas Chromatography Assays --- p.101 / Chapter 3.2.2.2.1 --- Cholesterol Analyses --- p.102 / Chapter 3.2.2.2.2 --- Fatty Acid Analyses --- p.105 / Chapter Chapter 4 --- Discussion --- p.115 / Chapter 4.1 --- The in vitro Model of Hypoglycorrhachia --- p.115 / Chapter 4.2 --- Decreased Glucose Level Triggers Changes of Gial Cells Proliferation --- p.117 / Chapter 4.3 --- Expression of Neurotrophic Factor under Glucose Deficiency viii - --- p.120 / Chapter 4.3.1 --- Alteration of the Expression of Neurotrophins --- p.120 / Chapter 4.3.1.1 --- NGF --- p.122 / Chapter 4.3.1.2 --- BDNF --- p.123 / Chapter 4.3.1.3 --- NT-3 --- p.126 / Chapter 4.3.1.4 --- NT-4/5 --- p.128 / Chapter 4.3.2 --- Alteration of the mRNA Expression of Calcium Binding ProteinS100B --- p.128 / Chapter 4.4 --- Alteration of Lipid Metabolism in Decreased Glucose Supply --- p.130 / Chapter 4.4.1 --- Up-regulation of ApoE mRNA Expression in Glucose Deficiency --- p.133 / Chapter 4.4.2 --- Cholesterol Homeostasis in Glial Cells --- p.133 / Chapter 4.4.3 --- Fatty Acids Homeostasis in Glial Cells --- p.135 / Chapter 4.4.4 --- Decreased Ketone Bodies synthesis in Glucose Deficiency --- p.143 / Chapter 4.5 --- Limitations of the Current Study --- p.144 / Chapter 4.6 --- Future Directions --- p.145 / Chapter Chapter 5 --- Conclusion --- p.147 / References --- p.148 / Appendix --- p.169