Thesis (Ph. D.)--University of Virginia, 1997. / Spine title: Structure & function of uhpA. Includes bibliographical references (138-146). Also available online through Digital Dissertations.

Thesis (Ph.D.)--University of Alabama at Birmingham, 2009. / Title from first page of PDF file (viewed on June 10, 2009). Includes bibliographical references.

Thesis (Ph. D.)--University of Washington, 2007. / Vita. Includes bibliographical references (leaves 126-149).

by Tsui Hong Teng. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1999. / Includes bibliographical references (leaves 174-181). / Abstracts in English and Chinese. / A CKNO WLED GMENTS --- p.7 / ABSTRACT --- p.8-10 / Chapter Chapter 1: --- Introduction: --- p.11-44 / Chapter 1.1) --- Glucose transporters / Chapter 1.2) --- Glucose transporters and cancers / Chapter 1.3) --- Antisense strategies / Chapter 1.4) --- Cellular uptake of oligonucleotides / Chapter 1.5) --- Hyperthermia and combined treatments / Chapter Chapter 2: --- Materials and methods --- p.45-60 / Chapter 2.1) --- Materials: / Chapter 2.1a) --- Cell lines and culture media / Chapter 2.1b) --- Oligonucleotides synthesis / Chapter 2.1c) --- Chemicals / Chapter 2.2) --- Methods: / Chapter 2.2a) --- Oligonucleotide design / Chapter 2.2b) --- Oligonucleotide treatment / Chapter 2.2c) --- Flow cytometry / Chapter 2.2d) --- Confocal microscopy / Chapter 2.2e) --- MTT assay for cytotoxicity or cell proliferation / Chapter Chapter 3: --- Cellular uptake of oligonucleotide spontaneously and Lipofectin-aided: --- p.61-85 / Chapter 3.1) --- Introduction / Chapter 3.2) --- Flow cytometric studies / Chapter 3.3) --- Confocal microscopic studies / Chapter 3.4) --- Cytotoxic effect of Lipofectin alone on MCF-7 cells / Chapter 3.5) --- Discussion / Chapter Chapter 4: --- Hyperthermia can enhance oligonucleotide uptake: --- p.86-118 / Chapter 4.1) --- Introduction / Chapter 4.2) --- Flow cytometric studies / Chapter 4.3) --- Confocal microscopic studies / Chapter 4.4) --- Cytotoxic effect of hyperthermia on MCF-7 cells / Chapter 4.5) --- FITC-ODN uptake in survival cells by propidium iodide (PI) exclusion method for hyperthermia / Chapter 4.6) --- Discussion / Chapter Chapter 5: --- The antiproliferative effects of antisense molecules against Glut-1 and 5 on MCF- 7 cells transfected by Lipofectin: --- p.119-146 / Chapter 5.1) --- Introduction / Chapter 5.2) --- The growth curve of MCF-7 cells / Chapter 5.3) --- The calibration of MTT assay / Chapter 5.4) --- The effect of antisense Glut-1 concentration without Lipofectin on MCF-7 cells / Chapter 5.5) --- The effect of antisense Glut-1 concentration with Lipofectin on MCF-7 cells / Chapter 5.6) --- The effect of antisense Glut-5 concentration without Lipofectin on MCF-7 cells / Chapter 5.7) --- The effect of antisense Glut-5 concentration with Lipofectin on MCF-7cells / Chapter 5.8) --- The effect of transfection time of antisense Glut-1 on MCF-7 cells / Chapter 5.9) --- The effect of transfection time of antisense Glut-5 on MCF-7 cells / Chapter 5.10) --- The effect of transfection time of antisense Glut-5 for higher concentration on MCF-7 cells / Chapter 5.11) --- The effect of antisense Glut-1 to Lipofectin (w/w) ratio on MCF-7 cells / Chapter 5.12) --- The effect of antisense Glut-1 to Lipofection (w/w) ratio for higher transfection time on MCF-7 cells / Chapter 5.13) --- The effect of antisense Glut-5 to Lipofectin (w/w) ratio on MCF-7 cells / Chapter 5.14) --- Discussion / Chapter Chapter 6: --- Combined treatments: --- p.147-162 / Chapter 6.1) --- Introduction / Chapter 6.2) --- The effect of combined treatment of antisense Glut-1 combined with antisense Glut-5 on MCF-7 cells / Chapter 6.3) --- The chronic effect of hyperthermia for 5 hours on MCF-7 cells / Chapter 6.4) --- The effect of combined treatment between antisense Glut-1 and hyperthermia on MCF-7 cells / Chapter 6.5) --- The net effect of antisense Glut-1 in combined treatment between hyperthermia and antisense Glut-1 on MCF-7 cells / Chapter 6.6) --- The effect of combined treatment between antisense Glut-5 and hyperthermia on MCF-7 cells / Chapter 6.7) --- The net effect of antisense Glut-5 in combined treatment between hyperthermia and antisense Glut-5 on MCF-7 cells / Chapter 6.8) --- Discussion / Chapter Chapter 7: --- Discussion: --- p.163-173 / Chapter Chapter 8: --- References: --- p.174-181

Chan Chung Sing. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2002. / Includes bibliographical references (leaves 93-101). / Abstracts in English and Chinese. / Acknowledgement --- p.i / Abstract --- p.ix / List of Abbreviations --- p.xvii / Chapter CHATPER ONE --- INTRODUCTION / Chapter 1.1 --- Glucose Homeostasis --- p.1 / Chapter 1.1.1 --- Function --- p.1 / Chapter 1.1.2 --- Origins and regulation of glucose --- p.2 / Chapter 1.1.3 --- Glucoregulatory factors --- p.4 / Chapter 1.1.4 --- Insulin --- p.6 / Chapter 1.1.4.1 --- Function of Insulin --- p.7 / Chapter 1.1.4.2 --- Discovery and Production of Insulin --- p.7 / Chapter 1.1.4.3 --- Insulin Signaling Pathway --- p.8 / Chapter 1.1.4.3.1 --- Insulin Receptor --- p.8 / Chapter 1.1.4.3.2 --- MAPK Pathway --- p.9 / Chapter 1.1.4.3.3 --- Phosphatidylinositol 3-kinase (PI3-K) Pathway --- p.10 / Chapter 1.1.5 --- Glucose Transporters --- p.11 / Chapter 1.1.6 --- Role of skeletal muscle in glucose homeostasis --- p.13 / Chapter 1.1.7 --- Insulin Resistance --- p.14 / Chapter 1.1.8 --- Glucose abnormality and its complications --- p.16 / Chapter 1.2 --- Actin --- p.19 / Chapter 1.2.1 --- Function of Actin --- p.20 / Chapter 1.2.2 --- Actin Accessory Protein --- p.22 / Chapter 1.2.3 --- Actin Polymerization --- p.23 / Chapter 1.3 --- "Interaction between Insulin, GLUT4 and Actin in Glucose Homeostasis" --- p.24 / Chapter 1.3.1 --- Insulin-Induced Actin Remodeling --- p.25 / Chapter 1.3.2 --- Actin Remodeling and Insulin-Induced GLUT4 Translocation --- p.26 / Chapter 1.3.3 --- Involvement of Insulin Signaling Molecules in Actin Remodeling --- p.27 / Chapter 1.3.4 --- Actin Remodeling and Insulin Resistance --- p.30 / Chapter 1.4 --- Hypothesis and Objective --- p.30 / Chapter 1.4.1 --- Rationale --- p.30 / Chapter 1.4.2 --- Hypothesis --- p.31 / Chapter 1.4.3 --- Objective --- p.31 / Chapter CHAPTER TWO --- MATERIALS AND METHODS / Chapter 2.1 --- Materials --- p.33 / Chapter 2.2 --- Cell Culture --- p.36 / Chapter 2.2.1 --- Cell Culture --- p.36 / Chapter 2.2.2 --- Reagents Preparation and Incubation --- p.39 / Chapter 2.3 --- 2-Deoxyglucose Uptake --- p.39 / Chapter 2.4 --- Immunofluorescence Microscopy --- p.41 / Chapter 2.4.1 --- Permeabilized cell staining --- p.41 / Chapter 2.4.2 --- Membrane-intact cell staining --- p.43 / Chapter 2.4.3 --- The analysis of actin remodeling reduction --- p.44 / Chapter 2.5 --- Live Image Microscopy --- p.44 / Chapter 2.6 --- Transmission Electron Microscope Study --- p.44 / Chapter 2.7 --- Statistical Analysis --- p.46 / Chapter CHAPTER THREE --- RESULTS / Chapter 3.1 --- Cell Growth --- p.48 / Chapter 3.2 --- Acute Effect of Insulin on L6 myotubes --- p.48 / Chapter 3.2.1 --- Immunofluorescence Microscopy --- p.49 / Chapter 3.2.1.1 --- The time profile of insulin on actin cytoskeletonin permeabilized L6 myotubes --- p.49 / Chapter 3.2.1.2 --- The concentration effect of insulin on actin cytoskeletonin permeabilized L6 myotubes --- p.50 / Chapter 3.2.1.3 --- Relationship between actin cytoskeleton and GLUT4mycin permeabilized L6 myotubes --- p.51 / Chapter 3.2.1.4 --- Translocation of GLUT4myc in membrane-intact L6 myotubes --- p.51 / Chapter 3.2.1.5 --- "Effect of methyl-β-cyclodextrins, MeOH or EtOHin permeabilized and membrane-intact L6 myotubes" --- p.52 / Chapter 3.2.2 --- 2-Deoxyglucose Uptake --- p.52 / Chapter 3.2.2.1 --- "Effects of insulin, methyl-β-cyclodextrins, MeOH and EtOH in L6 myotubes" --- p.52 / Chapter 3.2.3 --- TEM Study --- p.53 / Chapter 3.2.3.1 --- Effects of insulin on actin cytoskeleton and GLUT4myc in L6 myotubes --- p.53 / Chapter 3.3 --- Effect of high glucose and high insulin incubation in L6 myotubes --- p.54 / Chapter 3.3.1 --- Immunofluorescence Microscopy --- p.54 / Chapter 3.3.1.1 --- High insulin and high glucose preincubation in permeabilized L6 myotubes --- p.55 / Chapter 3.3.1.2 --- Effect of high insulin and high glucose incubationin membrane-intact L6 myotubes --- p.55 / Chapter 3.3.2 --- 2-Deoxyglucose Uptake --- p.56 / Chapter 3.3.2.1 --- Effect of high insulin and high glucose incubation in L6 myotubes --- p.56 / Chapter 3.3.3 --- TEM Study --- p.57 / Chapter 3.3.3.1 --- Effect of high insulin and high glucose incubation in L6 myotubes --- p.57 / Chapter 3.4 --- Effect of FFA incubation in L6 myotubes --- p.58 / Chapter 3.4.1 --- Immunofluorescence Microscopy --- p.58 / Chapter 3.4.1.1 --- FFA preincubation in permeabilized L6 myotubes --- p.58 / Chapter 3.4.1.2 --- FFA incubation in membrane-intact L6 myotubes --- p.59 / Chapter 3.4.2 --- 2-Deoxyglucose Uptake --- p.59 / Chapter 3.4.2.1 --- FFA incubation in L6 myotubes (24 hours) --- p.60 / Chapter 3.4.3 --- TEM Study --- p.62 / Chapter 3.4.3.1 --- FFA incubation in L6 myotubes --- p.62 / Chapter 3.5 --- Effect of CHO incubation in L6 myotubes --- p.62 / Chapter 3.5.1 --- Immunofluorescence Microscopy --- p.62 / Chapter 3.5.1.1 --- CHO preincubation in permeabilized L6 myotubes --- p.63 / Chapter 3.5.1.2 --- CHO incubation in membrane-intact L6 myotubes --- p.63 / Chapter 3.5.2 --- 2-Deoxyglucose Uptake --- p.64 / Chapter 3.5.2.1 --- CHO incubation in L6 myotubes (24 hours) --- p.64 / Chapter 3.5.3 --- TEM Study --- p.65 / Chapter 3.5.3.1 --- CHO incubation in L6 myotubes --- p.65 / Chapter 3.6 --- Overall changes in glucose uptake after preincubation experiment --- p.65 / Chapter CHAPTER FOUR --- DISCUSSION / Chapter 4.1 --- Effect of insulin on L6 myotubes --- p.69 / Chapter 4.2 --- "Effect of methyl-β-cyclodextrins, MeOH and EtOH on L6 myotube" --- p.75 / Chapter 4.3 --- Effect of pretreatment of cells in conditions of insulin resistance --- p.76 / Chapter 4.3.1 --- Effect of high glucose and high insulin preincubation on L6 myotubes --- p.76 / Chapter 4.3.2 --- Effect of FFA preincubation on L6 myotubes --- p.78 / Chapter 4.3.3 --- Effect of CHO preincubation on L6 myotubes --- p.82 / Chapter 4.3.4 --- Effect of cell preincubation in conditions of insulin resistance on L6 myotubes (TEM) --- p.83 / Chapter 4.4 --- Summary of the effects of cell preincubation in conditions of insulin resistance --- p.84 / Chapter 4.5 --- Possible mechanisms involved in insulin resistance induction --- p.86 / Chapter 4.5.1 --- Possible changes in GLUT expression and activities --- p.87 / Chapter 4.5.2 --- Possible changes in insulin signaling propagation --- p.88 / Chapter 4.5.3 --- Altered functioning of various actin accessory proteins --- p.89 / Chapter 4.6 --- Limitation of the study --- p.90 / Chapter 4.7 --- Conclusion --- p.90 / Chapter 4.8 --- Future study --- p.91 / REFERENCES --- p.93 / TABLES

by Au Kwong Keung. / Thesis (Ph.D.)--chinese University of Hong Kong, 1998. / Includes bibliographical references (p. 212-227). / 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.

Kwan Pui-Chun. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2003. / Includes bibliographical references (leaves 140-155). / Abstracts in English and Chinese. / Chapter Chapter 1 --- Introduction / Chapter 1.1 --- Overview --- p.1 / Chapter 1.2 --- Iron homeostasis --- p.5 / Chapter 1.3 --- Natural Resistance Associated Marcophage Protein (Nramp) Family --- p.15 / Chapter 1.4 --- Divalent Metal Transporter 1 (DMT1) --- p.18 / Chapter 1.5 --- Iron Responsive Element (IRE) and Iron Regulatory Protein (IRP) --- p.23 / Chapter 1.6 --- Expression and localization of DMT-1 in human --- p.27 / Chapter 1.7 --- Iron and the developing feus --- p.31 / Chapter 1.8 --- Objectives of the study --- p.36 / Chapter Chapter 2 --- Materials and Method / Chapter 2.1 --- Study population --- p.37 / Chapter 2.2 --- Procedure of surgical termination of pregnancy --- p.38 / Chapter 2.3 --- Tissues collection and preparation --- p.39 / Chapter 2.4 --- Semi-quantitative Reverse Transcription-Polymerase Chain Reaction --- p.44 / Chapter 2.5 --- Immunohistochemistry --- p.49 / Chapter 2.6 --- Statistical analysis --- p.55 / Chapter Chapter 3 --- Results / Chapter 3.1 --- Description of subjects --- p.56 / Chapter 3.2 --- Existence of human DMT-1 isoforms at early pregnancy --- p.58 / Chapter 3.3 --- Relative expression of DMT-1 isoforms to β -actin mRNA expression at different week gestation --- p.67 / Chapter 3.4 --- Cellular localization of DMT-1 isoforms at early pregnancy --- p.91 / Chapter 3.5 --- Relative expression of DMT-1 proteins at early pregnancy --- p.101 / Chapter Chapter 4 --- Discussion / Chapter 4.1 --- Existence of DMT-1 at early pregnancy --- p.116 / Chapter 4.2 --- Expression of DMT-1 isoforms at early pregnancy at gene level --- p.118 / Chapter 4.3 --- Expression of DMT-1 isoforms at early pregnancy at protein level --- p.120 / Chapter 4.4 --- "Comparison expression of DMT-1 between human fetus, human adult and animal studies" --- p.121 / Chapter 4.5 --- Functional importance of DMT-1 at developing fetus at early pregnancy --- p.130 / Chapter 4.6 --- Conclusion --- p.138 / Chapter 4.7 --- Further study --- p.139 / Chapter Chapter 5 --- Reference --- p.140 / Appendix I: Calculation of EM --- p.156

The causes of autism spectrum disorder (ASD) are not all known, but it is suspected that the serotonin transporter (SERT) plays an important role for some subjects with ASD. Mutations in the SLC6A4 gene, that encodes SERT, including the Ala56 mutation (Gly56Ala), have been found in some autism patients. This mutation makes the transporter more active and reduces the probability of serotonergic neurotransmission in the brain, which is linked to behavioral changes that are associated with core domain deficits of ASD 1. Depression also has been linked to decreases in the availability of serotonin (5-hydroxytryptamine; 5-HT) in the central nervous system (CNS), and is associated with reduced hippocampal neurogenesis. Selective serotonin reuptake inhibitors (SSRIs), drugs used to block SERTs, are used to treat depression and/or anxiety by inhibiting SERT to increase synaptic 5-HT levels. / Includes bibliography. / Thesis (M.S.)--Florida Atlantic University, 2019. / FAU Electronic Theses and Dissertations Collection

Thesis (Ph. D.)--Case Western Reserve University, 2004. / [School of Medicine] Department of Pathology. Includes bibliographical references. Available online via OhioLINK's ETD Center.

Thesis (Ph. D.)--University of Missouri--Columbia, 2003. / "May 2003." Typescript. Vita. Includes bibliographical references (leaves 102-113).