by Chan Shuk Chong. / Thesis (M.Phil.)--Chinese University of Hong Kong, 1995. / Includes bibliographical references (leaves 135-142). / Statement --- p.i / Acknowledgment --- p.ii / Abbreviations --- p.iii / Abstract --- p.iv / Chapter Chapter 1: --- General Introduction / Chapter 1.1 --- Haematopoiesis --- p.1 / Chapter 1.1.1 --- Sites of haematopoiesis / Chapter 1.1.1.1 --- Bone marrow stroma / Chapter 1.1.1.2 --- Thymus / Chapter 1.1.1.3 --- Spleen and lymph node / Chapter 1.1.1.3.1 --- Spleen / Chapter 1.1.1.3.2 --- Lymph Nodes / Chapter 1.1.2 --- Blood Cell / Chapter 1.1.2.1 --- Development of T and B cells / Chapter 1.1.2.1.1 --- T cells / Chapter 1.1.2.1.2 --- B cells / Chapter 1.1.2.2 --- Development of Granulocytes and monocytes / Chapter 1.2 --- White Cell Disorder -Leukemia --- p.13 / Chapter 1.2.1 --- Leukemia - general concept / Chapter 1.2.1.1 --- Classification of leukemia / Chapter 1.2.1.2 --- Pathophysiology and Clinical features / Chapter 1.2.1.3 --- Etiology of myeloid leukemia / Chapter 1.2.2 --- Genetic basis of leukemia / Chapter 1.3 --- Acute myeloid leukemia (AML) cell model --- p.19 / Chapter 1.3.1 --- Cell Model for human acute myeloid leukemia / Chapter 1.3.2 --- Murine leukemia cell lines / Chapter 1.4 --- Induction of leukemia cell differentiation --- p.21 / Chapter 1.4.1 --- Overview of different inducers / Chapter 1.4.2 --- Cytokines as Inducers / Chapter 1.5 --- Objectives and Research Strategy --- p.26 / Chapter 1.5.1 --- Objectives / Chapter 1.5.2 --- Research strategy / Chapter Chapter 2 : --- Materials and Methods / Chapter 2.1 --- Materials --- p.29 / Chapter 2.1.1 --- Cell line / Chapter 2.1.2 --- Tissue culture medium / Chapter 2.1.3 --- Tumor necrosis Factor - alpha (TNF-α) / Chapter 2.1.4 --- Interleukin 1- alpha (IL-lα)and Interleukin 1- beta (IL-1β) / Chapter 2.1.5 --- "Monoclonal hamster anti-mouse IL-lα monoclonal hamster anti-mouse IL-1β, and Polyclonal rabbit anti-mouse TNF-α antibodies" / Chapter 2.1.6 --- Lipopolysaccharides (LPS) / Chapter 2.1.7 --- Buffers and solutions / Chapter 2.2 --- Methods : --- p.33 / Chapter 2.2.1 --- Cell culture / Chapter 2.2.2 --- Cytotoxicity assay / Chapter 2.2.3 --- Proliferation assay / Chapter 2.2.4 --- Cell morphology / Chapter 2.2.5 --- Phagocytosis assay / Chapter 2.2.6 --- Preparation of undifferentiated and differentiated murine leukemia WEHI3B (JCS) cells for cell lysate / Chapter 2.2.7 --- Isolation of total cellular RNA / Chapter 2.2.8 --- Extraction of the total RNA / Chapter 2.2.9 --- Spectrophotometry / Chapter 2.2.10 --- Electrophoresis of RNA in agarose gel containing formaldehyde / Chapter 2 2.11 --- First strand cDNA synthesis / Chapter 2.2.12 --- Cytokines phenotyping of the uninduced and induced WEHI 3B (JCS) by The Reverse Trancription Polymerase Chain Reaction method / Chapter 2.2.13 --- Gel electrophoresis of PCR- product / Chapter 2.2.14 --- Southern blot / Chapter 2.2.15 --- Dot blot / Chapter 2.2.16 --- Hybridization with oligonucleotides / Chapter 2.2.17 --- Chemiluminescent detection / Chapter Chapter 3 : --- Growth Inhibitory and Differentiation Effects of Lipopolysaccharides ( LPS ) on WEHI 3B (JCS) cells / Chapter 3.1 --- Introduction --- p.51 / Chapter 3.1.1 --- Chemical structure of LPS / Chapter 3.1.2 --- Biological activity of LPS / Chapter 3.2 --- Results --- p.55 / Chapter 3.2.1 --- Anti-proliferative effects of LPS / Chapter 3.2.2 --- Differentiation inducing effect of LPS on WEHI 3B (JCS) cells / Chapter 3.2.3 --- Phagocytic activity LPS treated WEHI 3B (JCS) cells / Chapter 3.2.4 --- Anti-proliferative effect of TNF-α / Chapter 3.2.5 --- Differentiation inducing effect of TNF-α / Chapter 3.2.6 --- Phagocytic activity of TNF-α treated WEHI3B (JCS) cells / Chapter 3.3 --- Discussion --- p.67 / Chapter 3.4 --- Summary --- p.69 / Chapter Chapter 4 : --- The Cytokine Genes Expression of the TNF-α and LPS Treated WEHI 3B (JCS) cells / Chapter 4.1 --- Introduction --- p.70 / Chapter 4.1.1 --- Differentiation of leukemia cell line / Chapter 4.1.2 --- Study of the cytokine genes expression of WEHI 3B (JCS) cells / Chapter 4.2 --- Results --- p.72 / Chapter 4.2.1 --- Isolation of total RNA from uniduced and induced WEHI 3B (JCS) cells / Chapter 4.2.2 --- The cytokine genes expression during differentiation / Chapter 4.2.2.1 --- "Up-regulation of IL-lα, IL-1β,TNF-α and IFN-γ in both TNF-α induced and LPS induced WEHI 3B (JCS) cells" / Chapter 4.2.2.1.1 --- Southern blot / Chapter 4.2.2.1.2 --- Semi-quantitation of PCR-products by gel electrophoresis and dot-blot hybridization / Chapter 4.2.2.2 --- up-regulation of GM-CSF and G-CSF in LPS induced WEHI 3B (JCS) cells / Chapter 4.3 --- Discussion --- p.92 / Chapter 4.4 --- Summary --- p.95 / Chapter Chapter 5 : --- Growth inhibitory and Differentiation Inducing Effect of IL-l( IL-1α and IL-1β) on WEHI 3B (JCS) cells / Chapter 5.1 --- Introduction --- p.96 / Chapter 5.1.1 --- The interleukin 1 (IL-1) family / Chapter 5.1.1.1 --- Structure of IL-1 / Chapter 5.1.1.2 --- The biological function of IL-1 / Chapter 5.1.2 --- Tumor necrosis factor - alpha ( TNF-α) / Chapter 5.1.2.1 --- Structure of TNF-α / Chapter 5.1.2.2 --- Biological functions of TNF-α / Chapter 5.1.3 --- The similarity between TNF and IL-1 / Chapter 5.2 --- Results --- p.102 / Chapter 5.2.1 --- Anti-proliferative effect of IL-1 / Chapter 5.2.2 --- Differentiation inducing effect of IL-1 / Chapter 5.2.3 --- Phagocytic activity of IL-1 treated JCS cells / Chapter 5.2.4 --- "Role of endogenously produced IL-lα, IL-1β and TNF-α in LPS cytokines differentiation of WEHI 3B (JCS) cells" / Chapter 5.2.4.1. --- "Effect of neutralizing anti- ILl-α,anti - IL-l-β, and anti-TNF-α antibodies on the growth inihbition of the treated WEHI 3B (JCS) cells" / Chapter 5.2.4.2 --- "Effects of neutralizing anti-IL-lα, anti- IL-1β, and anti-TNF-α antibodies on differentiation of the treated WEHI 3B (JCS) cells" / Chapter 5.3 --- Discussion --- p.124 / Chapter 5.4 --- Summary --- p.127 / Chapter Chapter 6 --- : Concluding Discussion --- p.128 / References --- p.135

by Tang Shuk Chun. / "September 1998." / Thesis (Ph.D.)--Chinese University of Hong kong, 1998. / Includes bibliographical references (p. 157-178). / 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.

Bibliography: leaves 154-185 / iv, 185 leaves, [15] leaves of plates : ill. (some col.) ; 30 cm. / Title page, contents and abstract only. The complete thesis in print form is available from the University Library. / Thesis (Ph.D.)--University of Adelaide, Dept. of Science, 1987

Typescript (photocopy)

Graduation date: 1998

Graduation date: 1997

Primary cultures of stromal-vascular (S-V) cells from adipose tissue were used to investigate the regulation of preadipocyte development. Differentiation of S-V cells was found to be under hormonal control. Insulin and glucocorticoids are essential for S-V cell differentiation in culture. S-V cells from both newborn and mature pig adipose tissue and sera from both ages were used to examine the effect of age on preadipocyte development. S-V cells from newborn pigs replicated faster and appeared more responsive to serum borne factors influencing S-V cell growth and development in culture. Serum source (newborn vs mature) did not affect differentiation of S-V cells from newborn or mature pig adipose tissue. When sera from fed or fasted pigs were used to culture newborn pig S-V cells, fasted pig sera stimulated greater differentiation and decreased cell replication as indicated by DNA content of rat S-V cell culture. Lean pig serum compared to obese pig serum, increased differentiation activity in culture of S-V cells an effect which may be influenced by sex. When sera from rat and pig were subjected to gel filtration fractionation on Sephacryl S-200 column, the elution profiles of both sera were similar. Rat serum contained six additional peaks (280 nm) not present in pig serum. Rat serum fraction two (apparent molecular size 67-150 kD) promoted greater differentiation of S-V cells than other rat serum fractions or pig serum fraction two. Fraction three (apparent molecular size 17-43 kD) of both sera inhibited differentiation and lipid filling in cultures of S-V cells but only rat fraction three promoted cell proliferation. Rat and pig S-V cells have different morphology when differentiated. Differentiated rat S-V cells appeared as individual cells when cultured in serum free or serum supplemented medium while differentiated pig S-V cells appeared as individual cells in serum free medium and as a tight cluster of cells in serum supplemented medium. Both cells responded differently to sera obtained from pigs of differing ages and development of rat S-V cells was influenced by anatomic site. / Graduation date: 1992

Thesis (Ph. D.)--University of Texas at Austin, 2001. / Vita. Includes bibliographical references (leaves 109-118). Available also in a digital version from Dissertation Abstracts.

Dishevelled (Dvl) proteins are key transducers of Wnt signaling and are encoded by members of a multi-gene family in vertebrates. We report here divergent, tissue-specific expression patterns for all three Dvl genes in Xenopus embryos, which contrast dramatically with their expression in the mouse. Moreover, we find that the expression patterns of Dvl genes in the chick diverge significantly from those of Xenopus. In addition, in hemichordates, one of the outgroups to chordates, we find that the one Dvl gene is dynamically expressed in a tissue-specific manner. Using knockdowns, we find that Dvl1 and Dvl2 are required for early neural crest specification and for somite segmentation. Most strikingly, we report a novel role for Dvl3 in the maintenance of differentiated muscle and the development of the Xenopus sclerotome. Together, these data demonstrate that that the expression patterns and developmental functions of specific Dvl genes have diverged significantly during chordate evolution. The planar cell polarity (PCP) signaling pathway is essential for embryonic development because it governs diverse cellular behaviors, and the "core PCP" proteins, such as Dishevelled and Frizzled, have been extensively characterized. By contrast, the "PCP effector" proteins, such as Intu and Fuz, remain largely unstudied. These proteins are essential for PCP signaling, but they have never been investigated in a mammal and their cell biological activities remain entirely unknown. We report here that Fuz mutant mice display neural tube defects, polydactyly, and skeletal dysmorphologies that stem from defective ciliogenesis. Using bioinformatics and imaging of an in vivo mucociliary epithelium, we establish a central role for Fuz in membrane trafficking, showing that Fuz is essential for apical trafficking of ciliogenesis factors in ciliated cells and also for exocytosis in secretory cells. We identify a novel, Rab-related small GTPase as an interaction partner for Fuz, and this GTPase also is essential for ciliogenesis and secretion. These results are significant because they provide novel insights into the mechanisms by which developmental regulatory systems like PCP signaling interface with fundamental cellular systems such as the vesicle trafficking machinery. / text

published_or_final_version / Dentistry / Master / Master of Orthodontics