• Refine Query
  • Source
  • Publication year
  • to
  • Language
  • 162
  • 46
  • 32
  • 31
  • 22
  • 5
  • 3
  • 3
  • 2
  • 2
  • 1
  • 1
  • 1
  • 1
  • 1
  • Tagged with
  • 352
  • 101
  • 98
  • 87
  • 53
  • 51
  • 47
  • 46
  • 41
  • 39
  • 30
  • 29
  • 26
  • 25
  • 24
  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
1

Effects of novel microenvironments and factors on hematopoiesis. / Effects of novel microenvironments & factors on hematopoiesis

January 2005 (has links)
Ng Yuen Wah. / Thesis (M.Phil.)--Chinese University of Hong Kong, 2005. / Includes bibliographical references (leaves 118-144). / Abstracts in English and Chinese. / Abstract (English) --- p.ii / (Chinese) --- p.vii / Acknowledgements --- p.x / Publications --- p.xii / Abbreviations --- p.xiv / List of Tables --- p.xix / List of Figures --- p.xx / Table of Contents --- p.xxii / Chapter CHAPTER ONE: --- Introduction --- p.1 / Chapter 1.1 --- Ex Vivo Expansion of Cord Blood CD34+ Cells --- p.1 / Chapter 1.1.1 --- Hematopoiesis --- p.1 / Chapter 1.1.2 --- Hematopoietic Stem Cells --- p.2 / Chapter 1.1.2.1 --- Properties --- p.2 / Chapter 1.1.2.2 --- Functions and Sources of Hematopoietic Stem Cells --- p.3 / Chapter 1.1.2.3 --- Umbilical Cord blood Transplantation --- p.4 / Chapter 1.1.3 --- Ex Vivo Expansion of Hematopoietic Stem Cells --- p.5 / Chapter 1.1.3.1 --- The Need for Ex Vivo Expansion --- p.5 / Chapter 1.1.3.2 --- Ex Vivo Expansion for Clinical Transplantation --- p.6 / Chapter 1.1.3.3 --- Factors Promoting Ex Vivo Expansion of Hematopoietic Stem Cells --- p.7 / Chapter 1.1.3.3.1 --- Cytokines --- p.7 / Chapter 1.1.3.3.2 --- Stromal Feeder Support of Hematopoiesis --- p.9 / Chapter 1.1.3.3.3 --- Regulation of Self-Renewal --- p.11 / Chapter 1.1.4 --- Hematopoiesis and Neurogenesis --- p.12 / Chapter 1.1.4.1 --- Possible Crosstalks --- p.12 / Chapter 1.1.4.2 --- Neurotrophic Factors --- p.13 / Chapter 1.1.4.2.1 --- Brain-Derived Neurotrophic Factor --- p.13 / Chapter 1.1.4.2.2 --- Neurotrophin-3 --- p.14 / Chapter 1.2 --- Embryonic Stem Cells --- p.15 / Chapter 1.2.1 --- Embryonic Stem Cells and Potential Applications --- p.15 / Chapter 1.2.2 --- Maintenance of Undifferentiated State --- p.17 / Chapter 1.2.2.1 --- Mouse Embryonic Stem Cells --- p.17 / Chapter 1.2.2.2 --- Human Embryonic Stem Cells --- p.19 / Chapter 1.2.2.3 --- Embryonic Stem Cell-Specific Markers --- p.20 / Chapter 1.2.3 --- Controlled Differentiation of Embryonic Stem Cells to Hematopoietic Lineages --- p.21 / Chapter 1.2.3.1 --- Formation of Embryoid Body --- p.21 / Chapter 1.2.3.2 --- Hematopoietic Development in Embryoid Body --- p.22 / Chapter 1.2.3.3 --- Factors Promoting Hematopoietic Differentiation --- p.23 / Chapter 1.2.3.3.1 --- Cytokines --- p.23 / Chapter 1.1.3.3.2 --- Stromal Cells --- p.24 / Chapter 1.2.3.3.3 --- Mechanism of Hematopoietic Differentiation --- p.25 / Chapter 1.2.3.4 --- Potential Applications of Embryonic Stem Cells-Derived Hematopoietic Cells --- p.26 / Chapter 1.2.3.5 --- Culture Methods --- p.26 / Chapter 1.2.4 --- Issues Concerning Clinical Applications of Embryonic Stem Cells --- p.28 / Chapter 1.2.4.1 --- Teratoma Formation --- p.28 / Chapter 1.2.4.2 --- Contamination by Mouse Cells --- p.29 / Chapter 1.2.4.3 --- Ethical Issues --- p.29 / Chapter CHAPTER TWO: --- Objectives --- p.31 / Chapter CHAPTER THREE: --- Materials and Methods --- p.33 / Chapter 3.1 --- Ex Vivo Expansion of Cord Blood CD34+ Cells --- p.33 / Chapter 3.1.1 --- Collection of Human Umbilical Cord Blood --- p.33 / Chapter 3.1.2 --- Enrichment of Cord Blood CD34+ Cells --- p.33 / Chapter 3.1.3 --- Ex Vivo Expansion of CD34+ Cells --- p.36 / Chapter 3.1.3.1 --- Establishment of Two Stromal Cell Feeder Layers --- p.36 / Chapter 3.1.3.1.1 --- Primary Mouse AGM Stromal Cells --- p.36 / Chapter 3.1.3.1.2 --- Mouse C17.2 Neural Stem Cell Line --- p.37 / Chapter 3.1.3.2 --- Cryopreservation and Thawing of Stromal Cells --- p.37 / Chapter 3.1.3.3 --- Characterization of AGM --- p.38 / Chapter 3.1.3.4 --- Coculture of Cord Blood CD34+ Cells and Stromal Cells --- p.39 / Chapter 3.1.3.4.1 --- Preparation of Stromal Cells --- p.39 / Chapter 3.1.3.4.2 --- Contact Cocultures of CD34+ Cells and Stromal Cells --- p.39 / Chapter 3.1.3.4.3 --- Effects of Neurotrophic Growth Factors on Ex Vivo Expansion of Enriched CD34+ Cells --- p.40 / Chapter 3.1.4 --- Flow Cytometry Analysis of Human Cell Surface Markers --- p.41 / Chapter 3.1.5 --- Human Progenitor Colony-Forming Unit Assays --- p.42 / Chapter 3.1.6 --- Detection of mRNA Expressions of Hematopoietic and Neurotrophic Growth Factors in Mouse AGM and C17.2 Cells --- p.45 / Chapter 3.1.6.1 --- Cell Culture and Extraction of Total Cellular Ribonucleic Acid (RNA) --- p.45 / Chapter 3.1.6.2 --- Reverse Transcriptase -Polymerase Chain Reaction (RT-PCR) --- p.47 / Chapter 3.1.6.3 --- Gel Electrophoresis and Alkaline Transfer of RT-PCR Products and Southern Blot Analysis and Detection --- p.48 / Chapter 3.1.7 --- Detection of mRNA Expressions of Receptors of Neurotrophic Factors in Enriched CD34+and Expanded Progenitor Cells --- p.51 / Chapter 3.1.7.1 --- Culture of CD34+ Cells --- p.51 / Chapter 3.1.7.2 --- "Extraction of Total Cellular RNA, RT-PCR and Gel Electrophoresis" --- p.51 / Chapter 3.1.7.3 --- DNA Sequencing --- p.52 / Chapter 3.1.8 --- Statistical Analysis --- p.53 / Chapter 3.2 --- In Vitro Differentiation of Mouse Embryonic Stem Cells to Hematopoietic Stem Cells --- p.53 / Chapter 3.2.1 --- Maintenance of Mouse Embryonic Stem Cell --- p.53 / Chapter 3.2.1.1 --- Preparation of Mouse Embryonic Fibroblast Stromal Layer --- p.53 / Chapter 3.2.1.2 --- Culture of Embryonic Stem Cells --- p.55 / Chapter 3.2.2 --- Two-Step In Vitro Differentiation of Embryonic Stem Cells --- p.56 / Chapter 3.2.2.1 --- Collection of Stromal Cells - Conditioned Medium --- p.56 / Chapter 3.2.2.1.1 --- Establishment of Two Stromal Cell Feeder Layers --- p.56 / Chapter 3.2.2.1.2 --- Collection of Conditioned Medium --- p.56 / Chapter 3.2.2.2 --- Primary Differentiation of Embryonic Stem Cell into Embryoid Body --- p.57 / Chapter 3.2.2.2.1 --- Methylcellulose-Based Culture --- p.57 / Chapter 3.2.2.2.2 --- Conditioned Medium-Based Culture --- p.58 / Chapter 3.2.2.3 --- Detection of Hematopoietic Progenitors --- p.59 / Chapter 3.2.3 --- Detection of Embryonic Stem Cell Surface Marker --- p.60 / Chapter CHAPTER FOUR: --- Effects of Novel Microenvironments on the Ex Vivo Expansion of Cord Blood CD34+ Cells --- p.65 / Chapter 4.1 --- Characterization of Primary AGM Stromal Cells --- p.65 / Chapter 4.2 --- Effects of Two Mouse Stromal Cells on Ex Vivo Expansion of CD34+ Cells --- p.65 / Chapter 4.2.1 --- Effects of Primary AGM Cells --- p.66 / Chapter 4.2.2 --- Effects of Neonatal Neural Stem Cell line C17.2 Stromal Cells --- p.66 / Chapter 4.3 --- Expressions of Growth Factors in AGM and C17.2 Cells --- p.67 / Chapter 4.4 --- Effects of Two Neurotrophic Factors on the Clonogenicity of Hematopoietic Progenitor Cells --- p.67 / Chapter 4.4.1 --- Effects of Brain-Derived Neurotrophic Factor --- p.68 / Chapter 4.4.2 --- Effects of Neurotrophin-3 --- p.68 / Chapter 4.5 --- Effects of Two Neurotrophic Factors on the Ex Vivo Expansion of CD34+ Cells --- p.69 / Chapter 4.5.1 --- Effects of Brain-Derived Neurotrophic Factor --- p.69 / Chapter 4.5.2 --- Effects of Neurotrophin-3 --- p.70 / Chapter 4.6 --- Expressions of Receptors of Neurotrophic Factors in Enriched CD34+ Cells and Expanded Progenitor Cells --- p.71 / Chapter 4.6.1 --- mRNA Expressions of BDNF-R(Trk B) and NT-3-R (Trk C) --- p.71 / Chapter 4.6.2 --- DNA Sequencing --- p.72 / Chapter 4.7 --- Discussion --- p.73 / Chapter CHAPTER FIVE: --- Maintenance of Mouse Embryonic Stem Cells and Differentiation to Hematopoietic Lineage in the Presence of AGM and C17.2 Conditioned Media --- p.98 / Chapter 5.1 --- Maintenance of Embryonic Stem Cells --- p.98 / Chapter 5.2 --- Primary (Embryoid Body Formation) and Hematopoietic Differentiation of Embryonic Stem Cells --- p.99 / Chapter 5.2.1 --- Methylcellulose-Based Culture --- p.99 / Chapter 5.2.2 --- Conditioned Medium-Based Culture --- p.100 / Chapter 5.3 --- Discussion --- p.101 / Chapter CHAPTER SIX: --- General Discussion and Conclusion --- p.115 / References
2

Factors for hematopoiesis in dogs on milk diets

Frost, Douglas Van Anden, January 1940 (has links)
Thesis (Ph. D.)--University of Wisconsin--Madison, 1940. / Typescript. Includes abstract and vita. Includes (as Parts I. and II.) two reprints from Journal of nutrition: Iron utilization in dogs on milk diets / Douglas V. Frost, Conrad A. Elvehjem and Edwin B. Hart. Vol. 19, no. 4 (Apr. 1940), p. 311-320 -- Iron and copper versus liver in treatment of hemorrhagic anemia in dogs on milk diets / D.V. Frost, V.R. Potter, C.A. Elvehjem and E.B. Hart. Vol. 19, no. 2 (Feb. 1940), p. 207-211. Includes bibliographical references.
3

Cell type-specific Runx1 enhancer-reporter mouse lines to study hemogenic endothelium

Rode, Christina January 2016 (has links)
Hematopoietic stem cells emerge from a specialized subset of endothelial cells in the midgestation mouse aorta. This subset, the so-called hemogenic endothelium (HE), undergoes a morphological and molecular change to a hematopoietic cell type, as part of the endothelial-to- hematopoietic transition (EHT). Previously, lack of specific markers prevented mechanistic studies of HE, as well as studies into its developmental origin. Runx1 is a critical regulator of developmental hematopoiesis and is expressed in all cell intermediates of EHT. Identification of the Runx1 +23 enhancer led to the development of enhancer-reporter tools in order to isolate HE for further analysis. Here, I investigated the cell-type specific activity of another Runx1 enhancer, located 204 kb downstream of the ATG in exon 1. I generated a novel enhancer-reporter mouse line (204GFP) and determined the expression pattern and lineage potential of 204GFP+ cells. It was established that the +204 enhancer marks all HE and part of the HSCs. Hematopoietic progenitor cells, in contrast, were not marked by the 204GFP transgene. Interestingly, the 204GFP reporter also marks part of the Runx1- expressing sub-aortic mesenchyme. To test whether the 204GFP reporter could enrich for HE when combined with a Runx1 +23 enhancer-reporter transgene, I generated and characterized a 23Cherry transgenic mouse line. Expression analysis of aortic endothelial cells marked by both the 204GFP and 23Cherry transgenes using the Fluidigm platform indicated an enrichment of cells with a HE expression signature. This enrichment will facilitate further analysis of the molecular networks active in HE using whole genome expression profiling. The Runx1 enhancer-reporter models are also valuable tools to track the developmental origin of HE, which remains to be established in the mouse embryo. To this end, I mapped the precise spatio-temporal expression pattern of the 23GFP transgene in pre- somitic embryos and established lineage tracing experiments. This provides the basis to revisit fate mapping of the primitive streak to determine the origin(s) of the HE lineage.
4

Genetic investigations of human hemopoiesis : studies of clonality and gene transfer to hemopoietic progenitors

Hogge, Donna Eileen January 1987 (has links)
In most neoplasms malignant change occurs in a single cell which then proliferates. My purpose was to explore methods to study the cell that gives rise to hemopoietic cancer and to investigate the abnormalities at a molecular level. Cytogenetic analysis of cells from individual hemopoietic colonies revealed that monosomy 7 syndrome, a hematologic disorder of childhood, arises in a primitive cell capable of differentiating down both myeloid and erythroid pathways. Long-term bone marrow cultures (LTC) from patients with chronic myelogenous leukemia (CML) favor the growth of Philadelphia chromosome (Ph) negative progenitors which, although cytogenetically normal, could have been part of the malignant clone at a stage prior to the development of the Ph. LTC's were initiated with cells from 2 women with CML who were heterozygous for 2 electrophoretically distinct glucose-6-phosphate dehydrogenase (G6PD) enzyme variants. In one patient, 2/11 progenitors were Ph-negative after 4 to 6 weeks in LTC and 4/30 were nonclonal by G6PD enzyme analysis, i.e. the colonies expressed the enzyme not found in the malignant clone. In this case, karyotypically normal cells were truly normal. Next, gene transfer to human hemopoietic cells was demonstrated using recombinant retrovirus carrying the selectable marker gene, neor. With the K562 human leukemic cell line as targets up to 60% of infected cells became G418 resistant (G418r). Cloned populations of G418r cells showed unique patterns of retroviral integration in K562 DNA. When the target cells were progenitors from normal marrow, CML blood or fetal liver, the highest frequencies of G418r granulocyte-macrophage or large erythroid colonies was 16% and 5% respectively. Experiments infecting bone marrow cells in LTC with neor virus produced up to 2% G418r colonies after as long as 3 weeks in culture. Using v-src virus to infect LTC failed to perturb hemopoiesis, although infection of bone marrow-derived cells in these cultures was documented. In summary: 1. Unique populations of hemopoietic progenitors can be identified in culture using several genetic markers including chromosomes, G6PD analysis or gene transfer. 2. The feasibility of retroviral-mediated gene transfer for use on human hemopoietic cells has been demonstrated. / Medicine, Faculty of / Pathology and Laboratory Medicine, Department of / Graduate
5

The JAK/STAT pathway in Drosophila hematopoiesis function and regulatory mechanisms /

Shen, Ying. January 2007 (has links)
Thesis (Ph.D.)--Ohio University, November, 2007. / Title from PDF t.p. Includes bibliographical references.
6

Hematotoxicity of heptachlor

Dodson, Sarah Vanessa Meads. January 2004 (has links)
Thesis (Ph. D.)--West Virginia University, 2004. / Title from document title page. Document formatted into pages; contains xi, 196 p. : ill. (some col.). Vita. Includes abstract. Includes bibliographical references.
7

Understanding human mononuclear phagocyte ontogeny using human induced pluripotent stem cells (iPSCs)

Buchrieser, Julian January 2016 (has links)
Tissue-resident macrophages (MΦ) such as microglia, Kupffer and Langerhans cells derive from Myb-independent yolk sac (YS) progenitors generated before the emergence of hematopoietic stem cells (HSCs). Myb-independent YS-derived resident MΦ self-renew locally, independently of circulating adult monocytes and HSCs. In contrast, adult blood monocytes as well as infiltrating, gut and dermal MΦ derive from Myb-dependent HSCs and are less proliferative. These findings are derived from the mouse, using gene knock-outs and lineage tracing, but their applicability to human development has not been formally demonstrated. Here I use a human pluripotent stem cell (hPSC) differentiation model of hematopoiesis, capable of monocyte/MΦ production over prolonged periods of time, as a tool to investigate human mononuclear phagocyte ontogeny. Using a transcriptomic approach I showed that hiPSC-derived monocytes/MΦ (iPS-Mo/MΦ) produced early in differentiation (first weeks) are more proliferative and less immunologically mature than iPS-Mo/MΦ produced at a later time point. I therefore hypothesised either that iPS-Mo/MΦ only become fully mature after several weeks of differentiation or that there are two developmentally distinct waves of MΦ produced over time. By comparing the transcription profile of iPS-Mo/MΦs to that of primary adult blood monocytes and fetal microglia I then showed that early and late iPS-Mo/MΦs were transcriptionally closer to fetal microglia than to adult blood monocytes. To further investigate if iPS-Mo/MΦs are indeed of the same developmental origin as MYB-independent MΦ such as microglia, I used a CRISPR-Cas9 knock-out strategy to show for the first time, that human iPS-Mo/MΦs develop in a MYB-independent, RUNX1 and SPI1 (PU.1)-dependent fashion. This result makes human iPS-Mo/MΦs developmentally related to, and a good model for, MYB-independent tissue-resident \Macros such as alveolar and kidney MΦs, microglia, Kupffer and Langerhans cells. Interestingly, while MYB was not required for the generation of iPS-Mo/MΦs, its knock-out resulted in an increase in iPS-Mo/MΦ production. To investigate this increase I developed two methods for quantifying the differentiation bottleneck occurring during hiPSC differentiation to iPS-Mo/MΦs. Those techniques highlighted a potential increase in progenitor cell generation in MYB KO cells and thus lay foundation to improve our technical understanding of EB differentiation and will enable enhanced manipulation of the EB model.
8

Studies of histone demethylase JARID1B in hematopoiesis and leukemogenesis

Zhang, Jingxuan, 張璟璇 January 2014 (has links)
Post-translational modifications of histone proteins serve as one of the key epigenetic regulatory mechanisms in the development of organisms. It is well-known that methylation on histone lysine residues is an important epigenetic modification for the transcriptional regulation of normal hematopoiesis and leukemogenesis. JARID1B, a member of the JARID1 histone H3 lysine 4 (H3K4) demethylases, was found essential for the self-renewal of both embryonic stem cell and melanoma stem-like cell, and was involved in regulating genes, such as Egr1, Bmi-1 and p27, during embryo development. In addition, JARID1B is involved in the differentiation of neural cells and macrophages. Although JARID1B is believed to have important functions in stem cell biology, its role in hematopoiesis and leukemogenesis has not been systematically studied. We therefore examined the expression profile of JARID1B in different hematopoietic lineage cells. We observed an up-regulation of JARID1B in differentiated hematopoietic cells by comparing with hematopoietic stem cells and progenitor cells, suggesting that the enhanced cellular level of JARID1B is associated with hematopoietic lineage commitment. Interestingly, JARID1B expression is generally low in human leukemia cell lines and in CML (Chronic Myeloid leukemia) patient samples compared to 〖CD34〗^+ cord blood cells and normal peripheral white blood cells, which indicates the down-regulation of JARID1B is associated with leukemia development. We further modulated the expression of JARID1B in human leukemia cell lines, K562 and SEM, and in mouse hematopoietic stem/progenitor cells (〖Lin〗^-/〖Sca〗^(-1+)/c-〖Kit〗^+, LSK cells). We found that knockdown of Jarid1b in LSK cells did not alter their cell-cycle pattern. However, total colony formation number was reduced in serial re-plating assays, suggesting Jarid1b is required for the maintenance of colony-forming ability and self-renewal property. Knockdown of JARID1B in K562 cells did not change their cell proliferation and cell-cycle pattern, but did consistently inhibit their colony-forming ability during serial re-plating assays. On the other hand, overexpression of JARID1B in K562 and SEM leukemic cells inhibited cell proliferation and colony formation, but with no significant changes on cell-cycle patterns. Furthermore, apoptosis staining did not show any correlations between JARID1B overexpression and apoptosis. Previously, JARID1A, another JARID1 family member, was found as a fusion partner in AML (Acute Myeloid Leukemia); its third PHD domain, which locates at C-terminus, is associated with leukemogenesis. By amino acid sequence alignment, the differences between JARID1A and JARID1B protein are mainly occurred at their C-terminal regions, after the second PHD domain. Therefore, GST fusion protein pull-down experiments for this region was performed. Preliminary results showed that the C-terminus of JARID1B protein interacts with proteins of RNA transcriptional machinery complex. However, further investigation is needed to demonstrate these interactions are directly associated with JARID1B inhibitory effects on gene expression. To conclude, our results suggest that JARID1B plays an essential role in the biology of hematopoietic stem cells and leukemic cells. Investigation on its interacting partners and downstream target genes would lead us a detailed understanding of JARID1B function in hematopoietic cells. / published_or_final_version / Pathology / Doctoral / Doctor of Philosophy
9

Distinctive functions of the polycomb group protein BMI-1 in hematopoiesis and leukemogenesis

Lam, Yuk-man, 林旭文 January 2014 (has links)
abstract / Pathology / Doctoral / Doctor of Philosophy
10

Early molecular events conferring haematopoietic potential to human pluripotent stem cells

Jayasundar, Smruthi January 2013 (has links)
No description available.

Page generated in 0.0422 seconds