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1
Pat, Sze Wa. „Cell metabolism in cell death and cell growth“. HKBU Institutional Repository, 2007. http://repository.hkbu.edu.hk/etd_ra/775.
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2
Stocking, Carol E. „Autonomous growth of haematopoietic cells“. Thesis, Brunel University, 1989. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.290956.
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3
Greene, Elizabeth Ann 1964. „The effects of growth factors on bovine satellite cells“. Thesis, The University of Arizona, 1989. http://hdl.handle.net/10150/277202.
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This study examined the effects of basic fibroblast growth factor (bFGF), insulin-like growth factor I (IGF-I) and transforming growth factor beta (TGF-β) on the proliferation and differentiation of bovine satellite cells (BSC) in vitro. Cells were treated with serum-free defined media containing varying concentrations of bFGF, IGF-I and TGF-β. On day 3 of treatment total cell nuclei and myotube nuclei were determined. bFGF stimulated BSC proliferation in a dose-dependent fashion with half-maximal stimulation observed at a concentration of 5 ng/ml (p < .05). Similar results were found for IGF-I and TGF-β in the presence of FGF, with half-maximal stimulation observed at 5 ng/ml and 1 ng/ml, respectively. With regard to differentiation, TGF-beta inhibited myotube formation at concentrations above 0.05 ng/ml. IGF-I stimulated myotube formation at concentrations as low as 10 ng/ml (p < .05). These results demonstrate that proliferation and differentiation of BSC in vitro are affected by growth factors, and consequently, similar effects may be found in vivo. This information may prove to be useful in future methods of manipulating muscle growth in vivo.
4
Li, Jing. „Effects of intrinsic & extrinsic factors on the growth and differentiation of human mesenchymal stem cells“. View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36434450.
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5
Hou, Yuen-chi Denise, und 侯元琪. „A comparative study on the effects of feeder cells on culture of human embryonic stem cells“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2009. http://hdl.handle.net/10722/210317.
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6
McGuiness, Lindsay. „Transgenes targeted to growth hormone cells“. Thesis, University College London (University of London), 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405167.
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7
Anilkumar, Thapasimuthu Vijayamma. „The pathobiology of hepatic stem cells (oval cells)“. Thesis, Imperial College London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.244072.
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8
Barry, Megan M. Crockett Robert S. „Three-dimensional scaffolds for mammary epithelial cell growth : a thesis /“. [San Luis Obispo, Calif. : California Polytechnic State University], 2008. http://digitalcommons.calpoly.edu/theses/12/.
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Thesis (M.S.)--California Polytechnic State University, 2008.Major professor: Robert S. Crockett, Ph.D. "Presented to the faculty of California Polytechnic State University, San Luis Obispo." "In partial fulfillment of the requirements for the degree [of] Master of Science in Engineering." "May 2008." Includes bibliographical references (leaves 38-45). Also available on microfiche (1 sheet).
9
Johansson, Magnus. „Role of Islet Endothelial Cells in β-cell Function and Growth“. Doctoral thesis, Uppsala universitet, Institutionen för medicinsk cellbiologi, 2006. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-6801.
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The pancreatic islets are collections of endocrine cells, dispersed throughout the pancreas. In adult islets, endocrine cells are closely associated with capillary endothelial cells and receive a high blood perfusion. Transplanted pancreatic islets, on the other hand, have a vascular disturbance, manifested as decreased blood vessel density. Besides impaired islet blood perfusion and oxygenation, this means that the normal close proximity between endothelial cells and β-cell in adult islets is interrupted. The aim of the thesis was to investigate if, and to what extent, β-cells and islet endothelial cells can interact with one another. This hypothesis was investigated during physiological growth of pancreatic islets, following transplantation and in vitro. We observed that islet endothelial and endocrine cell replication coincided immediately after birth, as well as during pregnancy. In pregnant animals, β-cell proliferation colocalized to islets with increased endothelial cell replication, indicating that the two processes were interconnected. The pregnancy hormone prolactin favored endothelial cell replication, and these activated cells could then augment β-cell proliferation. We found that prolactin pretreatment increased blood vessel density and oxygen tension in islets after transplantation. Furthermore, prolactin pretreatment improved endocrine function in a minimal islet transplant model. Partial pancreatectomy performed in association with islet transplantation improved revascularization, oxygen tension and glucose stimulated insulin release from the graft. In conclusion, the findings suggest that endocrine and endothelial cells interact with one another to regulate growth and function in pancreatic islets. This may form the basis for interventions aiming to improve revascularization and function of transplanted islets.
10
Mittal, Nikhil 1979. „Cell-cell and cell-medium interactions in the growth of mouse embryonic stem cells“. Thesis, Massachusetts Institute of Technology, 2010. http://hdl.handle.net/1721.1/62602.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Physics, 2010.This electronic version was submitted by the student author. The certified thesis is available in the Institute Archives and Special Collections.
Cataloged from student-submitted PDF version of thesis.
Includes bibliographical references (p. 100-108).
Embryonic stem cells serve as powerful models for the study of development and disease and hold enormous potential for future therapeutics. Due to the potential for embryonic stem cells (ESCs) to provide a variety of tissues for use in regenerative medicine, there has been great interest in the identification of factors that govern the differentiation of ESCs into specific lineages. Much of this research builds on previous studies of the role of intercellular signaling in the specification of various cell types in the developing embryo. However, relatively little work has been done on understanding the role of cell-cell communication in the self-renewal of ESCs. In the first part of this thesis I describe the development and testing of new devices for studying intercellular signaling - the nDEP microwell array and the Bio Flip Chip (BFC). We used the BFC to show that cell-cell interaction improves the colony-forming efficiency and the self-renewal of mouse ESCs. Further, we demonstrate that the interaction is at least partly diffusible. In the next part of the thesis I describe our use of more traditional assays to validate the results obtained using the BFC and to further explore the role of diffusible signaling in the survival of mouse ESCs. We demonstrate the existence of an optimal density for 2-day culture of mouse ESCs. Further, we demonstrate that the increase in growth with plating density (103-104 cells/cm2) is at least partly due to the existence of one or more survival-enhancing autocrine factor(s) in mouse ESC cultures, and that one of these factors is Cyclophilin A. Finally, we demonstrate that changes in the low molecular weight composition of the medium are likely responsible for the decrease in growth at high plating densities (>104 cells/cm2). We use a numerical model to show that competition between the positive effect (on growth) of autocrine survival factors and the negative effect of nutrient depletion can account for the observed optimal growth density. Our study provides new insight into the processes underlying, and optimization of, growth in cell types that lack contact inhibition such as cancer cells and stem cells.
by Nikhil V. Mittal.
Ph.D.
11
Seshareddy, Kiran Babu. „Human Wharton’s jelly cells-isolation and characterization in different growth conditions“. Thesis, Kansas State University, 2008. http://hdl.handle.net/2097/1054.
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Master of ScienceDepartment of Anatomy and Physiology
Mark L. Weiss
Wharton's jelly is a non-controversial source of mesenchymal stromal cells. Isolation of the cells is non-invasive and painless. The cells have been shown to have a wide array of therapeutic applications. They have improved symptoms when transplanted in a variety of animal disease models, can be used in tissue engineering applications to grow living tissue ex vivo for transplantation, and can be used as drug delivery vehicles in cancer therapy. The cells have also been shown to be non-immunogenic and immune suppressive. This thesis focuses on optimizing isolation protocols, culture protocols, cryopreservation, and characterization of cells in different growth conditions. Results from the experiments indicate that isolation of cells by enzyme digestion yields cells consistently, a freezing mixture containing 90% FBS and 10% DMSO confers maximum viability, and the expression of mesenchymal stromal cell consensus markers does not change with passage and cryopreservation. The results of the experiments also show that cells grow at a higher rate in 5% oxygen culture conditions compared to 21% oxygen culture conditions, serum does not have an effect on growth of the cells, serum and oxygen do not have effects on the expression of mesenchymal stromal cell consensus markers and the cells are stable without nuclear abnormalities when grown in 5% oxygen and serum free conditions for six passages after first establishing in serum conditions.
12
Abraham, Samuel D. M. „Activation of multiple hemopoietic growth factor genes in Abelson virus transformed myeloid cells“. Thesis, University of British Columbia, 1988. http://hdl.handle.net/2429/27786.
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The stringent requirement for hemopoietic growth factors (HGF) in the induction of hemopoiesis in vitro has raised questions as to their possible role(s) in leukemogenesis. Several recent clinical studies have shown aberrant cell growth factor gene activation in patient derived leukemic cells. Assessment of growth factor activity is often based on in vitro bioactivity assays of conditioned media or body fluids. The specificity of this type of endpoint is, however, open to question due to the overlap in biological activities of many HGFs.
In assessing the role of growth factor gene expression in a murine myeloid leukemia model I have used a sensitive RNA detection procedure coupled with a vector-probe system that enables the synthesis of uniformly labelled radioactive DNA probes to detect unambiguously the expression of particular growth factor genes. The Abelson murine leukemia virus (A-MuLV) derived myeloid transformants used in this study had previously been shown to produce a multi-lineage colony stimulating activity (CSA). While these A-MuLV transformants were shown to produce GM-CSF, it seemed likely that the multi-lineage CSA was due to another factor. In addition to confirming the expression of GM-CSF mRNA, I was able to show that the cells of all four A-MuLV transformed lines tested also expressed interleukin-3 mRNA. This finding was strongly corroborated by bio-activity data obtained using the CM from the A-MuLV myeloid transformants. Additional preliminary analysis by bioactivity assays have also shown the possible presence of interleukin-6 (IL-6) and a recently described pre-B cell factor suggesting perhaps a common mechanism underlying the activation of these various growth factor genes.Medicine, Faculty of
Medical Genetics, Department of
Graduate
13
Luo, Shuang. „Transforming growth factor-beta on human normal and malignant trophoblast cells, role in cell growth and hormonogenesis“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape2/PQDD_0020/MQ56189.pdf.
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14
Wang, Yenfeng. „The role of mast cells in foam cell formation, growth inhibition, and apoptosis of smooth muscle cells“. Helsinki : University of Helsinki, 1999. http://ethesis.helsinki.fi/julkaisut/mat/bioti/vk/wang/.
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15
SIPES, NANCY JO. „GROWTH REGULATION OF HUMAN MELANOMA: FACTORS INVOLVED IN THE EXPRESSION OF THE TRANSFORMED PHENOTYPE (SOFT AGAR, GROWTH FACTORS, PLATELETS, ENDOTHELIAL CELLS, PARACRINE)“. Diss., The University of Arizona, 1986. http://hdl.handle.net/10150/183788.
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Cellular transformation is accomplished in vitro through the concerted action of growth factors and oncogenes. This association has demonstrated that malignant growth results from aberrations in pathways that normally operate to control proliferation. Activation of genes that code for growth factors, their receptors, and/or molecules essential in the transduction of signals from the cell surface to the nucleus are all potential mechanisms by which tumor cells could establish a selective growth advantage over normal cells. This dissertation addresses the question of what oncogenic mechanisms are important in the development and progression of human melanoma. These studies show that melanoma growth is regulated by endogenous substances produced by the melanoma cells themselves (autocrine stimulation), as well as by exogenous substances supplied by neighboring cells and platelets (paracrine stimulation). These factors work to drive the expression of the transformed phenotype for melanoma as evidenced by induction of serum-free soft agar growth. Human platelets were found to the the richest source of paracrine growth promoters. The factor from human platelets was characterized and partially purified. Melanoma cells respond to this 60,000 molecular weight, disulfide-bond-containing protein in colony formation assays. In addition, the protein has endothelial cell growth factor activity. Purified fractions which promoted optimal colony formation for human melanoma cells also maximally stimulated monolayer growth of bovine aortic endothelial cells, while melanocytes were nonresponsive. This implies that melanoma cells are expressing receptors for a protein which plays no known or apparent role in the normal growth of melanocytes. Melanoma cells are sensitive to growth regulatory molecules of autocrine and paracrine nature. This dissertation provides clues to the genetic lesions which have occurred in these melanoma cells to influence their proliferation. The aberrations appear to reside in those genes important in growth factor pathways at the level of endogenous production and misguided response to exogenous factors through receptor expression. We can not hope to fully inhibit the proliferation of tumor cells until we identify and understand those forces which drive their growth. These studies have increased our knowledge of those signals which stimulate melanoma cellular proliferation, and thus provide insight into important therapeutic targets.
16
Fernyhough, Melinda. „The growth and development of muscle and fat cells“. Online access for everyone, 2006. http://www.dissertations.wsu.edu/Dissertations/Spring2006/m%5Ffernyhough%5F042706.pdf.
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17
Wang, Lixin. „Mechanisms controlling growth of human lens cells“. Thesis, University of East Anglia, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405305.
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18
Keller, Christopher Philip. „The role of polysaccharidases in acid wall loosening of epidermal tissue from young Phaseolus vulgaris L. hypocotyls“. Thesis, University of British Columbia, 1987. http://hdl.handle.net/2429/26425.
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The extension of frozen-thawed epidermal strips prepared from the first centimetre below the hypocotyl hook of six day old dark grown Phaseolus vulgaris seedlings while immersed in various buffers and under various tensions was characterized. This was done in an attempt to determine if the acid wall loosening phenomenon, which according to the Acid-growth theory (Taiz, 1984) is thought to mimic part of the auxin mechanism of action, is mediated by unspecified wall loosening enzymes.
Epidermal strips were found to be significantly loosened by media pH 6.0 to pH 2.6 (0.05M citric acid-O.lOM disodium phosphate) relative to pH 7.5. A minimum stress between 1.6 and 7.6 grams was required for the acid-extension of strips 4.5±0.5 mm wide. Regardless of tension, extension by tissues in an acid medium was largely transient For example, tissues tensioned by a 16.0 gram load reached a maximum extension rate of 6.18 ±1.37% of initial length per hour (L°/hr) between 4 and 6 minutes after immersion in pH 4.8. The rate was 1.29±0.17% L°/hr between 55 and 60 minutes and 1.05±0.14% L°/hr between 220 and 240 minutes. Total acid-extension over four hours was 4.24±0.57% L°. The extension response was found to be stable; newly harvested tissues whether frozen or not performed similarly to strips aged up to 15 days at -12°C before being extended. The performance of strips immersed in unbuffered solutions indicated that tissues were self-buffering at an acid pH probably because of the fixed carboxyls within the wall. The capacity for acid-extension by epidermal strips was lost in mature tissues harvested 4-5 cm below the hypocotyl hook.
Temperature coefficients from extension rates were determined at several pHs. The results were highly variable. The acid-extension of strips boiled 15 minutes in ethanol or extracted in 3M NaCl for 4 hours at 4°C or 6M LiCl for 8 hours was determined in several pHs. The impact of the treatments was largely a suppression of the initial burst of acceleration. Extension rates following the initial surge were relatively unaffected. Glycosidase activities in untreated, ethanol-boiled, or salt extracted strips were determined. β-glucosidase was found to be most active in untreated strips with lesser levels of β-galactosidase and
β-xylosidase and a trace of α-galactosidase being detected. Ethanol-boiling and LiCl-extraction removed or deactivated all four activities from the strips and NaCl-extraction lowered all four activities 70-80%. NaCl proved to have solubilized most of the missing β-glucosidase and β-galactosidase when the extraction solution was assayed following desalting and concentration. LiCl solubilized most of β-xylosidase. It was concluded that glycosidases and any other similarly soluble enzyme cannot be responsible for long term acid wall loosening in bean epidermis. If an enzyme is involved, it must be extremely stable and tightly bound to the wall. The acid-extension performance of frozen-thawed longitudinally halved hypocotyl sections in comparison to epidermal strips, as well as other evidence was considered support for another hypothesized mechanism of acid wall loosening, the displacement of calcium bridges.Science, Faculty of
Botany, Department of
Graduate
19
Thornton, William H. „The role of extracellular zinc in IGF-1 receptor expression and proliferation in a normal and squamous cell carcinoma cell line“. free to MU campus, to others for purchase, 1999. http://wwwlib.umi.com/cr/mo/fullcit?p9946305.
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20
Haldankar, Raj. „A kinetic study of the growth of anchorage-dependent mouse L cells“. Ohio : Ohio University, 1994. http://www.ohiolink.edu/etd/view.cgi?ohiou1177097944.
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21
曹凱韻 und Hoi-wan Tso. „Effects of phagocytosis of apoptotic cells by mesenchymal stem cells on osteogenesis and T cells responses“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2007. http://hub.hku.hk/bib/B39707520.
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22
Richards, Sean Dennis. „Towards feeder-free and serum-free growth of cells“. Thesis, Queensland University of Technology, 2007. https://eprints.qut.edu.au/16598/1/Sean_D._Richards_Thesis.pdf.
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The in-vitro culture of human embryonic stem and keratinocyte cells has great potential to revolutionise the therapeutics industry. Indeed it is hoped that these cells will provide a superior alternative to current tissue and organ transplantation. However, both of these cell types require animal and/or donor products for their successful maintenance in-vitro. This requirement results in a significant risk of cross contamination from the animal or donor products to either the primary keratinocyte or hES cells. These potentially transplantable cells therefore need to be cultured in an environment free from animal or donor products to remove the risk of contamination to the patient.
The ideal growth conditions must comprise of two attributes; firstly they must be free from animal or donor products, and secondly the culture system must be fully defined. Recently, it was discovered that an extra-cellular matrix protein, vitronectin, could be used in conjunction with growth factors and growth factor-binding proteins (VN:GF combination), to promote enhanced cell migration and growth through the co-activation of integrin and growth factor receptors. Given that growth factors and serum are clearly important in supporting the in-vitro cultivation of mammalian cells, and that vitronectin is an abundant protein in serum, I hypothesised that these VN:GF combinations could be translated into a serum-free medium that would support the serial propagation and self renewal of primary keratinocytes and hES cells. As reported in this thesis I have developed a defined, serum-free media for the culture of these cells that incorporates the VN:GF combinations. While the two media differ slightly in their compositions, both support the serial, undifferentiated expansion of their respective cells types.
Together, this represents a significant advance that will ultimately facilitate the therapeutic use of these cells. However, the in-vitro expansion of these cells in these new media still required the presence of a feeder cell layer. In view of this I aimed to explore the in-vitro micro-environment of primary keratinocytes using a novel proteomic approach in an attempt to find candidate factors that could be used in conjunction with the VN:GF media to replace both serum and the feeder cells. The proteomic approach adopted examined the secretion of proteins into the defined, minimal protein content VN:GF media when the feeder cells were cultured alone, as well as in co-culture with primary keratinocytes. This strategy allowed assessment of proteins/factors that are secreted in response to both autocrine and paracrine cellular interactions and revealed a number of candidate factors that warrant further investigation.
Ultimately this proteomic information and the associated new insights into the keratinocyte in-vitro culture microenvironment may lead to the development of a culture system for these cells that is not reliant on either a feeder cell layer or serum for their successful propagation. Moreover, it is likely that this will also be relevant to the feeder cell-free propagation of hES cells. This has obvious advantages for the culture of primary keratinocytes and hES cells in that it will allow a safe defined culture system for the undifferentiated propagation of these cells. This will facilitate the generation of cells and tissues free from xenogeneic and allogeneic contaminants, thus ensuring any therapeutics developed from these cell types are approved for therapeutic applications and importantly, will minimise risks to patients.
23
Richards, Sean Dennis. „Towards feeder-free and serum-free growth of cells“. Queensland University of Technology, 2007. http://eprints.qut.edu.au/16598/.
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The in-vitro culture of human embryonic stem and keratinocyte cells has great potential to revolutionise the therapeutics industry. Indeed it is hoped that these cells will provide a superior alternative to current tissue and organ transplantation. However, both of these cell types require animal and/or donor products for their successful maintenance in-vitro. This requirement results in a significant risk of cross contamination from the animal or donor products to either the primary keratinocyte or hES cells. These potentially transplantable cells therefore need to be cultured in an environment free from animal or donor products to remove the risk of contamination to the patient. The ideal growth conditions must comprise of two attributes; firstly they must be free from animal or donor products, and secondly the culture system must be fully defined. Recently, it was discovered that an extra-cellular matrix protein, vitronectin, could be used in conjunction with growth factors and growth factor-binding proteins (VN:GF combination), to promote enhanced cell migration and growth through the co-activation of integrin and growth factor receptors. Given that growth factors and serum are clearly important in supporting the in-vitro cultivation of mammalian cells, and that vitronectin is an abundant protein in serum, I hypothesised that these VN:GF combinations could be translated into a serum-free medium that would support the serial propagation and self renewal of primary keratinocytes and hES cells. As reported in this thesis I have developed a defined, serum-free media for the culture of these cells that incorporates the VN:GF combinations. While the two media differ slightly in their compositions, both support the serial, undifferentiated expansion of their respective cells types. Together, this represents a significant advance that will ultimately facilitate the therapeutic use of these cells. However, the in-vitro expansion of these cells in these new media still required the presence of a feeder cell layer. In view of this I aimed to explore the in-vitro micro-environment of primary keratinocytes using a novel proteomic approach in an attempt to find candidate factors that could be used in conjunction with the VN:GF media to replace both serum and the feeder cells. The proteomic approach adopted examined the secretion of proteins into the defined, minimal protein content VN:GF media when the feeder cells were cultured alone, as well as in co-culture with primary keratinocytes. This strategy allowed assessment of proteins/factors that are secreted in response to both autocrine and paracrine cellular interactions and revealed a number of candidate factors that warrant further investigation. Ultimately this proteomic information and the associated new insights into the keratinocyte in-vitro culture microenvironment may lead to the development of a culture system for these cells that is not reliant on either a feeder cell layer or serum for their successful propagation. Moreover, it is likely that this will also be relevant to the feeder cell-free propagation of hES cells. This has obvious advantages for the culture of primary keratinocytes and hES cells in that it will allow a safe defined culture system for the undifferentiated propagation of these cells. This will facilitate the generation of cells and tissues free from xenogeneic and allogeneic contaminants, thus ensuring any therapeutics developed from these cell types are approved for therapeutic applications and importantly, will minimise risks to patients.
24
Curradi, Giacomo <1977>. „Airway Basal Cell Vascular Endothelial Growth Factor-mediated Cross-Talk Regulates Endothelial Cell Dependent Growth Support of Human Airway Basal Cells“. Doctoral thesis, Alma Mater Studiorum - Università di Bologna, 2013. http://amsdottorato.unibo.it/5925/.
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The human airway epithelium is a pseudostratified heterogenous layer comprised of cili-ated, secretory, intermediate and basal cells. As the stem/progenitor population of the airway epi-thelium, airway basal cells differentiate into ciliated and secretory cells to replenish the airway epithelium during physiological turnover and repair. Transcriptome analysis of airway basal cells revealed high expression of vascular endothelial growth factor A (VEGFA), a gene not typically associated with the function of this cell type. Using cultures of primary human airway basal cells, we demonstrate that basal cells express all of the 3 major isoforms of VEGFA (121, 165 and 189) but lack functional expression of the classical VEGFA receptors VEGFR1 and VEGFR2. The VEGFA is actively secreted by basal cells and while it appears to have no direct autocrine function on basal cell growth and proliferation, it functions in a paracrine manner to activate MAPK signaling cascades in endothelium via VEGFR2 dependent signaling pathways. Using a cytokine- and serum-free co-culture system of primary human airway basal cells and human endothelial cells revealed that basal cell secreted VEGFA activated endothelium to ex-press mediators that, in turn, stimulate and support basal cell proliferation and growth. These data demonstrate novel VEGFA mediated cross-talk between airway basal cells and endothe-lium, the purpose of which is to modulate endothelial activation and in turn stimulate and sustain basal cell growth.I risultati preliminari dello studio suggeriscono che il vascular endothelial growth factor A(VEGFA) e’ attivamente secreto dalle cellule basali dell’epitelio bronchiale e svolge una funzione paracrina nell’attivazione della cascata delle mitogen-activated protein kinases (MAPKs) nelle cellule endoteliali mediata dal VEGF receptor type 2. Utilizzando un sistema di co-coltura di cellule basali primarie delle vie aeree umane con cellule endoteliali umane, abbiamo mostrato come il VEGFA secreto dalle cellule basali sia in grado di attivare le cellule endoteliale che a loro volta, esprimono mediatori capaci di stimolare e sostenere la proliferazione delle cellule basali stesse. Questi dati dimostrano un cross-talk mediato dal rilascio di VEGFA tra le cellule basali dell’epitelio bronchiale e l’endotelio, il cui scopo è di modulare l'attivazione endoteliale e, a sua volta stimolare e sostenere la crescita delle cellule basali.
25
Cadart, Clotilde. „Cell size homeostasis in animal cells“. Thesis, Université Paris-Saclay (ComUE), 2017. http://www.theses.fr/2017SACLS103/document.
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Le mécanisme d’homéostasie de taille chez les cellules animales est très peu compris actuellement. Cette question est pourtant d’un intérêt majeur car le maintien de l’homéostasie de taille dans une population de cellules prolifératives doit se faire par une coordination entre la croissance et la division. Chez la levure S. pombe, il a ainsi été montré que la taille est une information cruciale pour déclencher l’entrée en mitose (Fantes, 1977). Chez plusieurs bactéries et les cellules filles de la levure S. cerevisiae au contraire, de récentes études ont au contraire montré que l’homéostasie de taille était le résultat d’une addition constante de volume, indépendamment de la taille initiale des cellules (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). Ce mécanisme est appelé « adder » et génère une régression des tailles à la moyenne, génération après génération. Ces résultats ont été possibles grâce au développement de techniques permettant la mesure dynamique du volume à l’échelle de la cellule unique et sur plusieurs générations. Une telle mesure est cependant très difficile chez les cellules de mammifère dont le volume fluctue constamment et qui cyclent sur des temps plus longs (environ 20 heures). Pour cette raison, la plupart des approches proposées sont indirectes (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) ou reposent sur une mesure de la masse plutôt que du volume (Mir et al. 2014; Son et al., 2012). Ensemble, ces études ont montré que les cellules de mammifère croissaient de manière exponentielle. Elles ont aussi remis en cause le modèle traditionnel qui proposait que l’homéostasie de taille reposait sur l’adaptation de la durée du cycle et mis en avant un rôle de la régulation de la vitesse de croissance. Cependant, aucun modèle n’a réellement été proposé ou démontré. La nature et l’existence même d’un mécanisme maintenant l’homéostasie de taille des cellules de mammifère est en fait discutée (Lloyd, 2013).Pour caractériser l’homéostasie de taille des cellules de mammifères, nous avons développé une technique permettant pour la première fois la mesure du volume de ces cellules sur des cycles complets (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). Nous montrons que plusieurs types cellulaires (HT29, MDCK et HeLa) se comportent d’une manière similaire à celle d’un « adder ». Pour tester davantage cette observation, nous induisons artificiellement des divisions asymétriques en confinant les cellules dans des micro-canaux. Nous observons que les asymétries de tailles sont réduites mais pas complètement corrigées au cours du cycle suivant, à la manière d’un « adder ». Pour comprendre comment la croissance et la progression dans le cycle sont coordonnées et génère cet « adder », nous combinons notre méthode de mesure de volume avec un suivi de la progression dans les différentes phases du cycle. Nous montrons que la durée de la phase G1 est inversement corrélée au volume initial des cellules. Cependant, cette corrélation semble contrainte par une durée minimale de G1 mise en évidence lors de l’étude de cellules artificiellement poussées à atteindre de grandes tailles. Néanmoins, même dans cette condition où la modulation de la durée du cycle est perdue, l’observation du « adder » est maintenue. Ceci suggère un rôle complémentaire de la régulation de la vitesse de croissance des cellules. Nous proposons donc une méthode pour estimer théoriquement la contribution relative de l’adaptation de la vitesse de croissance et de la durée du cycle dans le contrôle de la taille. Nous utilisons cette méthode pour proposer un cadre général où comparer le processus homéostatique des bactéries et de nos cellules. En conclusion, notre travail apporte pour la première fois la démonstration que les cellules de mammifères maintiennent l’homéostasie grâce à un mécanisme similaire au « adder ». Ce mécanisme semble impliquer à la fois une modulation de la durée du cycle et du taux de croissanceThe way proliferating mammalian cells maintain a constant size through generations is still unknown. This question is however central because size homeostasis is thought to occur through the coordination of growth and cell cycle progression. In the yeast S. pombe for example, the trigger for cell division is the reach of a target size (Fantes, 1977). This mechanism is referred to as ‘sizer’. The homeostatic behavior of bacteria and daughter cells of the yeast S. cerevisiae on the contrary was recently characterized as an ‘adder’ where all cells grow by the same absolute amount of volume at each cell cycle. This leads to a passive regression towards the mean generation after generation (Campos et al., 2014; Soifer et al., 2016; Taheri-Araghi et al., 2015). These findings were made possible by the development of new technologies enabling direct and dynamic measurement of volume over full cell cycle trajectories. Such measurement is extremely challenging in mammalian cells whose shape constantly fluctuate over time and cycle over 20 hours long periods. Studies therefore privileged indirect approaches (Kafri et al., 2013; Sung et al., 2013; Tzur et al., 2009) or indirect measurement of cell mass rather than cell volume (Mir et al. 2014; Son et al., 2012). These studies showed that cells overall grew exponentially and challenged the classical view that cell cycle duration was adapted to size and instead proposed a role for growth rate regulation. To date however, no clear model was reached. In fact, the nature and even the existence of the size homeostasis behavior of mammalian cells is still debated (Lloyd, 2013).In order to characterize the homeostatic process of mammalian cells, we developed a technique that enable measuring, for the first time, single cell volume over full cell cycle trajectories (Cadart et al., 2017; Zlotek-Zlotkiewicz et al. 2015). We found that several cell types, HT29, HeLa and MDCK cells behaved in an adder-like manner. To further test the existence of homeostasis, we artificially induced asymmetrical divisions through confinement in micro-channels. We observed that asymmetries of sizes were reduced within the following cell cycle through an ‘adder’-like behavior. To then understand how growth and cell cycle progression were coordinated in way that generates the ‘adder’, we combined our volume measurement method with cell cycle tracking. We showed that G1 phase duration is negatively correlated with initial size. This adaptation is however limited by a minimum duration of G1, unraveled by the study of artificially-induced very large cells. Nevertheless, the adder behavior is maintained even in the absence of time modulation, thus suggesting a complementary growth regulatory mechanism. Finally, we propose a method to estimate theoretically the relative contribution of growth and timing modulation in the overall size control and use this framework to compare our results with that of bacteria. Overall, our work provides the first evidence that proliferating mammalian cells behave in an adder-like manner and suggests that both growth and cell cycle duration are involved in size control
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ARTHUSO, FERNANDA dos S. „Adaptação de células CHO secretoras de prolactina humana e seus antagonistas para o crescimento em suspensão“. reponame:Repositório Institucional do IPEN, 2011. http://repositorio.ipen.br:8080/xmlui/handle/123456789/9623.
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Instituto de Pesquisas Energeticas e Nucleares - IPEN-CNEN/SP
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Cetinkaya, Cihan. „Control of growth and differentiation of human neuronal and hematopoietic tumour cells via Myc/Max/Mad-network proteins /“. Uppsala : Dept. of Plant Biology and Forest Genetics, Swedish University of Agricultural Sciences, 2005. http://epsilon.slu.se/200522.pdf.
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28
Wahlgren, Aida. „Growth factors in spermatogenesis /“. Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-579-4/.
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29
Sheikh, Farah. „Regulation of the fibroblast growth factor-2 axis in cardiac cells, effects on cardioprotection and cardiac muscle cell growth“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/NQ62665.pdf.
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30
Wang, Ying. „Phenotypic modulations of cultured canine airway smooth muscle cells and growth-arrested cells“. Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ32279.pdf.
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31
Patel, M. „Growth of human breast cells in primary culture“. Thesis, University of Glasgow, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.233149.
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Chambers, M. E. W. „Growth of animal cells on a novel substratum“. Thesis, University of Strathclyde, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.382324.
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Partridge, Maxine. „Studies of the growth control of epithelial cells“. Thesis, Imperial College London, 1990. http://hdl.handle.net/10044/1/46490.
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Delgado, Francisco Feijó. „Measuring compositional and growth properties of single cells“. Thesis, Massachusetts Institute of Technology, 2013. http://hdl.handle.net/1721.1/81666.
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Thesis (Ph. D.)--Massachusetts Institute of Technology, Dept. of Biological Engineering, 2013.Cataloged from PDF version of thesis.
Includes bibliographical references (p. 119-128).
The physical properties of a cell are manifestations of its most basic molecular and metabolic processes. In particular, size has been a sought metric, which can be difficult to ascertain with great resolution or for smaller organisms. The advancement of single-cell measurement techniques and the understanding of cell-to-cell variability have renewed the interest in size characterization. In addition, knowledge of how individual cells grow and coordinate their growth with the cell cycle is of fundamental interest to understanding cell development, but various approaches for describing cellular growth patterns have often reached irreconcilable conclusions. In this thesis, a highly sensitive microfabricated single-cell mass sensor - the suspended microchannel resonator - is used to demonstrate cellular growth measurements by mass accumulation for several microorganism, ranging from bacterial cells to eukaryotes and mammalian cells. From those measurements insights about cellular growth are derived, demonstrating that larger cells grow faster than smaller ones, consistent with exponential-like growth patterns and incompatible with linear growth models. Subsequently, the implementation of mechanical traps as means to optimize existing sensors is presented and the techniques are applied to the measurement of total mass, density and volume at the single-cell level. Finally, a method is introduced to quantify cellular dry mass, dry density and water content. It is based on weighing the same cell first in a water-based fluid and subsequently in a deuterium oxide-based fluid, which rapidly exchanges the intracellular water content. Correlations between dry density and cellular proliferation and composition are described. Dry density is described as a quantitative index that correlates with proliferation and cellular chemical composition.
by Francisco Feijó Delgado.
Ph.D.
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Major, Jonathan. „CdTe solar cells : growth phenomena and device performance“. Thesis, Durham University, 2008. http://etheses.dur.ac.uk/605/.
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A systematic study is presented on the control of CdTe and CdS layers during their growth, with the understanding gained being implemented in the production of solar cells with enhanced performance. In particular the growth mechanisms for close space sublimation (CSS) — grown CdTe were evaluated as a function of processing gas (N2, 02 and H2) and nitrogen pressure. Films were shown to form via the Volmer-Weber growth mode with films deposited under nitrogen showing well defined crystal facets. Inclusion of oxygen in the deposition ambient produced islands of a rounded morphology, reduced size and increased number density, whilst hydrogen was shown to increase the island number density and the level of substrate coverage. Growth mechanisms were deduced from the morphologies observed at different stages of growth by ex-situ AFM and SEM and by comparison with growth literature, especially the work of P. Barna. Nucleation density, step flow and impurity incorporation are all invoked in the discussion.Factors influencing the cell performance were evaluated with the aid of a optical beam induced current (OBIC) and external quantum efficiency (EQE) system built as part of this work and having the capacity to measure EQE or OBIC maps with a resolution of 12.5pm. The system was used to evaluate the photovoltaic response of CdTe/CdS devices as a function of wavelength with the impact of the nitric-phosphoric acid (NP) etch on the back surface, the uniformity of CdTe/CdS devices deposited by different methods and the effect of absorber layer thickness of PV uniformity being assessed. The performance of CdTe/CdS devices was evaluated as a function of variables that could be influenced by growth of the CdTe and CdS layers. The use of lower substrate temperature and the incorporation oxygen in CdS increased V„ from 0.51 to 0.65V is discussed. Oxygen in the CdTe was also shown to influence the junction position and hence efficiency, while oxygen in the CdS layer was also shown to be vital for the formation of hetero-junctions. The CdTe grain size was shown to be significantly increased for deposition under higher nitrogen pressures (Grain diameter = [0.027P + 0.9]gm, where P is the pressure in Torr), with the average grain diameters being 0.94pm at 2Torr and 5.63pm at 200Torr. Device performance was improved as a result with the peak device efficiency being increased from 2.1% at 2Torr to 14.1% at 100Torr. The series resistance was shown to be minimised for larger grain size, owing to the reduced contribution of grain boundaries. Suggestions for the fabrication of high efficiency solar cells are given with reference to the efficiency limiting factor.
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Ball, Jeremy. „The growth of silicon nanowires for solar cells“. Thesis, London South Bank University, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.587543.
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At present silicon wafer technologies dominate the market place with cost driven by the technological requirement for optically thick and electronically pure silicon. A solution to the high cost of wafer based panels is a thin film approach where micron thick layers of silicon replace the ~250 micron thick silicon wafers. Thin film silicon has gone to market in the form of amorphous and microcrystalline Si where performance is an issue as well as stability due to the hydrogenated amorphous Si structure. This project involves the growth of three dimensional wire structures based on crystalline silicon and their integration into solar cell devices. Nanowire solar cells featuring a radial junction have the potential to reduce the required volume and purity of the silicon used in cell fabrication compared to wafer based technologies. The vapour-liquid-solid effect (VLS) has been used to grow Si nanowires using Au and Sn as catalyst metals together with electron cyclotron resonance chemical vapour deposition (ECRCVD) for silicon deposition. Experimental results include the formation of seed particles from both gold and tin catalyst layers leading to the growth of silicon nanowires on both silicon wafer and glass substrates. The study of nanowire growth parameters from both gold and tin catalysts has led to the proposal of a model for growth in a low pressure environment as found in ECRCVD. Structural characterisation of the wires has taken place. Wires grown from gold catalyst layers on silicon are single crystal where the growth direction has a clear dependence on the orientation of the substrate. Those from tin exhibit a nanocrystalline shell over a single crystal core and have a tapered morphology. Furthermore, the growth direction is independent of substrate orientation. Reasons for this are discussed. Optical characterisation of the nanowire arrays has revealed high levels of broadband absorption. These results have been compared with finite difference time domain modelling (FDTD) and conclusions on the effects of wire density and catalyst layer thickness, along with that of the underlying silicon layer, have been drawn. The implication of these results for the design of solar cells based on these wires is discussed. Simple solar cell devices have been fabricated demonstrating photovoltaic response but with limited performance. The reasons for this are discussed with areas for improvement.
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Quinn, Thomas Edward. „Growth and crystallisation of silicon for solar cells“. Thesis, London South Bank University, 2011. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.570870.
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Polycrystalline silicon seed layer formation by aluminium-induced crystallisation (AIC) for solar cell applications was investigated. Precursor amorphous and microcrystalline silicon layers were deposited on SiO2 substrates using electron-cyclotron resonance plasma-enhanced chemical vapour deposition (ECR PECVD) and RF sputter deposition followed by thermal evaporation or RF sputter deposition of aluminium layers. Samples were then thermally annealed leading to layer exchange and crystallisation of the silicon layer. Selected samples were used as seed layers for ECR PECVD epitaxial thickening. Processing was usually done at temperatures less than 600°C compatible with glass substrates. Deposition parameters (substrate temperature, deposition time, gas flow rates, chamber pressure and magnetic currents) for ECR PECVD Si growth using SiH4 and H2 on bare and oxidised silicon wafers were varied to examine the effect on the crystallinity of deposited layers. This was related to properties of the plasma using diagnostic measurements. A method of adding argon to the chamber, found to be beneficial to material properties of deposited films, without causing the often observed reduction in growth rates was found. A study was then undertaken to optimise growth conditions of precursor silicon and aluminium layers for suitable seed layers by AIC. Using ECR PECVD deposited silicon and evaporated aluminium was found to lead to continuous layers after short annealing time, sometimes less than 15min, than using sputtered aluminium or silicon precursor layers which did not form continuous layers after several hours of annealing at 500°C. Using thin microcrystalline silicon was also found to lead to better film quality after annealing than thicker amorphous silicon films. Increasing the temperature during AIC from 250°C to 475°C was found to reduce the annealing time to typically 30 minutes at the highest temperature while allowing relatively large grains of several microns to form. Growth of a thick Si-Al interfacial oxide also lead to larger grain sizes. Under optimal preparation and annealing conditions, i.e. ECR PECVD μc-Si growth conditions and an annealing temperature of around 400°C, AIC produced continuous polycrystalline silicon seed layers with large grains up to 100μm, a preferential (001) orientation and a relatively smooth surface morphology with Ra values typically in the range of 20-30nm. Improvements in surface morphology and crystallinity were seen after subjecting AIC polycrystalline silicon to excimer laser irradiation at optimal fluence. Based on the above results and previous published work the process of AIC is discussed. ECR PECVD overgrowth on AIC seed layers was found to be epitaxial but the crystalline quality diminishes with thickness. Adding argon during deposition was found to be beneficial in producing thick, epitaxially grown layers with 2.5μm thick epitaxial layers achieved.
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Amarachintha, Surya P. „Optimal Growth Conditions for Tracheal Epithelial Stem Cells“. Bowling Green State University / OhioLINK, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=bgsu1187395530.
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Crew, Amanda Jayne. „Hormones and growth factors in ovarian cancer cells“. Thesis, University of Edinburgh, 1992. http://hdl.handle.net/1842/19654.
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Ovarian cancer is the most common cause of death among gynaecological malignancies in women in the UK. Despite this, the mechanisms which control the growth of ovarian cancer are unclear. However, the majority of epithelial ovarian cancers express oestrogen receptors (ER), which suggests that oestrogen may be involved with the growth control. In addition a proportion of ovarian tumours express EGF receptors. The majority also contain TGF-α and a smaller number produce EGF. It is therefore possible that GF and TGF-α are autocrine or paracrine growth regulators in ovarian cancer. Using three serous ovarian adenocarcinoma cell lines, PEO1, PEO4 and PEO14 as model systems, the aim of these studies has been to clarify the role of oestrogen, EGF and TGF-α in ovarian cancer. The PEO1 and PEO4 cell lines express moderate-high levels of oestrogen receptor, whereas the PEO14 cell line is ER-negative. The growth of the ER-positive cell lines was stimulated by the exogenous addition of 17 β-oestradiol, maximally at concentrations between 10-10- and 10-8 M whereas oestrogen produced negligible effects in the ER-ngative cell line, PEO14. Thus, the sensitivity to 17 β-oestradiol correlated with the expression of the ER. The 17β- oestradiol-stimulation of PEO1 and PEO4 cell lines was blocked by incubation with tamoxifen or the 'pure' anti-oestrogen ICI 164,384. Incubation with tamoxifen alone produced growth stimulatory effects at concentrations between 10-12 and 10-8 M in PEO1 and PEO4 cell lines. Similarly incubation with ICI 164,384 produced growth stimulation in these cells, although at concentrations between 10-12 and 10-10 M in the PEO1 cell line and 10-12 and 10-7 M in the PEO4 cell line. Neither anti-oestrogen produced growth stimulatory effects in the ER-negative cell line, PEO14. In all three cell lines, incubation with 17 β-oestradiol, tamoxifen or ICI 164,384 at concentrations greater than 10^-6 M of produced growth inhibitory effects.
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Chu, Yin-Ting. „Identification and growth of adrenal cortical progenitor cells“. Diss., Restricted to subscribing institutions, 2008. http://proquest.umi.com/pqdweb?did=1619830161&sid=1&Fmt=2&clientId=1564&RQT=309&VName=PQD.
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Liu, Ke. „Role of second messengers in controlling growth patterns of corneal epithelial cells /“. View thesis, 2002. http://library.uws.edu.au/adt-NUWS/public/adt-NUWS20030718.102224/index.html.
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Thesis (Ph. D.)--University of Western Sydney, 2002."This thesis is submitted in fulfilment of the requirements of the degree of Doctor of Philosophy to the University of Western Sydney School of Biological Sciences."t.p. Includes bibliographical references (leaves 138-150).
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Thompson, Steven Howard 1958. „The effect of trenbolone on skeletal muscle satellite cells“. Thesis, The University of Arizona, 1987. http://hdl.handle.net/10150/276633.
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Young female rats treated with trenbolone demonstrated an increase in weight gain per day and overall weight increase during the treatment period. Trenbolone treated rats also experienced improved feed efficiency. Muscles removed from the lower hind limb of trenbolone treated rats had a greater DNA to protein ratio than muscles from control animals. However, there was no significant difference in wet muscle weight between trenbolone treated and control muscles. Satellite cells from untreated female rats were not responsive to trenbolone added in vitro. In studies utilizing serum free medium, trenbolone alone, and in the presence of growth factors, could not stimulate proliferation above controls. In similar serum free medium studies, satellite cells from trenbolone treated rats were more responsive to growth factors than cells from control rats.
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Woodward, Terry L. „Inhibition of cellular proliferation by retinoids and transforming growth factor-betas in bovine mammary cells correlates with increased connexin43 expression“. Thesis, McGill University, 1996. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=40283.
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Bovine fibroblasts and epithelial cells were isolated from surgically biopsied mammary tissue. Characterization of population doubling time, cytoskeletal intermediate filaments, cryopreservation survival, and viability were performed on all fibroblast and epithelial cells. Several clonal fibroblast cell lines were cotransfected with a plasmid bearing the SV-40 Large-T-antigen, and the pSV-2 neo plasmid. Transfected cells were subsequently selected with G418 sulfate and cloned.MAC-T cells and non-clonal primary bovine mammary epithelial cells proliferated in response to IGF-I, insulin, serum and serum albumin. MAC-T cells did not proliferate when cultured in EGF, estrogen, progesterone, estrogen+progesterone, growth hormone, prolactin, and only modest proliferation was obtained after TGF-$ alpha$ treatment. Subsequent experiments used serum, insulin or IGF-I (and its analogues) to stimulate cellular proliferation. Serum albumin was not added to serum-free media preparations since it stimulated cellular proliferation.
TGF-$ beta$ receptors were characterized in MAC-T cells and normal fibroblasts. Affinity labelling studies revealed that MAC-T and MF-2 cells contained type I, II, and III autoregulatable receptors. Fibroblast proliferation, was inhibited 50% by TGF-$ beta$. TGF-$ beta$ inhibited MAC-T cellular proliferation at concentrations among the lowest ever reported, ED$ sb{ rm 50}$ = 4 pm. TGF-$ beta$ was not cytotoxic at concentrations 1000-fold higher.
Retinoic acid (RA) also inhibited proliferation of MAC-T cells. Inhibition of proliferation did not occur when cells were growth stimulated by IGF-I analogues that do not bind IGFBPs. Unlike TGF-$ beta$, RA treatment increased IGFBP-2 and decreased IGFBP-3 protein expression by cells into media and on the cell's membrane. RA was cytotoxic at concentrations 10-fold higher than ED$ sb{100}$.
Fibroblasts and epithelial cells expressed the gap junction (GJ) protein, connexin43, with transformed fibroblasts expressing significantly less connexin43. Perinuclear and cell surface connexin43 was immunodetected in epithelial and fibroblasts cells. TGF-$ beta$, RA or cAMP, increased connexin43 protein expression, especially phosphorylated species. Only cAMP noticeably altered immunolocalization patterns of connexin43, causing a shift from perinuclear pools to the cell surface. None of the growth inhibitors affected GJ communication as measured by dye transfer. Therefore, mammary epithelial cells are growth inhibited by TGF-$ beta$ and RA by distinct mechanisms and both growth inhibitors significantly enhance the gap junction protein, connexin43, without increasing GJ communication.
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Magnusson, Peetra. „Fibroblast Growth Factor Receptor-1 Function in Vasculo- and Angiogenesis“. Doctoral thesis, Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2005. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-5824.
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Mark, Melanie Danelle. „The mechanisms underlying EGF-stimulated neuronal differentiation in PC12 cells /“. Thesis, Connect to this title online; UW restricted, 1996. http://hdl.handle.net/1773/6261.
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List, Edward Owen. „Creating Growth Hormone Resistance in Cells using a Hammerhead Ribozyme Approach“. Ohio University / OhioLINK, 2001. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou997813564.
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Hoying, James B. „Cell-matrix interactions of microvessel endothelial cells in response to basic fibroblast growth factor“. Diss., The University of Arizona, 1994. http://hdl.handle.net/10150/186998.
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Vertebrate tissues consist of parenchyma and vascular elements all of which are necessary for the specific form and function of these tissues. In a unique process termed angiogenesis, vessels invade forming tissues to provide for proper tissue perfusion. Much is known about the molecular and cellular elements of angiogenesis, however, it is not clear how these elements are coordinated to produce specific microvascular beds. In an effort to answer this question, the effects of basic fibroblast growth factor (bFGF) on human microvessel endothelial cell (HMVEC) interactions with collagen I were examined. HMVEC migration on collagen I was chosen as the model angiogenic response. Utilizing two distinct migration assays, bFGF either induced migration or had no effect. Examination of HMVEC adhesion with two separate assays revealed that HMVEC adhesion to collagen I was altered by bFGF treatment and depended on the density of HMVEC at the time of treatment. Adhesion of HMVEC with or without bFGF treatment was mediated entirely by β1 integrins as demonstrated with a blocking antibody studies. Experiments were performed to determine the mechanism by which bFGF can alter HMVEC adhesion and focused on low density HMVEC. The reduction in adhesion of low density HMVEC following bFGF treatment correlated with no change in β1 integrin surface expression, delayed cell spreading, altered organization of β1 integrin into substrate contacts, and serine/threonine phosphorylation of the β1 subunit. To evaluate the coordinated effects of bFGF on angiogenesis, an in vitro model simulating a microvascular environment was developed utilizing isolated microvessel fragments from rat adipose tissue cultured in three dimensional collagen I gels. The addition of crude basic fibroblast growth factor to the cultures resulted in the growth of significantly longer microvessels and the expression of an endothelial cell protein, von Willebrand factor. Based on this work, it is apparent that cellular responses to physiological signals during angiogenesis are multifactorial and are sensitive to many coincidental environmental factors such as cell density. The influence of these environmental factors is such as to substantially alter the effects of a signalling factor acting alone.
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Li, Jing, und 李靜. „Effects of intrinsic & extrinsic factors on the growth and differentiation of human mesenchymal stem cells“. Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B37238310.
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Sharfe, Nigel. „Investigation of G protein expression in human lymphoid cells“. Thesis, University of Cambridge, 1993. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.308330.
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Midgley, Nicola-Ann. „Metabolic responses in melanoma cells to combined nutrient supplementation“. Thesis, Rhodes University, 1997. http://hdl.handle.net/10962/d1004096.
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This thesis examined the effect and biochemical mechanism by which combined vitamin E and C supplementation may influence tumour cell growth. The study initially addressed the effect of combined vitamin E succinate and Asc supplementation over a nutritional concentration range (5- 20μg/ml) and (25-50μg/ml) respectively, on the in vitro growth of non-malignant LLCMK and malignant BL6 cells. Supplementation of BL6 and LLCMK cells with combined vitamin E succinate and ascorbic acid, resulted in no significant increasing or decreasing trend in LLCMK cell growth, while in BL6 cells a significant decrease in cell growth was observed at all combined vitamin concentrations. It has been suggested that these vitamins may act synergistically to inhibit tumour cell growth through their antioxidant properties in quenching free radicals and lipid peroxidation and furthermore through their modulation of the activities of various enzymes and metabolites in the eicosanoid pathway. This study consequently investigated the effects of combined vitamin E succinate and ascorbic acid supplementation on these parameters. Throughout this study, emphasis was placed on the BL6 melanoma cells, as combined vitamin E succinate and ascorbic acid supplementation did not significantly affect growth or levels of secondary metabolites in the non-malignant LLCMK cells. Combined vitamin E succinate and ascorbic acid supplementation of BL6 cells resulted in a marked but non significant increase in free radical and a significant increase in lipid peroxidation levels. This prooxidant effect was accompanied by a significant decrease in BL6 cell growth, suggesting that the growth inhibitory effects of combined vitainin E succinate and ascorbic acid on BL6 cells in vitro was not mediated through their synergistic antioxidant properties. Vitamin E succinate is a nonphysiological antioxidant in its esterified form, hence cleavage of the succinate group must occur in order for ascorbic acid to interact with the free alcohol, vitamin E. The inability of combined vitamin E succinate and ascorbic acid to reduce free radicals and lipid peroxidation levels within BL6 cells may not be due to their ineffectiveness as antioxidants but rather the presence of other contributing factors which influence the oxidation state within the BL6 cells. Vitamin E is believed to modulate membrane-bound enzymes through membrane stabilization. Furthermore, the stabilizing effect of vitamin E may be enhanced by the ascorbic acid-sparing effect of vitamin E. Hence, this study investigated the effect of combined vitamin E succinate and ascorbic acid in modulating the activity of various enzymes and secondary messengers in the eicosanoid pathway. Supplementation with combined vitamin E succinate (5-20μg/ml) and ascorbic acid (25-50μg/ml) resulted in significant increases in phospholipase A₂, 5-lipoxygenase, cyclooxygenase and adenyl ate cyclase activity, with a significant decrease in BL6 cell growth. The possible synergistic action of these vitamins in terms of modulating membrane-bound enzymes was further substantiated by uptake and cellular distribution studies. Vitamin E succinate and vitamin E in the membrane fraction increased significantly compared to control cultures, while ascorbic acid levels were significantly higher in the stroma fraction when compared to membrane fractions. Consequently, another factor accounting for increased activities of phospholipase A2, 5-lipoxygenase and adenylate cyclase activities as a result of vitamin supplementation in BL6 cells may be an increased availability of Ca²+. Supplementation of BL6 cells with combined vitamin E succinate and ascorbic acid resulted in significant increases in intracellular Ca²+ levels at all combined vitamin groups. Furthermore, this increase in intracellular Ca²+ was positively correlated with cl1anges of the above-mentioned enzyme activities. Within the eicosanoid pathway, the rate of prostaglandin synthesis is regulated by phospholipase A₂ activity and arachidonic acid release, and the net prostaglandin production is dependent on cyclooxygenase activity, hence the effects of combined vitamin E succinate and ascorbic acid on arachidonic acid composition and prostaglandin production within BL6 cells was determined. The percentage arachidonic acid composition of the BL6 cells was elevated and inversely related to cell growth following combined vitamin E succinate and ascorbic acid supplementation. Prostaglandin E₂ and prostaglandin I₂ levels increased significantly, while those of prostaglandin D2 and prostaglandin F₂α increased markedly following supplementation of combined vitamin E succinate and ascorbic acid. These increases in prostaglandin levels were inversely related to BL6 cell growth, suggesting that the prostaglandins were involved in negative regulation of BL6 cell growth. When comparing the levels of prostaglandins, prostaglandin E2 levels were significantly higher when compared to prostaglandin D₂, prostaglandin F₂α and prostaglandin I₂ suggesting that vitamin E₂ succinate and ascorbic acid effects were mediated primarily through an increase in prostaglandin E2. Hence, prostaglandin E2 levels in combined vitamin E succinate and ascorbic acid appeared to be dependent on the amount of precursor present and the activity of its synthetic enzymes. This was confirmed when BL6 cells were supplemented with arachidonic acid. Arachidonic acid had an inhibitory effect on BL6 cell growth and also stimulated prostaglandin E₂ production. Prostaglandin E₂ levels are in turn believed to modulate adenylate cyclase activity in BL6 cells, hence it is reasonable to conclude that adenylate cyclase activity is dependent on prostaglandin E₂ levels. Combined vitamin E succinate and Asc supplementation to BL6 cells resulted in significant increases in adenyl ate cyclase and cyclic adenosine monophosphate, which again correlated with a significant decrease in cell growth. As cyclic adenosine monophosphate has a regulatory role in the cell cycle this study suggested that the effect of combined vitamin E succinate and ascorbic acid supplementation was mediated through the final effect provided by the second messenger, cyclic adenosine monophosphate. This was confirmed when BL6 cells were supplemented with dexamethasone, a phospholipase A₂ inhibitor. This treatment rsulted in combined vitamin E succinate and ascorbic acid having no inhibitory effect on BL6 cell growth. Cyclooxygenase activity, prostaglandin E₂ levels, adenylate cyclase activity and cyclic adenosine monophosphate levels were significantly lower in dexamethasone-treated cells compared to non-treated dexamethasone cultures. The reason for the increased free radical and lipid peroxidation levels in BL6 cells was further investigated. Cyclooxygenase enzymes are believed to generate free radical species during catalytic activity. Analysis of free radical and lipid peroxidation levels following supplementation with dexamethasone revealed markedly lower free radical and significantly lower lipid peroxidation levels in comparison with control cultures and non dexamethasone-treated cultures. These results suggest that the observed increases in free radical and lipid peroxidation levels in BL6 cells supplemented with combined vitamin E succinate and ascorbic acid were indirectly due to the increase in cyclooxygenase activity in these cells.