Dissertations / Theses: 'Cell biology research'

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Chen, Luxi. "Human Innate Lymphoid Cell Biology and Development." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1551901769401192.

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Li, Qiming. "IL-1 Receptor Biology: Promoter Complex and Cell Type Specific Function." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1280861203.

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Calderone, Carli E. "Stem Cell Research: Science Education and Outreach." Miami University Honors Theses / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=muhonors1268751337.

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Alvarado, Cabellos Alvaro Gonzalo. "Targeting Stem Cell Pathways in Glioblastoma." Case Western Reserve University School of Graduate Studies / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=case1459189591.

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Jaime-Ramirez, Alena Cristina. "HER2 and Folate Receptor Targeted Therapy is Enhanced by NK Cell-Activating Cytokines." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1364465780.

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Wray, Jason Patrick. "Characterisation of a novel culture condition for the establishment and maintenance of mouse embryonic stem cells and implications for the mechanisms of self-renewal." Thesis, University of Edinburgh, 2009. http://hdl.handle.net/1842/3215.

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Pluripotency is defined as the ability of a cell to give rise to all the cell types of the adult organism. In vivo this property is possessed transiently by the cells of the epiblast in the developing embryo but it can be maintained indefinitely by deriving embryonic stem (ES) cells. How the pluripotent state is established in the cells of the early embryo and how it is ‘captured’ and maintained in the form of ES cells is a fascinating question for biology with practical implications. It is hoped that ES cells will be of use in biomedical research and cell replacement therapy. Our understanding of their biology and our ability to manipulate the cells in vitro will be of great importance if these hopes are to be realised. The starting point for the work presented in this thesis was the development of a novel culture condition for the derivation and maintenance of mouse ES cells (Q-L. Ying and J. Nichols). The media is formed by the addition of three small molecule inhibitors to a previously described serum-free media, N2B27, and is termed 3i (three inhibitors).The inhibitors are SU5402, PD184352 and CHIRON99021, and they inhibit the FGF receptor, mitogen activated protein/extracellular signalregulated kinase (ERK) kinase (MEK), and glycogen synthase kinase 3 (GSK3) respectively. I attempt to further our understanding of pluripotency and self-renewal in ES cells by genetic and biochemical examination of ES cells cultured in 3i. Analysis of intracellular signalling pathways together with descriptions of genetic mutants for the targets of the inhibitors validates the mode of action and the specificity of the three inhibitors. Self-renewal of mouse ES cells is considered dependent on activation of STAT3 through provision of the cytokine leukaemia inhibitory factor (LIF). I demonstrate unequivocally that this pathway is not required for self-renewal in 3i by characterising Stat3-null ES cells. Further experiments reveal that preventing activation of ERK downstream of the growth factor FGF4, produced by the ES cells themselves, is key to preventing differentiation. Pleiotropic effects of GSK3 inhibition are observed and candidate GSK3 targets with known or predicted effects on self-renewal are investigated as potential downstream effectors. I propose that activation of canonical Wnt signalling, together with a global derepression of biosynthetic capacity, mediate the pro-self-renewal effects of GSK3 inhibition. The description of culture conditions that function independently of signalling pathways previously thought essential for self-renewal provides fresh insight into the nature of ES cell self-renewal and the relationship of ES cells to the pluripotent cells of the developing embryo. There are practical implications for ES cell biology as there is reason to hope that the new conditions will translate more readily to other mammalian species to facilitate the derivation of ES cells and will provide an optimal platform for differentiation of ES cells into somatic cell types of interest.

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Chakraborty, Rikhia. "Homeostatic Regulation of Interleukin-4-Mediated Cell Signaling." Cleveland State University / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=csu1258663290.

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Sprague, Leslee W. "Dendritic Cell Culture With 2D and 3D Collagen Substrates." Ohio University / OhioLINK, 2011. http://rave.ohiolink.edu/etdc/view?acc_num=ohiou1311616312.

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Hsu, En-Chi. "Targeting ILK to eliminate IL-6 induced cancer stem cell phenotype." The Ohio State University, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=osu1397560686.

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Nordén, Johan. "Assessment of methods for microRNA isolation, microRNA amplification, and development of a normalization strategy for sepsis biomarker research." Thesis, Högskolan i Skövde, Institutionen för biovetenskap, 2020. http://urn.kb.se/resolve?urn=urn:nbn:se:his:diva-18442.

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Sepsis, defined by organ dysfunction caused by an adverse immune response of the host to an infection, comes with considerable cost in human lives and as a substantial burden financially. Significant upgrades have been made over the past two decades when diagnosing and treating sepsis but still with room for improvements. Early detection is a cornerstone in the fight against sepsis, and the focus on strengthening diagnostics is in the forefront of modern research. The implementation of biomarkers may be the path of progression in this objective. This study aimed at establishing procedural foundations when using microRNAs as potential biomarkers. The study conducted looked at: (1) Isolation procedure, of microRNA from human plasma, of three kits: Total RNA Purification Kit (Norgen Biotech), miRNAeasy Serum/Plasma Kit (Qiagen), and miRNeasy Serum/Plasma Advanced Kit (Qiagen). (2) Amplification of miRNA through two Reverse Transcription Quantitative PCR methods: Two-tailed RT-qPCR (TATAA Biocenter), and miRCURY LNA miRNA PCR (Qiagen). (3) Developing a normalization strategy by identifying miRNA reference targets in a geNorm pilot experiment. Qubit analysis revealed that the two isolation kits from Qiagen performed similar, and better that the Norgen kit. The Two-tailed RT-qPCR failed to amplify miRNA samples, whereas the miRCURY LNA miRNA PCR showed consistent amplification across samples with a high call rate. The geNorm analysis concluded that hsa-miR-425-5p and hsa-miR-93-5p was the optimal reference target set. The study demonstrated that the isolation kits from Qiagen coupled with the miRCURY LNA miRNA PCR is a viable option for future miRNA biomarker studies.

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Koterba, Kristen L. "Regulation of Autophagy and Cell Death in Breast Carcinoma Cells." University of Toledo Health Science Campus / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=mco1276005638.

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Goschorska, Maja. "Investigating the mechanisms of cell competition in mammals using in vitro systems." Thesis, University of Cambridge, 2019. https://www.repository.cam.ac.uk/handle/1810/290214.

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Cell competition leads to elimination of a viable cell population, by fitter cells. Despite over forty years of research, the molecular mechanisms of competition in mammals are poorly understood. During my PhD I have investigated the mechanisms of competition by exploring an established mammalian cell culture system, in which wild-type MDCK cells eliminate scribble-deficient cells, and I have also developed a novel cell culture system to model mammalian competition. My work contributed to the discovery that scribble-deficient cells are eliminated not by biochemical exchange among cells, but by mechanical compaction. We termed this phenomenon mechanical competition. I employed transcriptional profiling to determine the molecular signature of mechanical losers, and identified activation of p53 signalling as their hallmark. My colleagues and I then demonstrated that elevation of p53 is both necessary and sufficient to trigger mechanical competition. In further investigating the mechanisms of mechanical competition, I found that compaction activates ROCK in scribble-deficient cells, and that this is required for their elimination. Inhibition of Src signalling in mechanical losers also protected them form out-competition, and integrin signalling is another pathway likely involved in mechanical competition. While investigating p53 competition, we observed that p53-high and p53-low cells engage in directional migration, with p53-high cells always at the migrating front. As a side-project, I investigated the role of p53 in directional migration, by exploring an established model with a single leader cell and multiple followers. We established a method to generate multinucleated leaders on demand. By creating leaders from p53-deficient cells, I established that p53 signalling is required for some, but not all multinucleated cells to trigger collective migration, thus implicating p53 signalling in a type of migration involved in wound healing. Finally, I successfully modelled p53-driven mechanical competition in a differentiated primary tracheal epithelial cell culture, thereby establishing a novel system to study mammalian competition, and also proving that p53 competition is conserved between different mammalian epithelia. Considering the involvement of p53, mechanical competition may play a major role in cancer.

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Feldges, Robert. "Mathematical Model of the Combined Effect of IL-6, TGF-beta and TNF-alpha on Pancreatic Stellate Cell Activation." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1428603582.

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Muniz-Feliciano, Luis. "Toxoplasma gondii Manipulates Host Cell Signaling To Prevent Autophagic Targeting And Promote Survival Within Host Cells." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1414520569.

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Moore, Janelle. "Establishment of CRISPR/Cas-9 Aided Knockout of the ZIC2 Gene in the African-American Prostate Cancer Cell Line E006AA-PR." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2019. http://digitalcommons.auctr.edu/cauetds/195.

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The largest U.S. cancer health disparity exists in prostate cancer, with African American men having the highest incidence and mortality rates. The present study evaluated the effects of ZIC2 and the underlying mechanisms in the E006 parental African-American cell line that produces tumors at accelerated growth rates because of the increase of ZIC2 genes in African-American males. We analyzed the experimental research that the overexpression of ZIC2 contributes to progression of prostate cancer. E006AA cells with overexpressed or suppressed ZIC2 were analyzed to determine phenotypic differences, PCR, cell proliferation and immunoblot assays. The expression levels of ZIC2 were analyzed by CRISPR-Cas9, Western blot and proliferation growth curves. We discovered using these experimental techniques to knockout ZIC2, reduced cell proliferation occurred. This research investigated the role of ZIC2 in prostate cancer progression and the effects of the loss or gain of function of ZIC2 by using CRISPR-Cas 9 genome editing technology.

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McCarty, Kenneth Dean. "Characterization of pulmonary surfactant apoproteins in the diabetic mouse." CSUSB ScholarWorks, 1989. https://scholarworks.lib.csusb.edu/etd-project/512.

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Weber, Grace E. "Memory B Cell Dysfunction in Human Malaria." Case Western Reserve University School of Graduate Studies / OhioLINK, 2018. http://rave.ohiolink.edu/etdc/view?acc_num=case1512731469728517.

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Kelly, Michael C. "Using Phage Display to Determine Mesenchymal Stem Cell Contribution to Collagen Synthesis." Youngstown State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1503615054387659.

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Ghaffari, Kevin A. "Zebrafish (Danio rerio) as a Model for Orofacial Research." VCU Scholars Compass, 2017. http://scholarscompass.vcu.edu/etd/4811.

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Across species, the face and more specifically the mouth, serves as an essential facet of everyday life. Amongst humans the mouth serves as a tool for the ingestion of food, a marker for facial recognition and a medium for communication. In order for the mouth to properly form, a series of precise growth and fusion events are needed. In order to insure that these events are orchestrated properly is a wide array of signals, transcription factors and epigenetic regulators. Due to the needed precision of these events, congenital birth defects of the face such as cleft lip and cleft palate are some of the most common worldwide. In order to support existing and identify new developmental processes involved in mouth formation, we have utilized the effective model, Danio to study the molecules and events implicated in orofacial development. This was accomplished by developing a novel confocal imaging technique that allows for visualization of the forward facing zebrafish. Using this imaging technique we were able to establish when the embryonic mouth first forms in zebrafish. Additionally, we recapitulated cleft-palate phenotypes shown in previous literature with the imaging method. Utilizing this technique, we then sought to further establish the role of Ca2+ signaling in proper orofacial morphogenesis and determine if the serine/threonine protein kinase, Ca2+/calmodulin-dependent protein kinase type-II (CaMK-II), has a role in proper orofacial developmental.

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Guzman, Nicole Denise. "Characterization and miRNA analysis of cancer cell-secreted microvesicles." The Ohio State University, 2012. http://rave.ohiolink.edu/etdc/view?acc_num=osu1338156013.

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Nyaboke, Roseline Nyaboke. "The Role of N2A and N2B Titin Isoforms in Muscle Cell Development." Youngstown State University / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=ysu1471612545.

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Estrada, Paula Joanne. "The effect of triiodothyronine on GLUT4 protein expression in skeletal muscle and adipose tissue of obese-diabetic (db/db) mice." CSUSB ScholarWorks, 1997. https://scholarworks.lib.csusb.edu/etd-project/1304.

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Dremann, David Michael. "Pluronic Activity in Hyperthermia-induced Cancer Cell Death." Case Western Reserve University School of Graduate Studies / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=case1247425426.

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DiVincenzo, Lola S. "DIRECTION OF INDUCED PLURIPOTENT STEM CELL DIFFERENTIATION BY ENDOTHELIAL CELL SECRETOME." Kent State University / OhioLINK, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=kent1438031276.

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Kotadiya, Preeyal. "Regulation Of Osteoclast Function By Alpha Gene Tropomyosins, TM-2/3 And TM-5a/5b." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1250612152.

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Habroun, Stacy Star. "Effects of Food Consumption on Cell Proliferation in the Brain of Python regius." DigitalCommons@CalPoly, 2017. https://digitalcommons.calpoly.edu/theses/1763.

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Neurogenesis is an important and vastly under-explored area in reptiles. While the ability to generate new brain cells in the adult mammalian brain is limited, reptiles are able to regenerate large populations of neuronal cells. Pythons exhibit a characteristic specific dynamic action (SDA) response after food intake with an increase in metabolic rate that facilitates processing the meal. Associated with this change in SDA, pythons (Python spp.) also exhibit impressive plasticity in their digestive and cardiovascular physiology due to the sheer magnitude of the increase in organ growth that occurs after a meal to speed digestion, absorption, and assimilation of nutrients. While this systemic growth in response following food consumption is well documented, whether the python brain exhibits associated changes in cell proliferation following food consumption and digestion is currently unexplored. For this study, juvenile male ball pythons (Python regius) were used to test the hypothesis that postprandial neurogenesis is associated with food consumption. We used the thymidine analog 5-bromo-12’-deoxyuridine (BrdU) to quantify and compare cell proliferation in the brain of fasted snakes and at two time points: two days and six days after a meal, which span time periods of during and after SDA response, respectively. Quantification of BrdU-labeled cells in the ventricular regions relealed that – consistent with other reptile species – the retrobulbar and olfactory regions had the highest numbers of proliferating cells in the python brain, regardless of sampling time. Throughout the telencephalon, cell proliferation was significantly greater in the six-day post-feeding group, with no difference between the two-day post-feeding group and controls. Most other postprandial systemic plasticity occurs within a day or two after a meal and decreases thereafter; however, the brain displays a more delayed response, with a surge of cell proliferation after most of the digestion and absorption is complete. Our results support our hypothesis that food consumption does affect cell proliferation in the python brain, and indicates that the degree of increased proliferation is dependent on the time since feeding.

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Kenyon, Jonathan Dallas. "Loss of Mismatch Repair in the Aging Human Hematopoietic Stem Cell." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1354917428.

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Clancy, Lauren R. "Platelet Transcriptome Heterogeneity: A Role for RNA Uptake in Vascular Health and Disease." eScholarship@UMMS, 2008. http://escholarship.umassmed.edu/gsbs_diss/922.

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As our understanding of the platelet’s systemic role continues to expand beyond hemostasis and thrombosis, interrogation of the platelet’s ability to affect diverse biological processes is required. Studies of the platelet’s non-traditional roles have focused on developing our understanding of the platelet’s relation to specific disease phenotypes as well as elucidation of platelet characteristics, content, and function. The generic content, traditional function and heterogeneity of platelets have long been accepted; more ambiguous and controversial has been how these factors are interrelated. Investigation of platelet content revealed the presence of biologically functional RNA in anucleated platelets, the correlation of platelet RNA to distinct phenotypes, and the ability of platelets to transfer RNA to other vascular cells; however how these processes occur is unclear. To further interrogate platelet RNA processes, we utilized sorting and RNA sequencing to develop platelet subpopulation transcriptome profiles. We found that platelet heterogeneity extends to the platelet transcriptome: distinct RNA profiles exist dependent on platelet size. We hypothesized that this RNA heterogeneity is the result of RNA transfer between platelets and vascular cells. Using in vitro and in vivo modeling, we were able to show the novel ability of platelets to take up RNA from vascular cells, correlating to the unique functional profile associated with small platelet transcriptomes. These findings reveal a role for platelet RNA transfer in platelet RNA heterogeneity, with potential correlation to platelet functional diversity previously proposed. The ability of the platelet to bidirectionally transfer RNA within circulation has implications for vascular health and beyond.

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Clancy, Lauren R. "Platelet Transcriptome Heterogeneity: A Role for RNA Uptake in Vascular Health and Disease." eScholarship@UMMS, 2017. https://escholarship.umassmed.edu/gsbs_diss/922.

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As our understanding of the platelet’s systemic role continues to expand beyond hemostasis and thrombosis, interrogation of the platelet’s ability to affect diverse biological processes is required. Studies of the platelet’s non-traditional roles have focused on developing our understanding of the platelet’s relation to specific disease phenotypes as well as elucidation of platelet characteristics, content, and function. The generic content, traditional function and heterogeneity of platelets have long been accepted; more ambiguous and controversial has been how these factors are interrelated. Investigation of platelet content revealed the presence of biologically functional RNA in anucleated platelets, the correlation of platelet RNA to distinct phenotypes, and the ability of platelets to transfer RNA to other vascular cells; however how these processes occur is unclear. To further interrogate platelet RNA processes, we utilized sorting and RNA sequencing to develop platelet subpopulation transcriptome profiles. We found that platelet heterogeneity extends to the platelet transcriptome: distinct RNA profiles exist dependent on platelet size. We hypothesized that this RNA heterogeneity is the result of RNA transfer between platelets and vascular cells. Using in vitro and in vivo modeling, we were able to show the novel ability of platelets to take up RNA from vascular cells, correlating to the unique functional profile associated with small platelet transcriptomes. These findings reveal a role for platelet RNA transfer in platelet RNA heterogeneity, with potential correlation to platelet functional diversity previously proposed. The ability of the platelet to bidirectionally transfer RNA within circulation has implications for vascular health and beyond.

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Gupta, Cherry. "DNA Translocation and Cell Electroporation in Micro and Nanofluidic Devices." The Ohio State University, 2015. http://rave.ohiolink.edu/etdc/view?acc_num=osu1448318827.

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Dudley, Brian Mason. "BMP Signaling Supports Primordial Germ Cell Development by Regulating Kit Ligand." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1278689341.

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Calderon-Salgado, Esther Lilia. "Effect of progesterone and RU486 on cisplatin resistance in OV2008 and C13 ovarian epithelial cancer cell lines." Kent State University / OhioLINK, 2008. http://rave.ohiolink.edu/etdc/view?acc_num=kent1208532125.

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Leslie, Kevin A. "Evaluation and Adaptation of Live-Cell Interferometry for Applications in Basic, Translational, and Clinical Research." VCU Scholars Compass, 2018. https://scholarscompass.vcu.edu/etd/5562.

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Cell mass is an important indicator of cell health and status. A diverse set of techniques have been developed to precisely measure the masses of single cells, with varying degrees of technical complexity and throughput. Here, the development of a non-invasive, label-free optical technique, termed Live-Cell Interferometry (LCI), is described. Several applications are presented, including an evaluation of LCI’s utility for assessing drug response heterogeneity in patient-derived melanoma lines and the measurement of CD3+ T cell kinetics during hematopoietic stem cell transplantation. The characterization of mast cells during degranulation, the measurement of viral reactivation kinetics in Kaposi’s Sarcoma, and drug response studies in patient-derived xenograft models of triple-negative breast cancer are also discussed. Taken together, data from these studies highlight LCI’s versatility as a tool for clinical, translational, and basic research applications.

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Swaminathan, Ganesh. "Evaluation Of Adult Stem Cell Derived Smooth Muscle Cells For Elastic Matrix Regenerative Repair." University of Akron / OhioLINK, 2016. http://rave.ohiolink.edu/etdc/view?acc_num=akron1462209321.

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Kisgeropoulos, Effie Christine. "Inhibition of Ovarian Cancer Cell Proliferation by Oleoylethanolamide and its Metabolically Stable Analog AM3102." Kent State University Honors College / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=ksuhonors1386429690.

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Beal, Robert William John. "Investigating the role of Junctional Adhesion Molecule-C (JAM-C) in endothelial cell biology in vitro and in vivo using human and mouse models." Thesis, Queen Mary, University of London, 2018. http://qmro.qmul.ac.uk/xmlui/handle/123456789/44687.

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Junctional adhesion molecule C (JAM-C) is a component of endothelial cell (EC) tight junctions that has been implicated in a number of endothelial functions, such as angiogenesis and trafficking of leukocytes through the endothelium during inflammation. Work within our lab has identified that loss of JAM-C at EC junctions results in increased reverse transendothelial migration (rTEM) of neutrophils back into the circulation, a response that has been associated with the dissemination of inflammation to distant organs. Whilst the mechanism by which JAM-C is lost or redistributed away from EC junctions has begun to be elucidated, little is known about how loss of endothelial JAM-C impacts the functions of ECs. As such, this thesis aimed to investigate the effect of JAM-C deficiency on EC functions to unravel possible molecular and cellular mechanisms of mediating neutrophil rTEM. To address the effect of JAM-C deficiency on EC functions, an in vitro RNA interference (RNAi) approach was used to efficiently knock-down (KD) JAM-C in human umbilical vein ECs (HUVECs). Importantly, KD of JAM-C did not affect expression of other key EC junctional markers such as JAM-A and VE-Cadherin and cell proliferation and apoptosis were similarly unaffected. Gene expression profiling using microarrays revealed that JAM-C depleted HUVECs exhibited a pro-inflammatory phenotype under basal conditions that was characterised by increased expression of pro-inflammatory genes such as ICAM1 and IL8. Following IL-1β-induced inflammation, no difference in expression of pro-inflammatory genes was detected between control and JAM-C KD HUVECs. However, protein levels of secreted chemokines such as IL-8 were reduced in JAM-C KD HUVECs following stimulation with IL-1β. This was corroborated by in vivo studies demonstrating reduced levels of secreted chemokines in the plasma of mice where JAM-C was conditionally deleted from ECs. A novel finding of this work is the demonstration that JAM-C KD HUVECs exhibit increased autophagy under basal conditions. This might provide a potential mechanism for the reduced chemokine secretion that is observed in this system, whereby chemokines are preferentially trafficked for autophagosome-mediated degradation. Taken together, these findings indicate a multi-functional role for JAM-C in regulating EC homeostasis under basal conditions. JAM-C KD ECs respond aberrantly to inflammatory stimuli by secreting reduced chemokine levels, a consequence that could provide novel insights into the mechanisms of neutrophil rTEM under conditions of endothelial JAM-C loss.

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Breckenridge, Mark T. "Cell Biological and Microfabrication Approaches Towards the Understanding of Transmigration and Nonmuscle Myosin II Assembly." Case Western Reserve University School of Graduate Studies / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=case1269961536.

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Zhang, Xudong. "3-D cell-based high-throughput screening for drug discovery and cell culture process development." Columbus, Ohio : Ohio State University, 2008. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1204701561.

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Perera, Hettiarachchige Dhanuja Deepamalee. "Molecular Basis of the Role of Kindlin 2 in Cell Adhesion." Cleveland State University / OhioLINK, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=csu1295461683.

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Allan, Kristin. "Exploring the Roles of Muller Glia and Activated Leukocyte Cell Adhesion Molecule A in Zebrafish Retinal Regeneration." Case Western Reserve University School of Graduate Studies / OhioLINK, 2021. http://rave.ohiolink.edu/etdc/view?acc_num=case1607705752486913.

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Moose, Holly Elizabeth. "Intrinsic Mechanisms Governing Retinal Progenitor Cell Biology: Retinal Homeobox Transcriptional Regulation and the Function of Forkhead Transcription Factors During Eye Development." The Ohio State University, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=osu1251827616.

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Santanam, Urmila. "Role of microRNA-29 in the Pathogenesis of B-Cell Chronic Lymphocytic Leukemia." The Ohio State University, 2010. http://rave.ohiolink.edu/etdc/view?acc_num=osu1281447982.

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Kanji, Suman. "Nanofiber-expanded human umbilical cord blood-derived CD34+ stem cell-mediated wound healing and underlying mechanisms." The Ohio State University, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=osu1376957233.

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Garlid, Anders Olav. "Mitochondrial Reactive Oxygen Species (ROS): Which ROS is Responsible for Cardioprotective Signaling?" PDXScholar, 2014. https://pdxscholar.library.pdx.edu/open_access_etds/1641.

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Mitochondria are the major effectors of cardioprotection by procedures that open the mitochondrial ATP-sensitive potassium channel (mitoKATP), including ischemic and pharmacological preconditioning. MitoKATP opening leads to increased reactive oxygen species (ROS), which then activate a mitoKATP-associated PKCε, which phosphorylates mitoKATP and leaves it in a persistent open state (Costa, ADT and Garlid, KD. Am J Physiol 295, H874-82, 2008). Superoxide (O2•-), hydrogen peroxide (H2O2), and hydroxyl radical (HO•) have each been proposed as the signaling ROS but the identity of the ROS responsible for this feedback effect is not known. Superoxide was excluded in earlier work on the basis that it does not activate PKCε and does not induce mitoKATP opening.To further examine the identity of the signaling ROS, respiring rat heart mitochondria were preincubated with ATP and diazoxide to induce the phosphorylation-dependent open state, together with agents that may interrupt feedback activation of mitoKATP by ROS scavenging or by blocking ROS transformations. Swelling assays of the preincubated mitochondria revealed that dimethylsulfoxide (DMSO), dimethylformamide (DMF), deferoxamine, trolox, and bromoenol lactone (BEL) each blocked the ROS-dependent open state but catalase did not interfere with this step. The lack of a catalase effect and the inhibitory effects of agents acting downstream of HO• excludes H2O2 as the endogenous signaling ROS and focuses attention on HO•. In support of the hypothesis that HO• is required, we also found that HO•-scavenging by DMF blocked cardioprotection by both ischemic preconditioning and diazoxide in the Langendorff perfused rat heart. HO• itself cannot act as a signaling molecule, because its lifetime is too short and it reacts immediately with nearest neighbor phospholipids and proteins. Therefore, these findings point to a product of phospholipid peroxidation, such as hydroperoxy-fatty acids. Indeed, this hypothesis was supported by the finding that hydroperoxylinoleic acid (LAOOH) opens the ATP-inhibited mitoKATP in isolated mitochondria. This effect was blocked by the specific PKCε inhibitor peptide εV1-2, showing that LAOOH activates the mitoKATP-associated PKCε. During ischemia, catabolism of mitochondrial phospholipids is accelerated, causing accumulation of plasmalogens and free fatty acids (FA) in the heart by the action of calcium independent phospholipases A2 (iPLA2). We first assessed the role of FAs and hydroxy FAs on mitoKATP opening and cardioprotection. Swelling assays of isolated rat heart mitochondria showed that naturally formed free FAs inhibit mitoKATP opening and that they are more potent inhibitors of the pharmacological open state of mitoKATP than the phosphorylation-dependent open state. That is, sustained mitoKATP opening induced by the phosphorylation-dependent feedback loop is more resistant to FA inhibition than direct mitoKATP opening by a potassium channel opener. Moreover, rat hearts perfused with micromolar concentrations of FA were resistant to cardioprotection by diazoxide or ischemic preconditioning. Racemic bromoenol lactone (BEL), a selective inhibitor of iPLA2, confers protection to otherwise untreated Langendorff perfused hearts by preventing ischemic FA release. To bring this story full circle, BEL blocks protection afforded by preconditioning and postconditioning by preventing the iPLA2-mediated release of FAOOH generated in the conditioned heart. HO• resulting from mitoKATP opening oxidizes polyunsaturated fatty acid components of the membrane phospholipids, resulting in a peroxidized side chain. FAOOH must be released in order to act on the mitochondrial PKCε, and this is achieved by the action of iPLA2. iPLA2 is essential for most modes of cardioprotection because it catalyzes the release of FAOOH. This fully supports the hypothesis that the second messenger of cardioprotective ROS-mediated signaling is hydroperoxy fatty acid (FAOOH), a downstream oxidation product of HO•.

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Qin, Xiao. "The role of ASPP2 in intestinal homeostasis and tumourigenesis." Thesis, University of Oxford, 2017. https://ora.ox.ac.uk/objects/uuid:a2d76d06-4361-4a39-8050-fd8a66a29218.

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The intestinal epithelium represents one of the most actively renewing tissues in the body, and is widely used as a model system to study epithelial cell biology. ASPP2, a member of the ASPP (apoptosis stimulating protein of p53) protein family, has been shown to act as a regulator of epithelial cell polarity and tumour suppressor. This study investigated whether the dual function of ASPP2 is involved in the regulation of intestinal homeostasis and tumourigenesis, with a particular interest in the distinction between epithelial cell autonomous and non-autonomous mechanisms. Germline and intestinal epithelial cell-specific ASPP2 conditional knockout mice were employed in this study. Deficiency of ASPP2 in the intestinal epithelium resulted in delayed recovery from dextran sulfate sodium (DSS)-induced acute colitis, concurrent with a reduction in the expression of proinflammatory cytokines such as interleukin (IL)-1β and IL-6. Moreover, ASPP2-deficient mice showed increased susceptibility to Azoxymethane/DSS-induced colorectal tumourigenesis. While wild-type and ASPP2-deficient crypts showed similar incidence of tumour formation, the local immune microenvironment of ASPP2-deficient mice favoured tumour progression. The intestinal organoid culture was established to supplement in vivo experiments. The feasibility of the system was demonstrated with small intestinal organoids, in the context of proliferation, differentiation, and cell death. Using the established workflow, a colonic organoid-based tissue regeneration model was developed. The intrinsic susceptibility of organoids to DSS-induced cell death was not affected by the loss of ASPP2. However, ASPP2-deficient colonic organoids were less responsive to the pro-proliferative effects of IL-6, but were more sensitive to tumour necrosis factor-α-induced cell death in the presence of IL-22. In conclusion, this project undertook parallel examinations of animal models and organoids, demonstrating that a deficiency of ASPP2 in the intestinal epithelium results in dysregulated epithelial-immune cell interactions. This may partially explain the pathological conditions observed in ASPP2-deficient mice. Importantly, this study highlights the possibility of using organoids to investigate epithelial cell non-autonomous factors implicated in intestinal pathogenesis.

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Yan, Kenneth. "Instructional Cues for Hierarchy Maintenance in Glioblastoma Multiforme." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1404169880.

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Burger, Lena F. "Characterisation of a novel tick-derived dendritic cell modulator, Japanin." Thesis, University of Oxford, 2014. http://ora.ox.ac.uk/objects/uuid:cbe8d327-8907-40ab-b410-36c21011f4db.

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Dendritic cells (DC) play a key role in immunity and represent a great target for modulation, because of their ability to prime T cells and direct their polarisation into effector subsets. Ticks release immunomodulatory compounds in their saliva, possibly in order to evade host immune responses during feeding. We have recently reported that Rhipicephalus appendiculatus ticks produce ‘Japanin’, a secretory lipocalin that arrests differentiation of monocytes into DC and reprogrammes maturation of DC in response to various stimuli towards a tolerogenic phenotype . Japanin was cloned and recombinantly expressed in a baculovirus system for subsequent immunological and biochemical analysis. This study was set out to further investigate the immunomodulatory activity of Japanin as well as the underlying mechanism of action. We have discovered that Japanin prevents DC-mediated proliferation and polarisation of allogeneic T cells. Experiments with labelled Japanin have demonstrated that it binds predominantly to ex vivo generated human monocyte-derived DC (moDC) and to a reduced degree to monocyte and DC populations in peripheral blood, yet to no other blood leucocytes. We have identified CD206, also known as the mannose receptor, as a Japanin-binding receptor on moDC. This identification has been achieved by crosslinking and subsequent pull-down of Japanin-receptor complexes from moDC. Affinity studies with recombinant CD206 constructs have confirmed the binding to Japanin. Moreover, the binding has been verified by specific siRNA knock-down of CD206 in moDC, which resulted in significantly decreased binding of Japanin. Unexpectedly, CD206 has appeared to be dispensable for at least most of the DC-modulatory activity of Japanin. Therefore, attempts were made to determine other factors in the mode of action of Japanin, through which we have found that IL-10 is not essentially involved. Further results have suggested that the activity of Japanin demands cell contact. Collectively, we have come to the conclusion that the mechanism of action of Japanin might require internalisation by DC, potentially enabling modulation of intracellular pathways involved in the regulation of DC maturation.

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Venugopal, Smrruthi Vaidegi. "Differential Roles of Mammalian Target of Rapamycin Complexes 1 and 2 in Migration of Prostate Cancer Cells." DigitalCommons@Robert W. Woodruff Library, Atlanta University Center, 2019. http://digitalcommons.auctr.edu/cauetds/189.

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In this study, we investigated differential activation and the role of two mTOR complexes in cell migration of prostate cancer cells. Specific knock-down of endogenous RAPTOR and RICTOR by siRNA resulted in decreased cell migration in LNCaP, DU145, and PC3 cells indicating that both mTORC1 and mTORC2 are required for cell migration. EGF treatment induced the activation of both mTORC1 and mTORC2 as determined by complex-specific phosphorylation of mTOR protein. Specific knock-down or inhibition of Rac1 activity in PC3 cells blocked EGF-induced activation of mTORC2, but had no effect on mTORC1 activation. Furthermore, the over-expression of constitutively active Rac1 (Rac1Q61L) resulted in significant increase in cell migration and activation of mTORC2 in PC3 cells, but had no effect on mTORC1 activation. Constitutively active Rac1 (Rac1Q61L) in PC3 cells was localized in the plasma membrane and was found to be in a protein complex which contained mTOR and RICTOR proteins, but not RAPTOR. In conclusion, we suggested that EGF-induced activation of Rac1 causes the phosphorylation/activation of mTORC2 via RICTOR, specific regulator of mTORC2 activation in numerous cancer cells. The major role played by mTOR in a wide array of cancers has in the recent decades led to the development of numerous mTOR inhibitors. One of the drawback of these first generation mTOR inhibitors are that m TORC1 activity is inhibited but effect on mTORC2 activity require high dosages and prolonged exposure in different cancer cell types including HeLa, PC3, LNCaP, and A549. High dosage of rapamycin and its associated rapalogs required for mTORC2 inhibition is clinically unsuitable. Studies have shown that the dual mTORC1/C2 inhibitors trigger feedback loops causing metastasis and affect the cell viability of normal tissues in vitro and in vivo. There is a need for specific mTORC1 and mTORC2 inhibitor, which overcome the disadvantages of the previously developed mTOR inhibitors. The Rac1-RICTOR axis suggested in this study could be used as a potential target for the development of mTORC2 inhibitor and lead to a potential therapeutic treatment for aggressive prostate cancer.

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Schumacher, Linus J. "A mathematical exploration of principles of collective cell migration and self-organisation." Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:bba68d2c-352b-4310-89c2-b9049b70515c.

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This thesis explores the role of collective cell migration and self-organisation in the development of the embryo and in vitro tissue formation through mathematical and computational approaches. We consider how population heterogeneity, microenvironmental signals and cell-cell interactions facilitate cells to collectively organise and navigate, with the aim to work towards uncovering general rules and principles, rather than delving into the microscopic molecular details. To ensure the biological relevance of our results, we collaborate closely with experimental biologists working on two model systems. First, to understand how neural crest cells obtain directionality, maintain persistence and specialise during their migration, we use computational simulations in parallel with imaging of chick embryos under genetic and surgical perturbations. We show how only a few cells adopting a leader state that enables them to read out chemical signals can lead a population of cells in a follower state over long distances in the embryo. Furthermore, we devise and test an improved mechanism of how cells dynamically switch between leader and follower states in the presence of a chemoattractant gradient. Our computational work guides the choice of new experiments, aids in their interpretation and probes hypotheses in ways the experiments can not. Secondly, to study the self-organisation of mouse skin cells in vitro, we draw on aggregation processes and scaling theory. Dermal and epidermal cells, after being dissociated and mixed, can reconstitute functional (transplantable and hair-growing) skin in culture. Using kinetic aggregation models and scaling analysis we show that the initial clustering of epidermal cells can be described by Smoluchowski coagulation, consistent with the dynamics of the "clustering clusters" universality class. Then, we investigate a potential mechanism for the size-regulation of cell aggregates during the later stages of the skin reconstitution process. Our analysis shows the extent to which this tissue formation follows a single physical process and when the transition to different dynamics occurs, which may be triggered by cellular biochemical changes.

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Chang, Hana. "Toward Clinical Stem Cell Sourcing And Definition Of Prescriptive Biophysical Protocols To Guide Stem Cell Fate During Healing." Case Western Reserve University School of Graduate Studies / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=case1370014612.

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Dissertations / Theses on the topic 'Cell biology research'

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