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1
Cheng, Wai. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation /". View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36433937.
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Cheng, Wai, i 鄭蔚. "The relationship between peroxisome proliferator-activated receptors (PPARs) and cell proliferation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010614.
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Jemec, Barbara. "Proliferation and action of an anti-proliferative agent in Dupuytren's fibroblast cultures". Thesis, University College London (University of London), 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.343601.
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Veerapen, Pierce Elaine. "Proliferation in astrocytomas". Thesis, University of Greenwich, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245348.
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Green, Daniel M. "Monitoring technology proliferation: an open source methodology for generating proliferation intelligence". Thesis, Monterey, California. Naval Postgraduate School, 1993. http://hdl.handle.net/10945/39686.
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Approved for public release; distribution is unlimited.This thesis develops a methodology to monitor technology proliferation. It is designed to provide proliferation intelligence on specific threat technologies and can be used to augment export controls or enhance counter proliferation initiatives. A high-te
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Miller, Nicholas L. (Nicholas LeSuer). "Hegemony and nuclear proliferation". Thesis, Massachusetts Institute of Technology, 2014. http://hdl.handle.net/1721.1/95553.
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Thesis: Ph. D., Massachusetts Institute of Technology, Department of Political Science, 2014.Cataloged from PDF version of thesis.
Includes bibliographical references (pages 277-292).
Contrary to longstanding of predictions of nuclear tipping points, the number of states interested in nuclear weapons has sharply declined in recent decades. In contrast to existing explanations, this dissertation argues that the decline is largely attributable to US nonproliferation policies, in particular the threat of sanctions that was instituted in the late 1970s. By credibly threatening to cut off economic and military support to countries pursuing nuclear weapons, I argue that this threat of sanctions deters states within the US sphere of influence from proliferating, reducing the overall rate of proliferation and also explaining why recent nuclear aspirants have exclusively been "rogue" states outside the US sphere of influence. Because states that depend on the United States have been deterred from proliferating in recent decades, the observed success rate of sanctions should be low, since they will generally be targeted at states that do not rely on US resources. This dissertation also offers a theory of the sources of US nonproliferation policy, arguing that fears of nuclear domino effects are necessary to explain (1) why US policy strengthened so dramatically in the wake of Chinese and Indian nuclear tests in the 1960s and 1970s, and (2) why the US abandoned a selective nonproliferation policy and decided to enforce nonproliferation across the board. To test these two arguments, this dissertation employs a mix of quantitative and qualitative methods. First, I draw on archival documents to show that fears of nuclear domino effects motivated US nonproliferation policy advances in the 1960s and 1970s, and that this motivation was prominent in individual cases of nonproliferation. Second, I show quantitatively that states dependent on the United States have been less likely to pursue nuclear weapons since sanctions policies were instituted in the late 1970s, that observed cases of sanctions have been largely ineffective, and that the deterrent effect of sanctions largely accounts for the temporal decline in proliferation. Case studies of US policy toward Pakistan and Taiwan demonstrate that a credible threat of sanctions can arrest ongoing nuclear programs when the proliferator is dependent on the United States and underestimated the likelihood of sanctions.
by Nicholas L. Miller.
Ph. D.
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Li, Xiaoling. "Peroxisome proliferation and division". Available to US Hopkins community, 2002. http://wwwlib.umi.com/dissertations/dlnow/3080712.
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Renda, Guido. "Resisting Nuclear Proliferation Through Design : a Systems Approach to Nuclear Proliferation Resistance Assessment". Thesis, University of Bristol, 2008. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.520167.
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Du, Zhenjian Cheung H. Tak. "Febrile condition and lymphocyte proliferation". Normal, Ill. Illinois State University, 1991. http://wwwlib.umi.com/cr/ilstu/fullcit?p9203029.
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Thesis (Ph. D.)--Illinois State University, 1991.Title from title page screen, viewed December 8, 2005. Dissertation Committee: H. Tak Cheung (chair), Herman E. Brockman, Lynne A. Lucher, Anthony J. Otsuka, Alan J. Katz. Includes bibliographical references (leaves 99-110) and abstract. Also available in print.
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Ashagbley, Anthony J. "Ethanolamine requirement and cell proliferation". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp04/mq23203.pdf.
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Falk, Anna. "Stem cells : proliferation, differentiation, migration /". Stockholm, 2005. http://diss.kib.ki.se/2006/91-7140-497-X/.
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Frankenstein, William. "Computational Models of Nuclear Proliferation". Research Showcase @ CMU, 2016. http://repository.cmu.edu/dissertations/782.
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This thesis utilizes social influence theory and computational tools to examine the disparate impact of positive and negative ties in nuclear weapons proliferation. The thesis is broadly in two sections: a simulation section, which focuses on government stakeholders, and a large-scale data analysis section, which focuses on the public and domestic actor stakeholders. In the simulation section, it demonstrates that the nonproliferation norm is an emergent behavior from political alliance and hostility networks, and that alliances play a role in current day nuclear proliferation. This model is robust and contains second-order effects of extended hostility and alliance relations. In the large-scale data analysis section, the thesis demonstrates the role that context plays in sentiment evaluation and highlights how Twitter collection can provide useful input to policy processes. It first highlights the results of an on-campus study where users demonstrated that context plays a role in sentiment assessment. Then, in an analysis of a Twitter dataset of over 7.5 million messages, it assesses the role of ‘noise’ and biases in online data collection. In a deep dive analyzing the Iranian nuclear agreement, we demonstrate that the middle east is not facing a nuclear arms race, and show that there is a structural hole in online discussion surrounding nuclear proliferation. By combining both approaches, policy analysts have a complete and generalizable set of computational tools to assess and analyze disparate stakeholder roles in nuclear proliferation.
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Hooper, Nigel I. "Methylglyoxal, glyoxalases and cell proliferation". Thesis, Aston University, 1987. http://publications.aston.ac.uk/12548/.
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The metabolic function of the glyoxalase system was investigated in (a) the differentiation and proliferation of human tumour cells in vitro, (b) the cell-free assembly of microtubules and (c) in the red blood cells during hyperglycaemia associated with Diabetes Mellitus. Chemically-induced differentiation of human promyelocytic HL60 leukaemia cells to neutrophils, and K562 erythroleukaemia cells, was accompanied by a decrease and an increase in the activity of glyoxalase I, respectively. Growth-arrest of Burkitt's lymphoma Raji cells and GM892 lymphoblastoid cells was accompanied by an increase and a decrease in the activity of glyoxalase I respectively. However, differentiation and growth arrest generally proceeded with an increase in the activity of glyoxalase II. Glyoxalase I activity did not consistently correlate with cell differentiation or proliferation status; hence, it is unlikely that glyoxalase I activity is either an indicator or a regulator of cell differentiation or proliferation. Conversely, glyoxalase II activity consistently increased during cell differentiation and growth-arrest and may be both an indicator and regulator of cell differentiation or proliferation. This may be related to the control of cellular microtubule assembly. S-D-Lactoylglutathione potentiated the cell-free, GTP-promoted assembly of microtubules. The effect was dose-related and was inhibited by glyoxalase II. During assembly, S-D-lactoylglutathione was consumed. This suggests that the glyoxalase system, through the influence of S-D-lactoylglutathione, may regulate the assembly of microtubules in cellular systems The whole blood concentrations of methylglyoxal and S-D-lactoylglutathione were increased in Diabetes Mellitus. There was no significant difference between red blood cell glyoxalase activities in diabetics, compared to healthy controls. However, insulin-dependent diabetic patients with retinopathy had a significantly higher glyoxalase I activity and a lower glyoxalase II activity, than patients without retinopathy. Diabetic retinopathy correlated with high glyoxalase I activity and low glyoxalase II activity and suggests the glyoxalase system may be involved in the development of diabetic complications.
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Hutley, Louise Joyce. "Human preadipocyte proliferation and differentiation". Thesis, Queensland University of Technology, 2002. https://eprints.qut.edu.au/37117/6/37117_Digitised_Thesis.pdf.
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Obesity represents a major health, social and economic burden to many developing and Westernized communities, with the prevalence increasing at a rate exceeding almost all
other medical conditions. Despite major recent advances in our understanding of adipose tissue metabolism and dynamics, we still have limited insight into the
regulation of adipose tissue mass in humans. Any significant increase in adipose tissue mass requires proliferation and differentiation of precursor cells (preadipocytes) present in the stromo-vascular compartment of adipose tissue. These processes are very
complex and an increasing number of growth factors and hormones have been shown to modulate the expression of genes involved in preadipocyte proliferation and
differentiation. A number of transcription factors, including the C/EBP family and PP ARy, have been identified as integral to adipose tissue development and preadipocyte
differentiation. Together PP ARy and C/EBPa regulate important events in the activation and maintenance of the terminally differentiated phenotype. The ability of
PP ARy to increase transcription through its DNA recognition site is dependent on the
binding of ligands. This suggests that an endogenous PP ARy ligand may be an important regulator of adipogenesis. Adipose tissue functions as both the major site of
energy storage in the body and as an endocrine organ synthesizing and secreting a number of important molecules involved in regulation of energy balance. For optimum
functioning therefore, adipose tissue requires extensive vascularization and previous studies have shown that growth of adipose tissue is preceded by development of a
microvascular network. This suggests that paracrine interactions between constituent cells in adipose tissue may be involved in both new capillary formation and fat cell
growth. To address this hypothesis the work in this project was aimed at (a) further development of a method for inducing preadipocyte differentiation in subcultured
human cells; (b) establishing a method for simultaneous isolation and separate culture of both preadipocytes and microvascular endothelial cells from the same adipose tissue
biopsies; (c) to determine, using conditioned medium and co-culture techniques, if endothelial cell-derived factors influence the proliferation and/or differentiation of
human preadipocytes; and (d) commence characterization of factors that may be responsible for any observed paracrine effects on aspects of human adipogenesis.
Major findings of these studies were as follows:
(A) Inclusion of either linoleic acid (a long-chain fatty acid reported to be a naturally occurring ligand for PP ARy) or Rosiglitazone (a member of the thiazolidinedione class of insulin-sensitizing drugs and a synthetic PPARy ligand) in differentiation medium had markedly different effects on preadipocyte differentiation. These studies showed that human preadipocytes have the potential to accumulate triacylglycerol irrespective of their stage of biochemical differentiation, and that thiazolidinediones and fatty acids may exert their adipogenic and lipogenic effects via different biochemical pathways. It
was concluded that Rosiglitazone is a more potent inducer of human preadipocyte differentiation than linoleic acid.
(B) A method for isolation and culture of both endothelial cells and preadipocytes from the same adipose tissue biopsy was developed. Adipose-derived microvascular endothelial cells were found to produce factor/s, which enhance both proliferation and differentiation of human preadipocytes.
(C) The adipogenic effects of microvascular endothelial cells can be mimicked by exposure of preadipocytes to members of the Fibroblast Growth Factor family, specifically ~-ECGF and FGF-1. (D) Co-culture of human preadipocytes with endothelial cells or exposure of
preadipocytes to either ~-ECGF or FGF-1 were found to 'prime' human preadipocytes, during their proliferative phase of growth, for thiazolidinedione-induced differentiation. (E) FGF -1 was not found to be acting as a ligand for PP ARy in this system. Findings from this project represent a significant step forward in our understanding of factors involved in growth of human adipose tissue and may lead to the development of
therapeutic strategies aimed at modifying the process. Such strategies would have potential clinical utility in the treatment of obesity and obesity related disorders such as
Type II Diabetes.
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Reed, Brian K. "Models for proliferation interdiction response analysis". Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 1994. http://handle.dtic.mil/100.2/ADA288645.
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Thesis (M.S. in Operations Research) Naval Postgraduate School, September 1994.Thesis advisor(s): David Morton, Peter Lavoy. "September 1994." Includes bibliographical references. Also available online.
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Nichols, Patti J. "Understanding China's nuclear non-proliferation policy". Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 1999. http://handle.dtic.mil/100.2/ADA366857.
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Thesis (M.A. in National Security Affairs) Naval Postgraduate School, June 1999."June 1999". Thesis advisor(s): Rodney Kennedy-Minott, Denny Roy. Includes bibliographical references (p. 103-108). Also available online.
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McDermott, Paul B. "Proliferation mechanisms in Methanothermobacter thermautotrophicus DeltaH". Thesis, University of York, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.485452.
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Petersen, Cecilia. "Paracrine regulation of Sertoli cell proliferation /". Stockholm, 2003. http://diss.kib.ki.se/2003/91-7349-443-7/.
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Gan, Lisha. "Corneal cellular proliferation and wound healing /". Stockholm, 2000. http://diss.kib.ki.se/2000/91-628-4505-5/.
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Yamak, Fatimah Abir. "GATA4 Partners in Cardiac Cell Proliferation". Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23802.
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Cardiovascular diseases are the leading cause of death in humans throughout the world and “congenital heart defects” (CHDs) are the major cause of infant mortality and morbidity. GATA4 is one of the most critical and intensely studied cardiac transcription factor. It is important for proliferation of cardiomyocytes as well as their survival and adaptive response. The focus of the following thesis was to identify GATA4 mediators and cofactors in cardiac growth. The first part focused on cyclin D2 (CycD2), a growth inducible cell cycle protein. We identified Ccnd2 (gene encoding CycD2) as a direct transcriptional target of GATA4 in postnatal cardiomyocytes and Ccnd2 cardiomyocyte specific overexpression in Gata4 heterozygote mice was able to rescue their heart size and function. We further uncovered a novel regulatory loop between GATA4 and CycD2. CycD2 enhanced GATA4 activation of its target promoters. GATA4 was able to physically interact with CycD2 and its cyclin dependent kinase CDK4 suggesting that GATA4 recruits CycD2/CDK4 to its target promoters. Together, our data uncover a role of CycD2 in the developing and postnatal heart and provide novel insight for the potential of targeting the cell cycle in cardiac therapy. The second part of the project focused on KLF13, a cell specific cofactor of GATA4. KLF13 is a member of the Krϋppel-like transcription factors that are important regulators of cell proliferation and differentiation. Klf13 is highly enriched in the developing heart where it is found in both myocardial and endocardial cells. To determine its role in the mammalian heart, we deleted the Klf13 gene in transgenic mice. Klf13-/- mice were born at 50% reduced frequency and presented with variable cardiac phenotypes. Epithelial-mesenchymal transformation (EMT) was affected in these mice and reduced cell proliferation was evident in the AV cushion. These data uncover a role for a new class of transcription factors in heart formation and point to KLF13 as a regulator of endocardial cell proliferation and a potential CHD causing gene. Future discovery of more cardiac regulators and understanding the molecular basis of CHDs is essential for preventions of these defects and possible development of therapeutic approaches for myocardial repair.
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Åkesson, Lovisa. "Identifikation av proteinmarkörer för cellulär proliferation". Thesis, KTH, Skolan för bioteknologi (BIO), 2015. http://urn.kb.se/resolve?urn=urn:nbn:se:kth:diva-170359.
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Cheung, Man-keung, i 張文強. "FBI-1 and choriocarcinoma cell proliferation". Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2013. http://hdl.handle.net/10722/193565.
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Gestational trophoblastic disease (GTD) includes a spectrum of diseases that involve abnormal growth of trophoblastic cells inside the uterus. It can range from benign hydatidiform moles (HM) to frankly malignant choriocarcinoma, placental site trophoblastic tumor (PSTT) or epithelioid trophoblastic tumour (ETT).GTD are considered curable if the patient is correctly diagnosed and receive appropriate treatment during the early stage of the disease.
About 15% -30% of hydatidiform moles will develop persistent GTD, but majority of them can usually resolved by surgical intervention and post-operation weekly serial serum β-hCG level monitoring. In contrast, choriocarcinoma is a frankly malignant gestational trophoblastic neoplasm (GTN). Most choriocarcinoma arise from HM but can develop from any pregnancy related events such as ectopic pregnancy, live-birth or stillbirth. Being the most aggressive neoplasm in GTD, choriocarcinoma can develop widespread metastasis and can be fatal.
FBI-1 (Pokemon) is a transcription factor that is often overexpressed in various types of human cancer. We have reported overexpression of FBI-1 in ovarian cancer in association with cell proliferation and invasiveness. Our recent study also suggested that overexpression of FBI-1 in HM was related to subsequent development of gestational trophoblastic neoplasms(GTN).
In this study, we evaluated the role of FBI-1 inchoriocarcinoma cell proliferation. By MTT assay, the proliferation rates of two choriocarcinoma cell lines (JAR and JEG-3) was found to decrease when FBI-1 was downregulated by shRNA approach with statistical significance reached in JEG-3 (p < 0.05). By quantitative real time PCR, the relative levels of a panel of hedgehog pathway related genes, including SHH, SMO, GLI1, GLI2, GLI3, and KIF7 were assessed after knockdown of FBI-1 gene. Sonic hedgehog (SHH) was found to be consistently downregulated in JEG-3 and JAR transfected with FBI-1 shRNA constructs.
In conclusion, FBI-1 may play a role in choriocarcinoma cell proliferation and FBI-1 may be explored as a potential therapeutic target for GTD in the future.published_or_final_version
Pathology
Master
Master of Medical Sciences
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Bell, Alexander. "The molecular basis of peroxisome proliferation". Thesis, University of Nottingham, 1998. http://eprints.nottingham.ac.uk/10395/.
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Characterisation of expression of functional Peroxisome Proliferator Activated Receptora (PPARalpha)receptor in rodent species responsive and non-responsive to peroxisome proliferators is important for our understanding of the molecular mechanism of peroxisome proliferation and peroxisome proliferator induced hepatocarcinogenesis. In vitro electromobility shift assays, demonstrated that rodent liver nuclear proteins (LNP) bound to a Peroxisome Proliferator Response Element (PPRE) in a sequence specific manner and that LNP from methylclofenapate (MCP) treated mice do not have enhanced binding to a PPRE. These results demonstrate that in MCP treated mice, PPAR alpha levels with functional DNA binding do not increase. The diurnal expression of mouse PPAR alpha (mPPARalpha) protein in liver was examined by western blotting. There was no observable difference in the expression of mPPARalpha across a 24 hour period. In C57 BL/6 mice, PPARalpha protein levels are not regulated in a diurnal manner. A comparison of mouse and guinea pig LNP revealed a PPARalpha-immunoreactive protein in guinea pig. Guinea Pig PPARalpha (gPPAR a) was cloned and found to encode a 467 amino acid protein. Phylogenetic analysis of gPPARalpha showed a high substition rate: maximum likelihood analysis was consistent with rodent monophyly, but could not exclude rodent polyphyly (p~0.07). The gPPAR alpha cDNA was expressed in 293 cells, and mediated the induction of the luciferase reporter gene by the peroxisome proliferator Wy-14,643, dependent upon the presence of a PPRE. The gPPAR alpha mRNA and protein was expressed in guinea pig liver, although at lower levels compared to PPAR alpha expression in mice. The evidence presented here supports the idea that guinea pigs serve as a useful model for human responses to peroxisome proliferators. mPPAR alpha DNA binding domain (mPPARalpha-DBD) was cloned and expressed as a fusion protein. Both His*6-mPPARalpha-DBD and thioredoxin-mPPARalpha-DBD were produced as insoluble proteins when over expressed in E.coli. In vitro translated mPPAR alpha-DBD did not bind to a PPRE in an electromobility shift assay.
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Adenrele, Festus Oladipo Ayinla. "Proliferation of nuclear weapons in Africa". Thesis, University of Glasgow, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.337530.
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Braut-Hegghammer, Malfrid. "Nuclear entrepreneurs : drivers of nuclear proliferation". Thesis, London School of Economics and Political Science (University of London), 2009. http://etheses.lse.ac.uk/2760/.
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What determines whether states pursuing nuclear weapons ultimately acquire them. More specifically, why do so few states stay committed to their nuclear weapons programmes over time. Theories of nuclear proliferation have not accounted for the causal role of external systemic factors and domestic agents in defining the political sustainability of nuclear weapons programmes. The efforts of entrepreneurial alliances between nuclear bureaucrats and governmental sponsors determine whether states remain committed to pursuing, and thus acquire, nuclear weapons. These alliances employ three causal mechanisms in seeking to secure their states' commitment to their nuclear weapons programmes: linking nuclear weapons with external threats, overcome resistance to investing in a nuclear infrastructure, and institutional 'insulation' from domestic critics. The entrepreneurial alliances are enabled and constrained by the economic and security environments facing their states. The entrepreneurial alliance hypothesis is tested in a series of case studies. First, the hypothesis is applied to detailed analyses of Libya and Iraq's nuclear weapons programmes. The hypothesis is tested as an explanation for why these states pursued nuclear weapons yet failed to acquire them. Furthermore, these cases facilitate process-tracing of the causal mechanisms and processes determining the outcomes of each state's nuclear weapons programme. Then, the hypothesis is applied to a corroborative analysis of four smaller case studies: India, Pakistan, Egypt and Australia. These cases include two authoritarian and two non-authoritarian states comprising two successful nuclear weapons programmes (India and Pakistan) and two that failed to cross the nuclear weapons threshold (Egypt and Australia). The entrepreneurial alliance hypothesis is found to provide a strong and unique explanation for what determines whether states pursuing nuclear weapons ultimately cross the nuclear weapons threshold. This framework identifies the determinants of the political sustainability of a nuclear weapons programme and what factors influence a state's prospects for acquiring such weapons.
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Dunphy, Elizabeth Louise. "TAF1 HAT activity in cell proliferation /". Thesis, Connect to this title online; UW restricted, 2003. http://hdl.handle.net/1773/6250.
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Fiorentini, Enrico. "Avoiding non-proliferation atrophy: the effectiveness of multilateral cooperation, regime dynamics and the case of nuclear non-proliferation". Doctoral thesis, Università degli studi di Trento, 2018. https://hdl.handle.net/11572/367756.
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This project investigates the evolution multilateral nuclear non-proliferation arrangements to prevent state and non-state actors to access potentially destructive weapons and components thereof. While less scrutinized by political scientists and security experts, cooperative frameworks abound in practice. This begets questions as to the mechanisms and processes by which actors effectively cooperate in a crowded, complex and pluralist environment. Which factors determine the success and resilience of non-proliferation arrangements? How much explanatory power do cognitive beliefs and institutional practices command to understand and explain variance in governance effectiveness?
While previous studies have focused on the ‘front-end’ of cooperation by examining factors leading states to cut deals, others have focused on the ‘back-end’ by focusing on the role of military and diplomatic means, such as alliances, coercion and the role of law. In addition, while scholarship on cooperation neglects sovereignty-conscious issues, non-proliferation studies disregard what happens between the ‘front- and the backend’ of the cooperation loop.
This work analyzes three arrangements – the review process of the Nuclear Non- Proliferation Treaty, U.N. Security Council Resolution 1540 and the Nuclear Security Summits. Using case study analysis, elite interviews and participant observation, this study undertakes an investigation from a cognitivist perspective and examines the “principles, norms, rules, and decision-making procedures†governing non-proliferation.
While factors related to knowledge and learning affect actors' understandings of risks and their mitigation pathways, their impact is intertwined with idiosyncratic factors, with crisis as overarching and crosscutting thread. Theoretically, compared to neorealism and neoliberal institutionalism, cognitive approaches to international regimes provide the most cogent explanations to account for governance effectiveness, but cannot wholly explain a case. Operatively, effective and resilient nuclear non-proliferation governance should provide for permanent interaction whereby novel implementation and monitoring mechanisms are experimented in a sovereignty-respecting way.
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Fiorentini, Enrico. "Avoiding non-proliferation atrophy: the effectiveness of multilateral cooperation, regime dynamics and the case of nuclear non-proliferation". Doctoral thesis, University of Trento, 2018. http://eprints-phd.biblio.unitn.it/3085/1/PhD_Thesis_EnricoFiorentini.pdf.
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This project investigates the evolution multilateral nuclear non-proliferation arrangements to prevent state and non-state actors to access potentially destructive weapons and components thereof. While less scrutinized by political scientists and security experts, cooperative frameworks abound in practice. This begets questions as to the mechanisms and processes by which actors effectively cooperate in a crowded, complex and pluralist environment. Which factors determine the success and resilience of non-proliferation arrangements? How much explanatory power do cognitive beliefs and institutional practices command to understand and explain variance in governance effectiveness?
While previous studies have focused on the ‘front-end’ of cooperation by examining factors leading states to cut deals, others have focused on the ‘back-end’ by focusing on the role of military and diplomatic means, such as alliances, coercion and the role of law. In addition, while scholarship on cooperation neglects sovereignty-conscious issues, non-proliferation studies disregard what happens between the ‘front- and the backend’ of the cooperation loop.
This work analyzes three arrangements – the review process of the Nuclear Non- Proliferation Treaty, U.N. Security Council Resolution 1540 and the Nuclear Security Summits. Using case study analysis, elite interviews and participant observation, this study undertakes an investigation from a cognitivist perspective and examines the “principles, norms, rules, and decision-making procedures” governing non-proliferation.
While factors related to knowledge and learning affect actors' understandings of risks and their mitigation pathways, their impact is intertwined with idiosyncratic factors, with crisis as overarching and crosscutting thread. Theoretically, compared to neorealism and neoliberal institutionalism, cognitive approaches to international regimes provide the most cogent explanations to account for governance effectiveness, but cannot wholly explain a case. Operatively, effective and resilient nuclear non-proliferation governance should provide for permanent interaction whereby novel implementation and monitoring mechanisms are experimented in a sovereignty-respecting way.
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Lafenêtre, Pauline. "Regulation der Proliferation im Hippocampus adulter Mäuse". [S.l.] : [s.n.], 2005. http://deposit.ddb.de/cgi-bin/dokserv?idn=979107407.
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Barretta, Michael A. "Nuclear proliferation and the stability-instability paradox". Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 1995. http://handle.dtic.mil/100.2/ADA304388.
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Talay, Brian J. "Preventing ballistic missile proliferation : lessons from Iraq /". Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 1996. http://handle.dtic.mil/100.2/ADA326672.
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Thesis (M.A. in National Security Affairs) Naval Postgraduate School, December 1996.Thesis advisor(s): Peter R. Lavoy. "December 1996." Includes bibliographical references (p. 97-100), Also available online.
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Roshan, Amit. "Stochasticity and order : studies of keratinocyte proliferation". Thesis, University of Cambridge, 2014. https://www.repository.cam.ac.uk/handle/1810/252966.
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A central tenet of stem cell biology has been that proliferating tissues are maintained through a cellular hierarchy comprising of self-renewing stem cells at the apex, multiple lineage-restricted short-lived progenitor cells, and post-mitotic differentiated cells. The wide range of colony sizes in cultured human keratinocytes has been taken to support this hypothesis. Contrary to this model, researchers using genetic lineage tracing in mouse epidermis have inferred a single progenitor population for homeostasis, and a quiescent stem cell population activated upon wounding or genetic mutation. To study the proliferative behaviour of human keratinocytes, I used live imaging in vitro at single cell resolution. This shows two modes of proliferation: Type 1 cell division is stochastic with equal odds of generating dividing or non-dividing progeny, while Type 2 cell division predominantly produces two dividing daughters. These two modes are sufficient to explain the entire range of colony sizes seen after 7-12 days of culture and does not require a spectrum of proliferative ability. This insight provides a simple way to study the effects of external factors on cell fate. To exemplify this, I observed the effects of epidermal growth factor (EGF) and the Wnt agonist R-spondin on proliferation. Here I find proliferation in type 2 colonies changes by changing the proportion of cells dividing. This has implications for the limited success of EGF therapies in clinical trials following burns. To examine clonal contributions to wound repair, I used the mouse oesophageal epithelium which is exclusively composed of, and maintained by, a single progenitor population. I developed a micro-endoscopic wounding technique that produced localised superficial wounds. Here, I found that these wounds healed by uniform contribution from surrounding keratinocytes, demonstrating that reserve stem cells are not obligatory for wound repair. In summary, my work shows that human keratinocytes in vitro have two, and only two, modes of proliferation: a stochastic mode that is insensitive to external EGF signalling, and a EGF-sensitive exponential mode. Additionally, proliferation during wound repair can occur with stochastically dividing progenitors, and does not obligate stem cell recruitment in vivo.
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Currie, Ian Stewart. "Proliferation and maturation in developing human liver". Thesis, University of Edinburgh, 2006. http://hdl.handle.net/1842/27856.
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In order to understand how human liver cells can proliferate and differentiate in vitro, a culture system was developed to support second trimester fetal liver cells. Having characterised the culture system, and demonstrated viable hepatocytes after seven days in vitro, cells were incubated with growth factors and cytokines and subject to two-colour flow cytometry to assess which cell fraction might proliferate in vitro. Experiments were then carried out to determine which circulating endocrine stimuli might initiate morphologic and functional maturation in the developing hepatocytes. Finally, urea metabolism and protein secretion were assessed in the presence and absence of glucocorticoid and different growth factors, to assess the interaction of these various stimuli at a functional level. Incubation with growth factors and cytokines showed that EGF alone caused cellular proliferation. This proliferation occurred within a primitive epithelial fraction, positive for cytokeratin 18, but negative for fibrinogen. The results showed that glucocorticoid alone brought about functional maturation in terms of increased protein secretion, with significant increases observed in α-fetoprotein, fibrinogen and α-1-antichymotrypsin secretion. This represented increased secretion per cell, as there was no effect of glucocorticoid on cell proliferation. Final experiments showed that EGF and HGF had modest stimulatory effects on urea synthesis. By contrast, KGF reduced urea synthesis by channelling ammonia into anabolic pathways. With regard to protein secretion, EGF inhibited fibrinogen and α-1-antichymotrypsin secretion, whereas, tumour necrosis factor inhibited fibrinogen alone. All of these observations were made only in the presence of dexamethasone. These data provide a frame of reference from which to develop cell-based therapies for the treatment of liver failure in clinical practice.
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Walker, John Ronald. "British attitudes to nuclear proliferation, 1952-1982". Thesis, University of Edinburgh, 1987. http://hdl.handle.net/1842/27024.
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British attitudes to proliferation cannot really be understood without reference to the historical, strategic and economic background of Britain's own nuclear programmes. The experiences and lessons learned during the civil and military programmes in the 1950s and 1960s played a crucial role in shaping British perceptions of, and attitudes to, the proliferation issue. The relationship between civil and military technology is important here because nuclear energy cannot be used as a source of power without simultaneous production of material suitable for use in a bomb. Two issues are revelant here; first, the actual relationship between the British civil and military programmes; second, British conception of the longterm proliferation implications of these relationships. Successive British governments have regarded possession of nuclear weapons as fundamental to British national security, but they have also sought to prevent their spread to other states. However, in the British case American policies between 1946 and 1953, and subsequently, were instrumental in encouraging independent nuclear programmes. These sought to maintain the US monopoly over nuclear materials and technology by making it illegal for the US to provide either to other countries including Britain. However, this only encouraged proliferation. US unreliability and policies based on denial appear to have persuaded successive British governments of the value of a stable and predictable international non-proliferation regime. Consequently it was considered important to maintain stability and predictability in international nuclear trade through assurance of supplies of nuclear materials, equipment and information subject to legitimate security considerations. This, it was thought, would reduce states' incentives to build indigenous sensitive fuel cycle facilities, and reduce hostility to the nonproliferation regime. British nuclear policies have remained basically unchanged, and have been instrumental in moulding British attitudes to proliferation. In the 1950s the perceived unreliability of the coal industry posed a threat to British energy security. This was the context in which the first nuclear power programme was launched. Nuclear power was thought to have potential benefits for energy security since it could provide reliable and predictable energy supplies. Reactor and fuel exports have always been a major objective of British nuclear policy notwithstanding the potential proliferation implications. British governments have never opposed the principle of nuclear exports on nonproliferation grounds; on the contrary, British nonproliferation policies have sought to defend UK commercial interests. During the 1960s commercial objectives became integrated with non-proliferation policy: there is no contradiction between commercial objectives and security requirements. They are mutually reinforcing. It is necessary to examine the British civil-military relationship; programme rationales and objectives; nuclear export policy and the military programme, before seeing how these have influenced British attitudes to, and policies on, proliferation. Part 2 examines the relationship between these factors and the British role in the Non- Proliferation Treaty negotiations and its 1975 and 1980 Review Conferences; the IAEA and Euratom safeguards systems; the International Nuclear Fuel Cycle Evaluation; the Nuclear Suppliers' Group; Multinational/Regional Fuel Cycle Centres; International Plutonium Storage and the Committee on the Assurance of Supply.
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Sutton, Selina Kaye. "How does mitochondrial heteroplasmy affect cell proliferation?" Thesis, University of Canterbury. Biological Sciences, 2006. http://hdl.handle.net/10092/1306.
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Mitochondrial mutations and heteroplasmy have been associated with disease states that result from inadequate cellular energy production. As mitochondrial DNA (mtDNA) encodes many of the polypeptides involved in oxidative phosphorylation (OXPHOS), mtDNA mutations may lower energy production which is required for cell division and sustained ATP synthesis. In order to test the relationship between mtDNA mutations and the rate of cell division, a mammary epithelial cancer cell line, MCF-7, is used as a model. Nine proliferate single cell clones have been isolated from MCF-7. Population doubling times of six single cell clones and the MCF-7 stock have been determined. Clones with distinctly different growth rates were selected for mutational analysis. Growth rates of these clones appeared to be different from each other. Using polymerase chain reaction (PCR) and DNA sequencing, three cases of heteroplasmy have been identified in the mitochondrial genes of the MCF-7 stock and four single cell clones (ATPase C9119T, ND6 T14300G, Cytb G15807A). Heteroplasmy present in the Cytb gene is differs between single cell clones. Differences between the growth rates may be indicative of metabolic variations in these single cell clones. The OXPHOS enzymes encoded by the mutated genes were quantified by standard enzymatic assays. The assays demonstrated significant differences in specific activity between the clones, but were not correlated with mitochondrial heteroplasmy. This thesis determines that the differences in specific activity observed between clones is of nuclear origin.
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Dorward, Ann M. "Hydrogen peroxide production and autocrine proliferation control". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp03/NQ66202.pdf.
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Wang, Yanling. "cAMP-Regulated Cell Proliferation in Brown Preadipocytes". Doctoral thesis, Stockholms universitet, Institutionen för molekylär biovetenskap, Wenner-Grens institut, 2013. http://urn.kb.se/resolve?urn=urn:nbn:se:su:diva-88393.
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As a prototypical second messenger, cAMP is involved in the regulation of multiple cell functions. cAMP has a well established inhibitory effect on cell proliferation in smooth muscle and epithelial cell types. However, there is accumulating evidence also for stimulatory effect on proliferation, mainly in endocrine cell types. Mechanisms mediating the cAMP stimulatory effect are not well studied. cAMP, produced via β1-adrenoceptor activation, promotes cell proliferation in brown preadipocytes. Due to the importance of brown adipose tissue in energy metabolism and its implication in the treatment of obesity and type II diabetes, understanding the mechanisms of tissue recruitment has clinical implication for the treatment of these metabolic syndromes. We found that the Erk1/2 family of MAPK, often involved in regulation of cell proliferation, can be activated in response to the stimulation of G protein-coupled receptors, including adrenergic receptors (α1-, α2-, β1- and β3-Adrenoceptors) and mitogenic lysophosphatidic acid (LPA) in primary cultured brown adipocytes. In contrast to the case e.g. in many immortalized cell lines and various primary cultured cells, EGF receptor transactivation is not employed in Erk1/2 activation by any G protein-coupled receptor tested in brown adipocytes. This suggests that EGF receptor transactivation is not an universal mediation process for GPCR activation of MAPK. cAMP-activated cell proliferation in brown preadipocytes is mediated through PKA rather than Epac under serum-free conditions. This effect is independent of PI3K/Akt, mTOR or Erk1/2 MAPK pathways. Differential responses to two different MEK inhibitors PD98059 and U0126 suggested the involvement of a pathway sensitive to PD98059, but independent of the Erk1/2 family of MAPK. At the transcriptional level, by combining microarray and RT-qPCR, we have identified eight genes, under the regulation of cAMP, that may be involved in the further mediation of the cAMP effect on cell proliferation. An understanding of cAMP-induced cell proliferation may be of importance both in metabolic and cancer research.At the time of the doctoral defense, the following papers were unpublished and had a status as follows: Paper 2: Submitted. Paper 3: Manuscript. Paper 4: Manuscript.
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Sohi, Jasloveleen. "Investigation of factors regulating parathyroid cell proliferation". Thesis, McGill University, 1994. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=55530.
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Parathyroid glands are responsible for maintaining normal extracellular calcium concentrations through their release of PTH. Calcium and 1,25-(OH)$ rm sb2D sb3$ have been demonstrated to be potent regulators of PTH and CgA synthesis and release. Primary cultures of quiescent bovine parathyroid cells proliferate in response to high concentrations of serum. Next, I examined the role of c-myc in the proliferation of the PT-r cell line, which was cloned from rat parathyroid cells. In order to study the role of c-myc in PT-r cell proliferation more precisely, I used antisense RNA technology to inhibit c-myc mRNA.In summary, my studies have shown that parathyroid cells respond to selected growth factors. This proliferative response involves increased expression of c-myc, c-fos, c-jun and PTHrP. 1,25-(OH)$ rm sb2D sb3$ inhibits the expression or c-myc, and cell proliferation is inhited. The differentiated parathyroid cell expresses high levels of CgA and PTH. However, during proliferation these high levels are not sustained.
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Whitworth, Emma Jane. "Adrenocortical proliferation and signal transduction 'in vitro'". Thesis, Queen Mary, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.415058.
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Woodman, Anthony C. "Studies on the control of hepatocyte proliferation". Thesis, Imperial College London, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.364568.
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Kranc, Kamil. "The role of Cited2 in cellular proliferation". Thesis, University of Oxford, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.398233.
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Kuffer, Christian. "Proliferation and arrest of human tetraploid cells". Diss., Ludwig-Maximilians-Universität München, 2015. http://nbn-resolving.de/urn:nbn:de:bvb:19-182558.
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Durch Fehler entstandene tetraploide Zellen sind chromosomal instabil und können zu Zelltransformation führen. Die Beweise verdichten sich, dass die Propagation von tetraploiden Säugetierzellen durch einen p53-vermittelten Arrest eingeschränkt wird; jedoch ist weiterhin unklar, was die Ursache dieses p53-vermittelten Arrests ist.
Um die Ursache des p53-vermittelten Arrests zu identifizieren, wurden individuelle Zellen mittels zeitraffender Mikroskopie in Echtzeit verfolgt. Neu entstandene tetraploide Zellen können einen Zellzyklus vollenden, aber die Mehrzahl der Zellen starb oder verharrte in einem Arrest in der folgenden G1-Phase, abhängig davon ob die vorangegangene Mitose fehlerfrei verlief oder nicht. Tochterzellen, denen eine fehlerhafte Mitose voranging, akkumulierten p53 im Zellkern, was zum Zelltod oder einem irreversiblen Zellzyklusarrest führte. Es zeigte sich durch den Anstieg von 8-OHdG, einem Indikator für oxidative DNA Schädigung, dass tetraploide Zellen durch die vermehrten fehlerhaften Mitosen höheren Konzentrationen von reaktiven oxidativen Spezien (ROS) ausgesetzt sind. Der Anstieg von 8-OHdG korrelierte mit der p53-Akkumulation im Zellkern. Da keine vermehrte Phosphorylierung des Histons H2AX (γ-H2AX), ein Marker für DNA-Strangbrüche, detektiert wurde, lässt sich schlussfolgern, dass ROS entscheidend für den p53 vermittelten Arrest verantwortlich sind.
Mehrere p53-aktivierende Kinasen wurden mittels RNA Interferenz (RNAi) und chemischer Genetik untersucht, ob sie einen Einfluss auf den Zellzyklusarrest von tetraploiden Zellen haben. Von den getesteten Kinasen hatte nur ATM einen Einfluss auf die Aktivierung von p53 nach fehlerhaften tetraploiden Mitosen. Zwar wird ATM in der Regel durch DNA-Schäden aktiviert, jedoch wurde bereits zuvor gezeigt, dass ATM auch durch erhöhte ROS Konzentrationen aktiviert werden kann.
Um die Zusammenhänge des Zellzyklusarrests weiter aufzuklären, wurde ein genomübergreifender esiRNA Screen etabliert, der die Zellproliferation nach induzierter Tetraploidisierung analysiert. Durch Kombination der Zellzyklusanalyse an Hand des DNA-Gehalts zusammen mit den FUCCI-Zellzyklusindikatoren, konnten tetraploide und diploide Zellen nebeneinander mikroskopisch analysiert werden, ohne zuvor tetraploide und diploide Zellen isolieren zu müssen. Dieser neue experimentelle Ansatz ermöglichte die Identifikation von Genen, die spezifisch die Proliferation von tetraploiden Zellen verstärken oder einschränken
Im Primärscreen wurden 1159 Gene identifiziert, deren Inhibition die Proliferation einschränken. Weiter wurden 431 Gene identifiziert, deren Inhibition die Proliferation der tetraploiden Zellen verstärken. Von den 431 Genen, deren Inhibition die Proliferation verstärken, wurden 371 Gene einem Konfirmationsscreen unterzogen, in dem 158 der identifizierten 371 Gene bestätigt wurden. Die bioinformatische Analyse der 158 Gene zeigte eine signifikante Anhäufung von Genen, die mit DNA-Replikation, dem kanonischen Wnt-Signalweg oder mit Tumorsignalwegen assoziiert sind. Unter letzteren ist CCDC6 sehr interessant, da dessen Genprodukt durch ATM phosphoryliert wird und nachgeschaltet den Tumorsuppressor 14-3-3σ reguliert.
Des weiteren wurden mittels einer Meta Analyse der Ergebnisse des Primärscreens, zusammen mit den Daten aus dem “Project Achilles”, welches genomweit den Effekt von shRNA-vermittelter Geninhibition auf die Proliferation von 108 Krebszelllinien untersuchte, 18 Gene identifiziert, deren Inhibition sowohl die Proliferation von tetraploiden Zellen einschränkt, als auch die Proliferation von Zelllinien hemmt, welche von Krebsarten stammen, die zu meist chromosomale Instabilitäten (CIN) aufweisen.
Damit bilden die präsentierten Daten nicht nur eine gute Basis zur Aufklärung des Zellzyklusarrests tetraploider Zellen, sondern auch für die Identifikation neuer potentieller Zielmoleküle, welche benutzt werden können um Tumorerkrankungen mit chromosomaler Instabilität zu behandeln, welche häufig resistent gegen die bislang verfügbaren Behandlungen sind.Erroneously arising tetraploid mammalian cells are chromosomally unstable and may facilitate cell transformation. An increasing body of evidence suggests that the propagation of mammalian tetraploid cells is limited by a p53-dependent arrest, however, the triggers of this arrest have thus far not been identified. To elucidate the timing and causes of this arrest, time-lapse live cell imaging was performed to track the fate of individual cells immediately after tetraploidization. Newly formed tetraploid cells can progress through one cell cycle, but the majority of cells arrest or die in the subsequent G1 stage, with the fate of these tetraploid cells determined by the preceding mitosis. Daughter cells arising from defective mitosis accumulated p53 in the nucleus, which led to irreversible cell cycle arrest or death. Furthermore this p53 accumulation coincides and correlates with an increase of the oxidative DNA damage marker 8-OHdG, suggesting an increase in reactive oxygen species (ROS), but does not coincide with the phosphorylation of H2AX (γ-H2AX), a marker for canonical DNA damage. Using RNA interference and chemical genetics, several p53 activating kinases were tested for their contribution to the cell cycle arrest of tetraploid cells. Of the tested kinases, only ATM was shown to play a role in the activation of p53 after defects in mitosis. ATM kinase is a DNA damage-responsive kinase, however, it has been shown that increased ROS levels activate ATM in a non-canonical way. To gain further insights into arrest of tetraploid cells, an unbiased genome-wide esiRNA screen was performed to analyze cell proliferation after induced tetraploidization. Using FUCCI cell cycle probes, combined with DNA content cell cycle profiling, allowed an image-based assay to examine tetraploid and diploid cells side-by-side. This novel approach enabled us to screen for genes that specifically restricts or enhances cell proliferation after tetraploidization, if inhibited by esiRNA mediated knockdown. From the primary screen we identified 1159 genes that decreased and 431 genes that increased the cell proliferation after tetraploidization, if knocked down by esiRNA. From the 431 genes that increased proliferation upon knockdown, 374 were selected and subjected to a re-screen. Of these 374 genes, we were able to confirm the results for 158 of the genes. A bioinformatics analysis of the 158 genes for which the phenotype were confirmed by the re-screen revealed a significant enrichment of genes involved in DNA replication, the canonical Wnt signaling pathway and in pathways linked to cancer. Among the latter, CCDC6 is particularly interesting, because its gene product is a target of the ATM kinase and an upstream regulator of the tumor suppressor 14-3-3σ. Moreover, by comparing the results of the primary screen with the data of the “Project Archilles”, which measured the proliferation in genome wide pooled-shRNA screens for 108 cancer cell lines, 18 genes were identified that are essential for the proliferation of cells after tetraploidization, as well as for the proliferation of cancer cell lines that derive from cancer types with a high incidence for chromosomal instability (CIN). Taken together, the presented data builds an excellent resource not only for elucidating how the arrest after tetraploidization is mediated, but also to identify novel potential therapeutic targets against tumors with CIN, which are frequently resistant to many of today’s anti-cancer therapies.
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Wilshusen, John D. "Do U.S. security commitments discourage nuclear proliferation?" Monterey, California. Naval Postgraduate School, 1997. http://hdl.handle.net/10945/8275.
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Approved for public release; distribution is unlimitedU.S. policy makers claim that nuclear weapons are needed to guarantee security commitments and discourage the international spread of nuclear weapons. This thesis evaluates the link between security guarantees and efforts to prevent nuclear proliferation. It draws three conclusions based on case studies of the use of conventional security commitments and nuclear security guarantees to prevent nuclear weapons development in South Korea and Taiwan. First, nuclear security guarantees alone are not sufficient to prevent proliferation. Second, strong conventional commitments made credible by visible presence of forces are sufficient to prevent nuclear proliferation when the direct security threat is conventional. Third, when the security threat being faced includes nuclear weapons, nuclear proliferation prevention requires both a nuclear security guarantee and a physically evident conventional military guarantee. Two implications for security policy follow from these findings. First, nuclear weapons are necessary in the modem security environment. Second, nuclear security guarantees are not credible without the stationing of conventional forces
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Dixon, Mark. "Signal transduction mechanisms involved in hepatocyte proliferation". Thesis, University of Newcastle Upon Tyne, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245710.
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Livingstone, D. "Modelling cell proliferation in a structured tissue". Thesis, University of Reading, 1987. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.379764.
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Webster, Lynne. "Hypoxia and proliferation in murine tumour models". Thesis, University College London (University of London), 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.336415.
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Goodlad, J. R. "Germinal centre cell proliferation in murine spleens". Thesis, University of Aberdeen, 1994. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.241447.
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Germinal centres are dynamic structures in which a number of kinetic processes take place. This thesis was designed to investigate mechanisms whereby one of these kinetic events, germinal centre cell proliferation, is regulated in vivo. In order to achieve this, the proliferative rate of germinal centre cells was measured in C3H/HeN mice under a variety of experimental conditions. In particular, the effect on germinal centre cell proliferation of different classes of antigen and of variously timed doses of the immunosuppressant drug cyclosporin A, was examined. In some experiments, an immunohistochemical technique was employed to demonstrate the distribution of antigen within murine spleens and to correlate the presence of antigen within germinal centres with the germinal centre cell birth rate. The results showed that the type of antigen to which an animal is exposed does determine the subsequent rate of germinal centre cell proliferation. In addition it became apparent that specific regulatory mechanisms were at work within murine germinal centres which either stimulated or inhibited germinal centre cell proliferation depending on the stage of the germinal centre reaction. The proliferative response to antigen was also significantly affected by treatment of the animals with cyclosporin A. The effect of the drug varied depending on the timing of its administration in relation to antigen. These results indicated that T cell derived cytokines play a central role in regulating both stimulation and inhibition of germinal centre cell proliferation. It is proposed that interleukin-4 and interleukin-5 are involved in driving the former, while interferon-γ is a candidate for mediating the latter.
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Woodrow, Sarah Louise. "Mechanisms of human papillomavirus-induced benign proliferation". Thesis, University of London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.405572.
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Noordin, Liza. "Molecular mechanisms of cell proliferation in endometriosis". Thesis, University of Strathclyde, 2011. http://oleg.lib.strath.ac.uk:80/R/?func=dbin-jump-full&object_id=16808.
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Mitchell, Angela M. "Hepatic peroxisome proliferation : mechanisms and species differences". Thesis, University of Surrey, 1985. http://epubs.surrey.ac.uk/847808/.
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The present work has investigated the species differences and mechanisms involved in hepatic peroxisome proliferation. The suitability of primary hepatocyte cultures as an in vitro model for this phenomenon was determined. The effects of a range of peroxisome proliferators on cultured rat hepatocytes were both qualitatively and quantitatively similar to the effects observed in the liver of the rat in vivo. A species difference in the hepatic response to orally administered di-(2-ethyl hexyl)phthalate (DEHP) was demonstrated in the rat and the marmoset. This species difference phenomenon was further investigated using primary guinea pig and marmoset hepatocyte cultures. Peroxisome proliferation as seen in rat hepatocytes was not observed in guinea pig or marmoset hepatocytes with any agent tested. Similarly, peroxisome proliferation was not observed in cultured human hepatocytes. These observations are suggested to infer an inherent difference in sensitivity of the guinea pig, marmoset and human hepatocyte to peroxisome proliferation. The mechanism by which DEHP elicits peroxisome proliferation in the rat liver has been investigated. The metabolites of DEHP produced by o-1-oxidation of the monoester (metabolite IX [mono-(2-ethyl-5-hydroxy hexyl phthalate] and metabolite VI [mono-(2-ethyl-5 oxo hexyl phthalate]) were shown to be potent peroxisome proliferators in cultured rat hepatocytes. These metabolites produced a transient increase in intracellular neutral lipid in cultured rat hepatocytes. Metabolite Vis was further shown to interfere with hepatic lipid metabolism, causing an inhibition of mitochondrial medium chain acyl carnitine oxidation specifically. Hence it is proposed that the species difference in peroxisome proliferation is due to differences in response of guinea pig, marmoset and human hepatocytes to the accumulation of intracellular lipid.