Дисертації з теми "Proliferate"
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Shen, Qian. "Histoplasma circumvents nutrition limitations to proliferate within macrophages." The Ohio State University, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=osu1563371073816792.
Повний текст джерелаMmatli, Thato. "Do I belong here? Conditions and micro-diffussions in the South African milieu which proliferate the emigration of potential leaders." Thesis, Linnéuniversitetet, Institutionen för organisation och entreprenörskap (OE), 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-65126.
Повний текст джерелаFarmer, Michael L. "Why Iran proliferates." Thesis, Monterey, Calif. : Springfield, Va. : Naval Postgraduate School ; Available from National Technical Information Service, 2005. http://library.nps.navy.mil/uhtbin/hyperion/05Sep%5FFarmer.pdf.
Повний текст джерелаVillada, Castro Carolina. "O proliferar dos outros." reponame:Repositório Institucional da UFSC, 2016. https://repositorio.ufsc.br/xmlui/handle/123456789/175904.
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Esta pesquisa apresenta uma análise teórica da tradução para o espanhol do texto "Apontamentos para uma poética xamânica do traduzir" do escritor e tradutor Álvaro Faleiros (2012), assim como das traduções indiretas para o espanhol da seleção de cantos xamânicos marubo: ?Raptada pelo raio? (Kaná kawã,), ?Pajé Flor de Tabaco? (Rome owe romeya) e ?Origem da vida breve? (Roka), compendiados no trabalho etnopoético de Niemeyer Cesarino em: Quando a terra deixou de falar. Cantos da mitologia Marubo (2013). A fim de pesquisar imagens do traduzir nos cantos xamânicos araweté e marubo, estabeleceu-se uma articulação entre a enunciação polifônica do xamã e a tradução literária, como atos de reverberação e multiplicação de vozes outras. Nessa perspectiva, ao modo do xamã, o tradutor literário age como voz entre vozes e prolonga os caminhos dessas vozes alheias vindas de alhures, que proliferam no espaço literário. O corpus está composto pelas contribuições tradutológicas de Álvaro Faleiros (2012-2015), as contribuições etnopoéticas de Viveiros de Castro (1986) e Niemeyer Cesarino (2011 e 2013). Desse modo, articulam-se diversas ferramentas metodológicas tais como: análise conceitual, análise comparada de traduções, tradução direta e indireta comentada e análise poética das imagens dos cantos xamânicos. Tudo isto almeja responder à força ética do canto xamânico e seus ecos para a prática de tradução literária.
Abstract : This study presents a theoretical analysis of the Spanish translation of the text "Apontamentos para uma poética xamânica do traduzir" authored by the Brazilian writer and translator Álvaro Faleiros (2012a), as well as the Spanish indirect translation of a selection of Marubo shamanic singings: "Raptada pelo raio" (kaná kawã,), "Pajé Flor de Tabaco" (Rome owe romeya) and "Origem da vida breve" (Roka), assambled in the ethnopoetic work of Niemeyer Cesarino: Quando a terra deixou de falar. Cantos da mitologia Marubo (2013). Our main purpose is to investigate images of translation in the ?shamanic singing? Arawete and Marubo, articulating the polyphony of shamanic enunciations and literary translation as acts of reverberation and multiplication of other voices. From this perspective, as a shaman, we see the literary translator performing as a voice among other voices and extending the paths that distant voices bring with them; voices that proliferate within the literary space. Our framework is formed by the works of Álvaro Faleiros (2012-2015) and the ethnopoetic works of Viveiros de Castro (1986) and Niemeyer Cesarino (2011, 2013). We also put into play the following methodological tools: conceptual analysis, comparative analysis of translations, direct and indirect translation, and poetic analysis of shamanic singing images. With these instruments, we attempt to re-join the ethical strength of the shamanic singing and to direct its echoes to the practice of literary translation.
von, Hehl Stephanie. "Vergleich der Wirkung verschiedener Wachstumsfaktoren auf physiologische Parameter kultivierter humaner retinaler Pigmentepithelzellen." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-80080.
Повний текст джерелаVelde, Guillaume Paulus Marcus ten. "Cell proliferation and tumour growth of lung cancer a clinical, immunohistochemical and flow cytometric study /." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5493.
Повний текст джерелаBoers, James Evan. "Composition and proliferation of normal human tracheobronchial mucosa." Maastricht : Maastricht : Datawyse/Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1997. http://arno.unimaas.nl/show.cgi?fid=5926.
Повний текст джерелаMcOrist, S. "The aetiology of the proliferative enteropathies." Thesis, University of Edinburgh, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383022.
Повний текст джерелаSmith, Sionagh Helen. "Epidemiological features of porcine proliferative enteropathy." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/30774.
Повний текст джерелаBailey, Catherine Clare. "A prospective national survey of laser treatment for diabetic retinopathy." Thesis, University of Bristol, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285814.
Повний текст джерелаServián, Vives Pol. "Clinical significance of prostatic proliferative inflammatory atrohpy." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/386532.
Повний текст джерелаBackground: Proliferative inflammatory atrophy (PIA) has been involved in prostatic carcinogenesis. Proliferative epithelium in PIA may progress to high-grade prostatic intraepithelial neoplasia (HGPIN) or adenocarcinoma or both. However, little is known about the clinical significance of a PIA finding in negative prostate biopsies (PBs). A preliminary review of the current literature has been done.(1st article) Objectives: 1)Determine the incidence of PIA in PBs with and without prostate cancer (PCa) and RPs, its association to HGPIN and tumor aggressiveness.(2nd article) 2)Determine the prognostic value of PIA finding in a negative PB regarding PCa risk and agressiveness.(3rd article) Methods: Retrospective and observational study of PIA lesion in 528 extended PBs and 200 RPs. Outcome measurements: PIA, HGPIN, PCa incidence, Gleason score, clinical and pathologic tumor stage and insignificant tumor rate.(2nd article) Retrospective and observational study of 474 men scheduled to repeated PBs. Assessment of PIA and its extension in the previous biopsy. PCa detection rate and tumor aggressiveness. Age, serum total PSA, free PSA, percent free PSA (%fPSA), digital rectal exam (DRE), prostate volume (PV), PSA density (PSAD), PSA kinetics (PSAV and PSADT) findings of PIA and HGPIN and number of affected cores in previous PBs were included in the univariate and multivariate analysis. Aggressive tumors were considered when any Gleason pattern 4 was found.(3rd article) Results: Overall incidence of PIA and HGPIN was 30.3% and 54% in extended PBs. In RPS, the incidence was 30.5% and 72%, respectively. No significant association was found between PIA and HGPIN. Overall PCa detection rate in PBs was 38.1%. PCa was found in 27.5% PBs with PIA and 42.7% of those without PIA, p<0.001. In contrast, PCa was detected in 50.9% of PBs with HGPIN and 23% of those without HGPIN, p=0.001. Multivariate analysis revealed that PIA decreased the risk of PCa, OR: 0.59 (95%CI:0.37–0.95), p=0.029, while HGPIN increased OR: 3.16 (95%CI:2.04–4.90), p=0.001. PIA was not related to Gleason grade and clinical stage, however it was associated to an insignificant tumors increase, OR:3.08 (95%CI:1.09–8.7), p=0.033. The information in RPs suggests that PIA is associated with less aggressive tumors and a higher probability of insignificant tumors.(2nd article) In the analysis of 474 men that underwent repeated PBs, PCa was detected in 133 men (28.1%). Age, serum total PSA, %fPSA, PV, PSAD, PSAV, PSADT and PIA finding were significantly associated to PCa detection. However, only age, OR:1.061 (95%CI:1.025-1.098), p=0.001; DRE, OR:1.755 (95%CI:1.054-2.923), p=0.031; %fPSA, OR:0.963 (95%CI: 0.933-0.996), p=0.028; PV, OR:0.983 (95%CI:0.972-0.994), p=0.002 and PIA finding, OR:0.491 (95%CI:0.291-0.828), p=0.008, were independent predictors of PCa detection. PCa was found in 18% of 159 men with previous PIA finding while in 33% of 315 men without previous PIA (p=0.001). None of the studied parameters including PIA in the previous biopsy were related with subsequent PCa aggressiveness. (3rd article) Conclusions: 1)PIA lesion is found in 30% of extended prostate biopsies, only 27% of PBs with PIA had PCa. PIA incidence in RPs was 32%. 2)The finding of PIA in prostate biopsies is not related with HGPIN finding in PBs nor in RPs. PIA finding is related to a lower risk of associated PCa. If PCa is present in prostate biopsies, the finding of PIA is associated to less aggressive and insignificant tumors. The presence of PIA in RPs was associated to less aggressive and insignificant tumors. 3)PIA lesion can be identified in 30% of patients with a negative PB. PIA finding in negative prostatic biopsies represents a decreased risk of PCa detection in future repeated PBs due to persistent PCa suspicion. There is no relation between PIA lesion in negative prostate biopsies and PCa aggressiveness in further biopsies.
Anderson, Steven P. "Gene modulation during peroxisome proliferator-induced hepatocarcinogenesis." NCSU, 2001. http://www.lib.ncsu.edu/theses/available/etd-20011101-131940.
Повний текст джерелаANDERSON, STEVEN PAUL. Gene modulation in peroxisome proliferator-induced hepatocarcinogenesis. (Under the direction of Russell C. Cattley and John M. Cullen). Recognition that peroxisome proliferator chemicals are potent hepatic mitogens and carcinogens in rats and mice has generated concern about possible human health risks associated with exposure to several of these chemicals, many of which have medical or commercial utility. Our broad objective was to improve the estimation of human health risk following peroxisome proliferator exposure by defining a subset of the molecular events associated with the rodent tumors. Our working hypothesis was that peroxisome proliferator-induced tumors in rodents result from specific, peroxisome proliferator-activated receptor-a(Ppara)-modulated changes in gene expression. The research was directed toward three specific aims. First, we sought to identify genes associated with hepatocarcinogenesis induced by the peroxisome proliferator, Wy-14, 643, in the rat. The principle conclusion of these studies - that peroxisome proliferators dysregulate expression of hepatic acute-phase protein genes - suggested possible perturbations in cytokine signaling networks that also regulate cell growth. Second, although Ppara is necessary for the rodent hepatocarcinogenesis induced by peroxisome proliferators, we were interested in identifying more proximate mediators of the increased cell proliferation. Thus, we examined cytokine signaling in mice treated with peroxisome proliferators. We found that peroxisome proliferator-induced increases in cell proliferation is not mediated via Tnfasignaling, but instead may be mediated through interleukin-1b or interleukin-6. Third, because Ppara is necessary for the cell proliferation that follows peroxisome proliferator exposure, we hypothesized that the receptor may play a role in hepatocellular proliferation induced by other stimuli. Following partial hepatectomy, liver regeneration in Ppara-null mice is transiently impaired, and may result from altered expression of genes regulating the G1/S cell cycle checkpoint in hepatocytes from these mice. Overall, our studies suggest that hepatic Ppara activation (1) alters inflammatory mediators, (2) modulates several potentially mitogenic cytokines, and (3) is necessary for normal liver regeneration after partial hepatectomy. Our data, compared with data from similar experiments on human hepatocytes, may provide further clues about the differences and similarities between peroxisome proliferator exposure in humans and laboratory animals.
Randle, Suzanne Jane. "Anti-proliferative function of FBX07 in haematopoiesis." Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.607728.
Повний текст джерелаEsau, Luke Emmanuel. "Proliferative and survival pathways in oesophageal cancer." Doctoral thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/12279.
Повний текст джерелаIncludes bibliographical references.
Oesophageal squamous cell carcinoma (OSCC) is the 8th most common cancer worldwide with high incidence in areas that include China, Iran and South Africa. The current treatment available for OSCC does not significantly enhance patient survival. A better understanding of proliferative and survival pathways activated in OSCC could allow identification of more specific therapeutic targets, potentially improving management of OSCC. Cell surface receptors are known to play important roles in relaying signals from the extracellular environment...The aim of this study was to determine the role of EGFR, IGF-1R and CXCR2 in proliferation and survival of OSCC cells.
Nickkho-Amiry, Mahshid. "Peroxisome proliferator-activated receptors in endometrial cancer." Thesis, University of Manchester, 2011. https://www.research.manchester.ac.uk/portal/en/theses/peroxisome-proliferatoractivated-receptors-in-endometrial-cancer(2388ac43-ecd4-402f-a9c7-853be4902ec8).html.
Повний текст джерелаLord, James D. "Proliferative signaling by the interleukin-2 receptor /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8320.
Повний текст джерелаDay, Robert Charles, and n/a. "Transcript analysis of proliferative endosperm from Arabidopsis thaliana." University of Otago. Department of Biochemistry, 2008. http://adt.otago.ac.nz./public/adt-NZDU20080703.113233.
Повний текст джерелаTinfo, Nicole Shivonn. "The peroxisome proliferator-activated receptor in ovarian biology." [Ames, Iowa : Iowa State University], 2007.
Знайти повний текст джерелаSampaio, de Sousa Soeiro IneÌ‚s. "Proliferative signals in normal and malignant B cells." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441947.
Повний текст джерелаBrowne, P. O. "Analyses of the peroxisome proliferator-activated receptor gamma." Thesis, University of Cambridge, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.597020.
Повний текст джерелаDionisi, Mauro. "Endocannabinoid metabolism and peroxisome proliferator-activated receptor signalling." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11384/.
Повний текст джерелаKang, Ying. "Synthesis & evaluation of some anti-proliferative substances." Thesis, Nottingham Trent University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396372.
Повний текст джерелаEl-Ghrably, Ibraheem Ahmed. "Cytokine contribution to pathogenesis of proliferative vitreoretinopathy (PVR)." Thesis, University of Nottingham, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.367591.
Повний текст джерелаClarke, Helen Catherine. "Targeting Ras in models of proliferative renal disease." Thesis, King's College London (University of London), 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429183.
Повний текст джерелаHinze, Claudia. "Changes in endocytosis and trafficking during proliferative quiescence." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10060713/.
Повний текст джерелаReyes, Gaige Andres Jose. "Invasion potential and colonization dynamics of Fusarium proliferatum." Diss., Kansas State University, 2016. http://hdl.handle.net/2097/32804.
Повний текст джерелаDepartment of Plant Pathology
James Stack
The trade of food, plant, and animal products has increased the worldwide movement and establishment of exotic pathogens with dramatic negative impacts on plant systems. Fusarium proliferatum is a broad host-range pathogen and among the most common maize pathogens globally. It is often seed-borne and symptomless in maize, making it a high risk for introduction in maize and other grains. Considering the global distribution of maize and the wide host range and production of mycotoxins by F. proliferatum, a better understanding of its life history is needed. To provide markers for tracking F. proliferatum in laboratory experiments, strains of F. proliferatum were transformed to express a green fluorescent protein (GFP). Active dispersal (at least 1.5cm at 25°C and -50mb soil matric potential) and colonization of organic matter in nonsterile field soil was demonstrated in soil microcosms. Fusarium verticillioides is commonly isolated from maize seed also colonized by F. proliferatum. A red fluorescent (mRFP) F. verticillioides transformant was developed to study competition with F. proliferatum. For quantification in host tissues, a TaqMan multiplex qPCR protocol was developed using primer and probe sets targeting fragments of the green and red fluorescence genes to detect F. proliferatum and F. verticillioides, respectively. Prior colonization of maize tissues by F. verticillioides (p=0.6749) and other seed-borne microorganisms (p=0.1910) did not affect subsequent colonization by F. proliferatum. Genotyping-by-sequencing (GBS) was used to identify genetic markers in F. proliferatum. Primer sets based GBS markers were designed to allow detection of specific isolates in field experiments. F. proliferatum populations were characterized from maize seed prior to planting and again after harvest. End-point PCR identified F. proliferatum isolates containing the GBS marker. AFLP-fingerprinting indicated that 23 of the 817 F. proliferatum isolates contained the molecular marker and were genetically related to the original isolate. Based on the subclade and percentage similarity in UPGMA phylogenetic trees, and the population grouping observed in STRUCTURE and Principal Coordinate Analysis, these isolates could have a single origin and be clonal. Understanding the life cycle of F. proliferatum is critical for learning more about the risk of introducing seed-borne exotic isolates into new environments.
Lyndin, M. S. "Algorithmization diagnosis of proliferative processes of the breast." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/33588.
Повний текст джерелаHeß, Katharina Andrea. "Peroxisome proliferator-activated receptors (PPARs) und die Lymphozytenmigration." [S.l. : s.n.], 2006. http://nbn-resolving.de/urn:nbn:de:bsz:289-vts-56139.
Повний текст джерелаClifton-Hadley, R. S. "Studies of proliferative kidney disease in salmonid fishes." Thesis, University of Stirling, 1986. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.375392.
Повний текст джерелаRomesser, Paul Bernard. "Differential proteomic characterization of B cell proliferative states." Thesis, Boston University, 2006. https://hdl.handle.net/2144/27753.
Повний текст джерелаPLEASE NOTE: Boston University Libraries did not receive an Authorization To Manage form for this thesis. It is therefore not openly accessible, though it may be available by request. If you are the author or principal advisor of this work and would like to request open access for it, please contact us at open-help@bu.edu. Thank you.
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Schutte, Berend. "Cancer cell ploidy and proliferation in colorectal carcinoma." Maastricht : Maastricht : Rijksuniversiteit Limburg ; University Library, Maastricht University [Host], 1987. http://arno.unimaas.nl/show.cgi?fid=5360.
Повний текст джерелаComalada, Vila Mónica. "Decisiones en los macrófagos: proliferar, activarse o morir." Doctoral thesis, Universitat de Barcelona, 2002. http://hdl.handle.net/10803/3004.
Повний текст джерелаAdemás, también se ha analizado como el entorno celular puede afectar a las respuestas de proliferación y activación de los macrófagos. Se ha demostrado que un aumento de adhesión producido por la decorina y fibronectina inhibe la proliferación de los macrófagos a través de la expresión de p27Kip1 y la prolongación de la actividad ERK. La decorina aumenta la activación de los macrófagos a través del secuestro del TGF-beta? producido de forma endógena por estas células.
Por ultimo el LPS, aunque es un buen activador de los macrófagos, induce apoptosis en determinadas situaciones, por ejemplo cuando dicha estimulación se produce de forma incorrecta, es decir, en ausencia de IFN-gamma o bien debido a dosis elevadas de LPS, responsables del shock séptico. La apoptosis inducida por el LPS se produce a través de dos vías de señalización independientes. Una primera vía mas temprana debida a la secreción autocrina de TNF-alfa y una segunda vía mas tardía, basada en la producción de NO. La apoptosis de los macrófagos inducida por el LPS se da principalmente a través de la producción de TNF-alfa que esta regulada mayoritariamente por PKC-epsilon a través de la modulación de la actividad JNK.
Parker, Charles F. "Controlling weapons of mass destruction : an evaluation of international security regime significance /." Uppsala : Uppsala Univ. Library, 2001. http://www.gbv.de/dms/sub-hamburg/335328989.pdf.
Повний текст джерелаReynaud, Patrick. "Etude de la fraction proliferante tumorale apres incorporation in vivo de bromodesoxyuridine." Clermont-Ferrand 1, 1994. http://www.theses.fr/1994CLF1MS26.
Повний текст джерелаMcGurk, Charles. "Culture of malacosporeans (Myxozoa) and development of control strategies for proliferative kidney disease." Thesis, University of Stirling, 2005. http://hdl.handle.net/1893/37.
Повний текст джерелаJones, Simon. "Characterisation of the anti-proliferative properties of stromal cells." Thesis, Imperial College London, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.486913.
Повний текст джерелаMehl, Isaac R. "Regulation of gene expression by peroxisome proliferator activated receptors." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 2007. http://wwwlib.umi.com/cr/ucsd/fullcit?p3249923.
Повний текст джерелаTitle from first page of PDF file (viewed April 4, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
Gillett, Cheryl E. "Studies of cell proliferative indices in human breast cancer." Thesis, Institute of Cancer Research (University Of London), 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.315432.
Повний текст джерелаMorris, David John. "Studies on proliferative kidney disease using monoclonal antibody probes." Thesis, University of Stirling, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.320376.
Повний текст джерелаOwens, Joanna. "Regulation of peroxisome proliferator-activated receptor-alpha (PPAR#alpha#)." Thesis, University of Surrey, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341337.
Повний текст джерелаBanerjee, Philip James. "Proliferative vitreoretinopathy : strategies to improve anatomical and visual outcomes." Thesis, University College London (University of London), 2017. http://discovery.ucl.ac.uk/10024849/.
Повний текст джерелаBurghard, Alice [Verfasser]. "Einflussfaktoren auf proliferative Vorgänge nach Cochlea Implantation / Alice Burghard." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1046662295/34.
Повний текст джерелаLabbé, Jorquera Matías José. "Medidas de producción — objetos recolectores de contextos proliferantes vegetales." Tesis, Universidad de Chile, 2012. http://www.repositorio.uchile.cl/handle/2250/101359.
Повний текст джерелаWelikala, Roshan Alex. "Automated detection of proliferative diabetic retinopathy from retinal images." Thesis, Kingston University, 2014. http://eprints.kingston.ac.uk/30591/.
Повний текст джерелаLorgat, Faizel. "Proliferative and cytotoxic cellular immune responses in human tuberculosis." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26373.
Повний текст джерелаMerritt, Sonia Raquel. "Improving surgical efficacy via localized anti-proliferative drug delivery." Case Western Reserve University School of Graduate Studies / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=case1402017214.
Повний текст джерелаPandey, Sapkota Narmada. "ANTI-PROLIFERATIVE FUNCTIONS OF miR-644a IN PANCREATIC CANCER." Cleveland State University / OhioLINK, 2017. http://rave.ohiolink.edu/etdc/view?acc_num=csu1495023254188526.
Повний текст джерелаMartins, Beatriz Corte Real. "Regulation of proliferative response by SETD7 in breast cancer." Master's thesis, Universidade de Aveiro, 2017. http://hdl.handle.net/10773/21405.
Повний текст джерелаBreast cancer growth is dependent on stimulation by the ovarian hormone estrogen. Estrogen activates estrogen receptora (ERa) which is a ligandactivated transcription factor. Estrogen-bound ERa transactivates genes which stimulate proliferation and survival. Hormonal therapy is an effective strategy to treat hormone-related breast cancer. However, it is associated with endocrine resistance and recurrence. Activation of growth factors signaling pathways and alterations on ERα protein have been propossed as resistance mechanisms. ERa protein stability and activation of transcription is regulated by post transcriptional modifications such as methylation and by proteasome degradation. SETD7 is a methyltransferase which targets histones and others non-histone proteins important for cellular proliferation, including ERa. Methylation of ERa seems to contribute to ERa stability and activity; this would lead to an increase in cell survival. However, previous results from our lab indicate that SETD7 inhibits mammary epithelial cell proliferation. Therefore, in this project, we intent to study the co-regulation between ERa and SETD7 as well as the subsequent effects on proliferation in response to different mitogenic stimuli, with focus on estrogen. For this purpose, we used a SETD7 activity inhibitor known as R-PFI. In this study, we show that SETD7 levels decrease when cells are stimulated to proliferate. Inhibition of SETD7 activity by R-PFI leads to an increase in cell number. However, when cells were co-treated with R-PFI and estrogen the increase was not significant once cells suffer a cell cycle arrest. In the presence of R-PFI, we show an increase of ERa protein levels, identical to the levels obtained when ERa degradation is impaired by blocking the proteasome, suggesting that SETD7 may control ERa protein levels at this level. However, this increase of ERa levels did not translate into an increase of ERa activity. Thus, SETD7 can be dispensable for ERa activity. Our findings suggest an inhibitory role of SETD7 in breast cells growth in the absence of estradiol. But, on the other hand, our results do not support studies previously reported in relation to ERa regulation. Therefore, further studies are needed to establish SETD7 function in ERα- induced proliferation.
O crescimento e progressão do cancro da mama é maioritariamente dependente da estimulação hormonal, nomeadamente pela hormona ovariana estrogénica. Esta hormona liga-se e ativa o recetor de estrogénio a (ERα) que culmina na transativação de genes que por sua vez gera uma resposta celular ao nível da proliferação e sobrevivência celular. Uma das terapias para cancros dependentes de estrogénio é a terapia hormonal. Porém, apesar de eficaz, a longo tempo gera mecanismo de resistência endócrina e até recorrência. A ativação de vias de sinalização dependentes de fatores de crescimento e outras vias de sinalização alteram a estrutura do ERα, a sua estabilidade e função. Estes mecanismos são os propostos para explicar a resistência endócrina. A estabilidade e atividade do ERαsão processos regulados por modificações pós traducionais bem como a degradação da proteína mediada pelo proteossoma. A metilação do ERαpela SETD7 parece contribuir para a estabilidade e atividade transcricional do recetor. Tal, traduzir-se-ia num aumento de sobrevivência celular. Contudo, resultados anteriores do laboratório indicam que a SETD7 inibe a proliferação celular de células epiteliais mamárias. Assim, este estudo tem como objetivo principal estudar a regulação do ERα pela SETD7 e vice-versa, bem como os efeitos desta regulação ao nível da proliferação celular mediada por diversos estímulos mitogénicos, e com foco nos efeitos dos estrogénios. Para tal, realizámos vários estudos utilizando um inibidor da atividade da SETD7, RPFI. Neste estudo mostrámos que os níveis de SETD7 diminuem quando as células são estimuladas a proliferar. A inibição da atividade da SETD7 pelo R-PFI origina um aumento do número de células. Contudo, quando combinado com estrogénio, o aumento deixa de ser significativo devido a uma paragem no ciclo celular. Na presença de R-PFI, pudemos observar um incremento dos níveis proteicos de ERa idênticos aos que se verificam quando o proteossoma está inibido, sugerindo um controlo dos níveis proteicos de ERa pela SETD7 poderia estar associado ao controlo da degradação do ERα. Contudo, este aumento dos níveis de ER não se traduz num aumento de atividade do recetor, pelo que a SETD7 parece ser dispensável para a atividade do ERα. Os resultados obtidos sugerem um papel inibitório da SETD7 sobre o crescimento de células mamárias na ausência de estradiol. Por outro lado, os nossos resultados não estão de acordo com estudos já publicados, pelo que será necessário aprofundar os estudos para esclarecer qual a função da SETD7 na regulação da proliferação mediada pelo ERα.
Cuneo, Anthony. "THERAPEUTIC MECHANISMS OF INTERLEUKIN-19 FOR VASCULAR PROLIFERATIVE DISEASES." Diss., Temple University Libraries, 2012. http://cdm16002.contentdm.oclc.org/cdm/ref/collection/p245801coll10/id/78032.
Повний текст джерелаPh.D.
Cardiovascular disease is the leading cause of mortality in the western world. The pro-inflammatory and pro-proliferative etiology of vascular proliferative diseases is well characterized, while much less is known about the mechanisms of anti-inflammatory and anti-proliferative processes. Interleukin-19 (IL-19) is a newly described member of the IL-10 family of anti-inflammatory interleukins, and our group was the first to discover IL-19 expression in activated, synthetic, but not quiescent, contractile human vascular smooth muscle cells (hVSMC). We also found that IL-19 is anti-inflammatory and anti-proliferative for hVSMC. IL-19 is able to reduce the abundance of COX-2, IL-1β, IL-8, and Cyclin D1 transcripts which contain AU-rich elements (ARE) in their 3'-untranslated regions (3'-UTR). IL-19 is able to reduce the abundance of HuR, a stabilizing RNA-binding protein, which we feel provides a mechanism for these effects. The overall goal of this study is to elucidate IL-19's anti-inflammatory and anti-proliferative mechanism(s) in hVSMC in the context of vascular proliferative diseases. This goal has directed our overall hypothesis: IL-19's anti-proliferative and anti-inflammatory effects in hVSMC are mediated, at least in part, by modulation of HuR abundance and translocation, resulting in decreased stability of mRNA transcripts. HuR functions through a translocation mechanism, and IL-19 is able to reduce HuR cytoplasmic abundance. IL-19 also reduces HuR phosphorylation, which is a pre-requisite for HuR translocation, possibly through a PKCα-dependent mechanism. The stability of ARE-containing transcripts is reduced with IL-19 treatment, and reducing HuR expression by siRNA has the same inhibitory effect. VSMC are important mediators in the initiation of atherosclerosis. Oxidized low-density lipoprotein (ox-LDL) is able to induce IL-19 expression in these cells. VSMC are known to express scavenger receptors that take up ox-LDL. IL-19 is able to reduce the uptake of ox-LDL and the abundance of ox-LDL induced LOX-1 and CX-CL16 scavenger receptors. Interestingly, these scavenger receptors also have ARE in their 3'-UTR. IL-19 is able to reduce ox-LDL induced HuR cytoplasmic abundance. HuR knockdown by siRNA reduces the uptake of ox-LDL by hVSMC. These data suggest that IL-19 reduced scavenger receptor abundance may be due to decreased total and cytoplasmic HuR abundance. IL-19 reduces the abundance of ox-LDL induced COX-2 expression. Taken together, these results demonstrate that IL-19 down-regulates vital steps in vascular proliferative disease processes through an HuR-dependent mechanism.
Temple University--Theses
Peace, Tracy Ann. "Molecular and immunologic aspects of proliferative ileitis of hamsters." Connect to resource, 1993. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1193084550.
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