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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.
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Mmatli, 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.
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A plethora of interdisciplinary research has highlighted the increase of global mobility and diasporic communities. While talent emigration has shown to have a multiplicity of benefits, particularly as gaining diversified sets of skills is essential in the face of globalization. However, widely researched concepts such as the ‘brain drain’ have conveyed the dark side of talent emigration and the ramification of countries’ desiccation for scarce skills. With a history fraught with tensions and immense loss of talent, South Africa is a country in continuous transformation, but is on the cusp of another significant ‘brain drain’. Hence, this study aimed to explore the micro-diffusions and conditions in the South African context which proliferate the emigration of talented potential leaders. The research design was qualitative, with specific use of the actors approach as methodology to gain insight into perspectives of South Africans living, working and studying in Sweden. Twenty-one participants from five cities were involved in the focus group dialogues, namely; Gothenburg, Kalmar, Lund, Linköping and Stockholm. As a participant-observer, I too was involved in the sense-making of how talent delineated their identities and relation to South Africa. Certain aspects of the findings were expected regarding the conditions which serve as push factors for emigration, such as participants’ frustrations and despondency with increasing rates of crime, unemployment and corruption. However, the most accentuated and poignant micro-diffusion which perpetuates talent’s emigration derives from conflicts of identity and belongingness, deep-seated inherited guilt and helplessness. Whilst there is a desire to ameliorate the social ills which plague the country, there also seems to be a palpable need for escapism away from the persistent historical complexities of South Africa.
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Farmer, 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.
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Villada, Castro Carolina. "O proliferar dos outros." reponame:Repositório Institucional da UFSC, 2016. https://repositorio.ufsc.br/xmlui/handle/123456789/175904.
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Dissertação (mestrado) - Universidade Federal de Santa Catarina, Centro de Comunicação e Expressão, Programa de Pós-Graduação em Estudos da Tradução, Florianópolis, 2016.Made available in DSpace on 2017-05-23T04:23:21Z (GMT). No. of bitstreams: 1 345641.pdf: 1574506 bytes, checksum: d3d18fc7556d38743776ff17eb6e2511 (MD5) Previous issue date: 2016
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.
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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.
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Bei der proliferativen Retinopathie (PVR) kommt es aufgrund einer Netzhautablösung zu einer Störung der Blut-Retina-Schranke. Durch die daraus resultierende Milieuänderung wandern retinale Zellen und Bestandteile des Blutes in den Glaskörper ein. Wachstumsfaktoren regen die mitotisch inaktiven RPE-Zellen zur Migration und Proliferation an. Im weiteren Verlauf der Erkrankung führt dies zur Ausbildung von Traktionsmembranen und zur Ablösung der Netzhaut. Die dadurch entstehenden Zugkräfte verhindern eine Wiederanlegung der Netzhaut.
Ziel dieser Arbeit war es, zu untersuchen, welchen Einfluss Wachstumsfaktoren und deren Kombinationen auf die Proliferation und Migration humaner retinaler Pigmentepithelzellen, die VEGF-Sekretion durch RPE-Zellen und die mRNA-Expression von Kollagenen haben. Die beteiligten Signalwege sollten ebenfalls ermittelt werden. Im Ergebnis sollten Faktoren identifiziert werden, die die Entstehung einer PVR begünstigen.
Migration, Proliferation, VEGF-Sekretion und die TGF-ß-Sekretion konnten durch den Wachstumsfaktor PDGF (Platelet-derived growth factor) gesteigert werden. Die Wirkung des PDGF-Signals wurde durch die Aktivierung verschiedener intrazellulärer Signalwege (MAPK, p38MAPK, PI3K/AKT) vermittelt. PDGF wirkte hemmend auf die Kollagen mRNA-Expression.
Für TGF-ß (Transforming growth factor-ß) wurde eine hemmende Wirkung auf die Proliferation und eine induzierende Wirkung auf die Kollagensynthese nachgewiesen.
Beide Faktoren – PDGF und TGF-ß – steigerten die VEGF-Sekretion. Eine additive Erhöhung der VEGF-Sekretion wurde durch die Kombination beider Faktoren nachgewiesen.
Die untersuchten Wachstumsfaktoren interagieren mit den humanen retinalen Pigmentepithelzellen und tragen somit maßgeblich zur Ausbildung und auch zur Beschleunigung des Verlaufs der proliferativen Retinopathie sowie der pathologischen Gefäßneubildung bei.
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Velde, 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.
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Boers, 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.
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McOrist, S. "The aetiology of the proliferative enteropathies." Thesis, University of Edinburgh, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.383022.
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The entezopathogenicity and antigens of Campylobacter-like organisms and Campylobacter app associated with the proliferative enteropathies were investigated. Two gnotobiotic pigs exposed orally to a filtered suspension of intestinal mucosa designated 284/86 from a naturally infected pig subsequently developed lesions of proliferative enteritis. Culture of the successful mucosal inoculum only revealed a moderate number of C. coli, however an apparently greater number of Campylobacter-like organisms was evident in smears of this inoculum. The pathogenesis of porcine proliferative enteritis was clearer from the results of this study. Ten days after infection, curved bacilli had colonised the ileal and large intestinal crypts. Attachment and entry of Campylobacter-like organisms into crypt enterocytes was also evident, with some proliferation of both bacteria within cells and of the enterocytes themselves. Twenty days after infection there was similar intracellular colonisation of bacteria and proliferative activity, although no luminal bacteria were evident. A moderate sub-acute inflammatory reaction was evident throughout. Conventional hamsters dosed with C. jejuni developed varying degrees of localised acute intestinal inflammation. Hamsters dosed with C. hyointestinalis or C. cola did not develop any lesions. Lesions of proliferative enteritis were detected in hamsters dosed with porcine tissue 284/86. Numerous intra-cytoplasmic Campylobacter-like organisms were detected within enterocytes in affected portions of intestine. Weanling hamsters this proved to be susceptible to the agent of porcine proliferative enteritis by cross-species transmission. Whole cell antigen preparations were made of various Camoylobacter sp. -Indirect immunofluorescence assays incorporating rabbit antisera to each Campylobacter sp gave specific endpoints for each antiserum of 1: 160 to 1: 320. Rabbit antisera prepared to Campylobacter-like organisms partly purified from proliferative enteritis mucosa, by a homogenisation and filtration technique, also gave specific reactions in this assay, up to 1: 610. Intracellular Campylobacter-like organisms were also compared in gel electrophoresis protein profiles and immunoblotting reactions to Campylobacter spp. The intracellular organisms tested had a distinctive protein profile dissimilar to the profiles of the known Campylobacter spp. In immunoblotting reactions, each of the Camoylobacter sp antisera reacted strongly with homologous antigens, but none reacted with Camcylobacter-like organisms prepared from lesions, except for a minor reaction seen with one serum. Similarly antisera to Campylobacter-like organisms showed a strong reaction to 25K to 27K components of homologous antigens, with only minor reactions to various other components of the cultivated Campylobacter app. Therefore it is likely that the intracellular Campylobacter-like organisms have a distinctive antigenic profile and that the 25 and 27K components are major antigenic components. Mouse monoclonal antibodies were produced that were apparently specific to the intracellular Camoylobacter-like organisms. Immunoblotting results showed that these antibodies only bound to a 251 to 27K outer membrane component present in the intracellular organisms. Reactions with this component could not be detected in assays with normal pig intestine, or Camoylobacter sp antigen. Restriction endonuclease digestion of Camoylobacter sp with Bgl II gave suitably resolved DNA fragments of between 2kb and 25kb. Patterns obtained with Bgl II digestion of Camoylobacter sp were dissimilar to those of Camoylobacter-like organisms, and each Camoylobacter sp had a characteristic distinct pattern. Digestion of DNA from porcine tissue samples with Bgl II produced a diffuse smear of fragmented DNA bands between 0.5 and19kb, with no recognizable "ladder" effect. The genome of the Carylobacter-like organisms within enterocytes in proliferative enteritis therefore is different to that of known Camoylobacter spp associated with the disease. This suggests that the differences in antigenic structures between these bacteria axe due to genetic differences. Only a limited number of strains were examined. Looking at the evidence provided by this study, the overall tenor of the results suggests that the intracellular organisms could be a separate, new species of Camp lobacter. If indeed the intracellular organisms are a single, new Cammylobacter PGS/ABST ecies, then a new name may be proposed, such as "C. intracellulare". Verifica nthis side Oni of the validity of such a proposal would require further DNA studies.
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Smith, Sionagh Helen. "Epidemiological features of porcine proliferative enteropathy." Thesis, University of Edinburgh, 1997. http://hdl.handle.net/1842/30774.
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The polymerase chain reaction (PCR) assay was adapted and optimised for specific detection of Lawsonia intracellularis genomic DNA segment in swine faeces. Lawsonia intracellularis is the aetiological agent of porcine proliferative enteropathy (PPE) and the PCR represents the first diagnostic test suitable for ante-mortem use in affected swine. Various methods designed to extract bacterial DNA from faeces were evaluated to establish a convenient and optimum protocol. The PCR was utilised in pig challenge studies to investigate the excretion patterns of L. inracellularis in weaner pigs orally inoculated with pure cultures of L. intracellularis. This challenge work demonstrated that the PCR was a suitable tool for detection of infection, and indicated that individual animals could excrete L. intracellularis organisms for periods of up to ten weeks post-challenge. Such an excretion period has major implications for the transmission of organisms in the field. For example, if infected growers are still shedding L. intracellularis organisms upon entry to the breeding population, then this is a possible route for the transmission of disease to younger, susceptible pigs. A more extensive, two-part investigation of the epidemiological aspects of PPE in the field followed. The investigation comprised a farm sampling study and a questionnaire postal survey. In the farm sampling study, faeces samples were collected serially over a ten month period from breeding gilts and their litters. Samples were subjected to PCR for the detection of infection, allowing estimation of within-herd prevalence, as well as determination of possible transmission patterns. The assay successfully detected the presence of L. intracellularis in the weaners and/or growers of three of the five farms selected for this study. The within-herd prevalence for these age-groups ranged from 10 to 30%. The PCR also confirmed infection in several of the adult breeding boars and gilts.
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Bailey, 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.
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Servián, Vives Pol. "Clinical significance of prostatic proliferative inflammatory atrohpy." Doctoral thesis, Universitat Autònoma de Barcelona, 2016. http://hdl.handle.net/10803/386532.
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La atrofia proliferativa inflamatoria (PIA) se ha relacionado con la carcinogénesis prostática. El epitelio proliferativo en la lesión PIA podría progresar a neoplasia intraepitelial prostática de alto grado (HGPIN), adenocarcinoma o ambos. Sin embargo, se conoce poco acerca del significado clínico de detectar PIA en biopsias prostáticas (BPs) negativas. Se realizó una revisión de la literatura actual(1rartículo).
Objetivos: 1)Determinar la incidencia de PIA en BPs con y sin cáncer de próstata (CaP) y en prostatectomías radicales (PRs), su asociación con HGPIN y agresividad tumoral(2ºartículo). 2)Determinar el valor pronóstico del hallazgo de PIA en BPs negativas, riego de CaP y agresividad(3r artículo).
Métodos: Estudio retrospectivo y observacional de la lesión PIA en 528 BPs extendidas y 200 PRs. Variables de medida: PIA, HGPIN, incidencia CaP, suma Gleason, estadío clínico y patológico y ratio de tumor insignificante(2º artículo).
Estudio retrospectivo y observacional de 474 hombres sometidos a BPs de repetición. Evaluación de PIA y su extensión en la biopsia previa. Detección de CaP y agresividad tumoral. Edad, PSA total, PSA libre, porcentaje PSA libre(%PSAL), tacto rectal(TR), volumen prostático(VP), densidad PSA(DPSA), cinética PSA(VPSA y TDPSA), hallazgos de PIA y HGPIN y nº cilindros afectados en BPs previas se incluyeron en el análisis univariante y multivariante. Se consideró como tumor agresivo cuando se detectó algún patrón Gleason 4(3r artículo).
Resultados: La incidencia global de PIA y HGPIN fue 30.3% y 54% en BPs. En PRs, la inicidencia fue 30.5% y 72% respectivamente. No se encontró asociación estadística entre PIA y HGPIN. La detección global de CaP en BPs fue 38.1%. Se encontró CaP en 27.5% BPs con PIA y en 42.7% de éstas sin PIA, p>0.001. Por el contrario, se detectó CaP en 50.9% BPs con HGPIN y 23% sin HGPIN,p=0.001. El análisis multivariante mostró que PIA disminuía el riesgo de CaP, OR:0.59 (95%CI:0.37–0.95),p=0.029, mientras que HGPIN lo aumentaba OR:3.16 (95%CI:2.04–4.90),p=0.001. La PIA no se relacionó con el grado de Gleason y el estadío clínico, aunque sí con el aumento de tumores insignificantes OR:3.08 (95%CI:1.09–8.7),p=0.033. La información derivada de PRs sugiere que PIA está asociada con tumores menos agresivos y mayor probabilidad de tumores insignificantes(2º artículo).
En el análisis de 474 hombres sometidos a BPs repetidas, se detectó CaP en 133 hombres(28.1%). La edad, PSA total, %PSAL, VP, DPSA, VPSA, TDPSA y hallazgo de PIA se relacionaron con la detección de CaP. Sin embargo, solo la edad, OR:1.061 (95%CI:1.025-1.098),p=0.001; TR, OR:1.755 (95%CI:1.054-2.923),p=0.031; %PSAL, OR:0.963 (95%CI: 0.933-0.996),p=0.028; VP, OR:0.983 (95%CI:0.972-0.994),p=0.002 y hallazgo de PIA, OR:0.491 (95%CI:0.291-0.828),p=0.008, fueron factores predictores independientes de detección de CaP. Se encontró CaP en 18% de los 159 hombres con PIA previa y en 33% de los 315 hombres sin PIA previa(p=0.001). Ninguno de los parámetros estudiados incluido el hallazgo de PIA en la BP previa se relacionó con la agresividad del CaP(3r artículo).
Conclusiones: 1)PIA se encontró en el 30% de las BPs extendidas, sólo el 27% de las BPs con PIA tenían CaP. La incidencia de PIA en PRs fue 32%.
2)El hallazgo de PIA en BPs no se relacionó con la detección de HGPIN en BPs ni en PRs. El hallazgo de PIA se relaciona con un menor riesgo de CaP. En caso de deteción de CaP, el hallazgo de PIA se asoció con tumores menos agresivos e insignificantes en BPs y en PRs. 3)La lesión PIA se detectó en el 30% de los pacientes con BP negativa. El hallazgo de PIA en BPs negativas representa una disminución en el riesgo de detección de CaP en futuras BPs de repetición. No hay relación entre PIA en BPs negativas y agresividad tumoral en biopsias sucesivas.Background: 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.
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Anderson, Steven P. "Gene modulation during peroxisome proliferator-induced hepatocarcinogenesis." NCSU, 2001. http://www.lib.ncsu.edu/theses/available/etd-20011101-131940.
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ANDERSON, 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.
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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.
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Esau, Luke Emmanuel. "Proliferative and survival pathways in oesophageal cancer." Doctoral thesis, University of Cape Town, 2011. http://hdl.handle.net/11427/12279.
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Includes abstract.Includes 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.
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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.
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Endometrial cancer is a common gynaecological cancer. Improving outcomes for women with advanced disease remains a challenge and there is also a need to develop preventative strategies in those women at highest risk of developing disease. Peroxisome proliferator-activated receptors (PPARs) comprise of a group of transcription factors belonging to the nuclear hormone receptor subfamily. PPAR sub-types are involved in metabolic homeostasis and have been implicated in malignancy, particularly breast and colo-rectal malignancies both of which are associated with obesity. Endometrial cancer is also closely associated with both obesity and insulin resistance. The work described in this thesis examined the expression of PPARs in endometrioid endometrial cancer and investigated their effects on key pathways implicated in this disease. Immunoblotting revealed over expression of PPARα and loss of PPARγ in human endometrioid endometrial cancer tissues. Pull-down assays also demonstrated differential selectivity of different PPARs for heterodimerisation with different isoforms of the RXR family of transcription factors. PPARα was localized to tumour cells and vascular endothelium and ELISA demonstrated an increase in VEGF-A in PPARα silenced cells suggesting that PPARα may promote tumour angiogenesis. PPARγ was largely seen in epithelial cells and also macrophages within benign endometrium. Reduction of PPARγ expression in cultured endometrial cells led to increased proliferation and decreased apoptosis. Loss of PPARγ was correlated with a loss of the tumour suppressor PTEN in endometrial tissues. Furthermore, PPARγ silencing led to diminished expression of PTEN and a concomitant increase in phosphorylated AKT suggesting that PPARγ is protective against deregulated growth within the endometrium. Synthetic PPAR-specific ligands reduced proliferation and increased apoptosis in endometrial cell lines. These effects were present in PPAR-silenced cells too although reduced in magnitude, indicating that the actions of specific PPAR ligands are mediated via both receptor dependent and receptor independent pathways.In conclusion, this work has demonstrated the differential expression of PPARs and RXRs in endometrial cancers and identified possible mechanisms, both direct and indirect, by which these may modulate endometrial cancer growth. Different PPAR family members may provide targets for therapeutic intervention in endometrial cancer care and require further study in this regard.
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Lord, James D. "Proliferative signaling by the interleukin-2 receptor /." Thesis, Connect to this title online; UW restricted, 1999. http://hdl.handle.net/1773/8320.
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Day, 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.
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Arabidopsis has emerged as an important model system for molecular plant biology. The extensive resources available for Arabidopsis make it an attractive system to study the molecular mechanisms involved in early seed development. During the early stages of seed development Arabidopsis endosperm is syncytial and proliferates rapidly through repeated rounds of mitosis without cytokinesis. This stage of endosperm development is both important in determining final seed size and is a model for studying various aspects of cellular and molecular biology, such as the cell cycle and genomic imprinting. However, the small size of Arabidopsis seed, the syncytial nature of the proliferative endosperm, and the surrounding maternal tissues make high throughput molecular analysis of the early endosperm technically difficult.
To get around this we used laser capture microdissection to enable transcript analysis of the early proliferative endosperm of Arabidopsis at 4 days after pollination (DAP). Microarray results identified several thousand genes with endosperm expression, including many that were endosperm preferred. A number of genes were validated by relative quantification PCR and were consistent with the findings of the microarray. Meta analysis of the endosperm transcriptome revealed a developmental program dominated by mitosis and under the influence of several phytohormones, predominated by cytokinin signaling.
The list of endosperm-preferred genes included all characterised imprinted genes in Arabidopsis. Imprinting is an epigenetic phenomenon by which genes are expressed predominantly from either their paternal or their maternal allele and very few imprinted genes have been identified in plants. The mono-allelic expression of the characterised imprinted genes appears to be limited to the endosperm where they provide important regulatory controls for seed development via direct effects on endosperm development. Genes from the endosperm-preferred list were screened for mono-allelic expression using sequence polymorphisms between the Colombia and Landsberg erecta ecotypes. We generated PCR products that spanned the polymorphisms of 67 genes from template obtained by laser capture of endosperm tissue from hybrid seed. Sequence analysis revealed three genes which gave strong allelic bias toward the maternal allele (At2g32460, At1g55550 and At2g21420) and one biased for the paternal allele (At1g47840).
In summary, laser capture microdissection has enabled high-resolution transcript analysis of the proliferative stage of Arabidopsis endosperm development. The data generated provides a useful resource providing novel insight into early seed development, facilitating both identification of endosperm expressed and novel imprinted genes.
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Tinfo, Nicole Shivonn. "The peroxisome proliferator-activated receptor in ovarian biology." [Ames, Iowa : Iowa State University], 2007.
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Sampaio, de Sousa Soeiro Inês. "Proliferative signals in normal and malignant B cells." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.441947.
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Browne, 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.
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The peroxisome proliferator-activated receptor γ(PPARγ) plays a key role in the development of adipose tissue, and over the last few years has attracted increasing attention as the most likely target for a new and potent class for anti-diabetic drugs known as the thiazolidinediones (TZDs). The first part of this work investigated whether mutations in the gene encoding PPARγ are responsible for syndromes of aberrant adipose tissue development. The entire coding sequence of the PPARγ gene was screened in 9 individuals with inherited forms of lipodystrophy, and 98 children affected by severe early onset obesity were screened for activating mutations within the second exon of the PPARγ gene. Neither study identified any mutations that might contribute to these syndromes. The second part of this work investigated whether a common mutation in the amino-terminus of PPAR-γ (PPARγ Pro12A1a) was associated with body mass index (BMI) and/or insulin sensitivity in a UK Caucasian population. The results of this study suggest that there is a diet-dependent association of the PPARγ2 Prol2A1a mutation with BMI and as a consequence of this with insulin sensitivity. The final part of this work concerned the evaluation of an artificial dominant negative PPARγ mutant (PPARγm), and the generation of transgenic mouse lines in which PPARγ activity is blocked in skeletal muscle and adipose tissue by tissue specific expression of PPARγm. I hope that these transgenic will enable us to prove conclusively whether or not PPARγ is the mediator of insulin sensitisation by the TZDs.
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Dionisi, Mauro. "Endocannabinoid metabolism and peroxisome proliferator-activated receptor signalling." Thesis, University of Nottingham, 2010. http://eprints.nottingham.ac.uk/11384/.
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The fatty acid amides (FAAs) family includes endocannabinoids, such as anandamide, as well as endocannabinoid-like molecules, such as N-palmitoylethanolamine (PEA) and N-oleoylethanolamine (OEA). Members of the FAA family show agonist activity at transmitter-gated channels (TRPV1), as well as peroxisome poliferator-activated receptors (PPARs). Given that FAAs appear to be hydrolysed principally through the action of the enzyme fatty acid amide hydrolase, inhibition of FAAH should lead to accumulation of a variety of FAAs. Therefore, in this study it was investigated whether pharmacological inhibition of FAAH could influence PPAR activity in SH-SY5Y human neuroblastoma cells or HeLa human cervical carcinoma cells. FAAH activity was assessed by monitoring liberation of [3H]-ethanolamine from labelled anandamide. FAAH protein and RNA expression were measured by immunoblotting and qRT-PCR respectively. Endocannabinoid levels were measured by LC-MS/MS. In order to evaluate PPAR activation, a PPRE-linked luciferase construct was co-transfected with expression plasmids for either PPAR α, β or γ. Binding to PPAR receptors was assessed with a competitor displacement assay (Invitrogen). In intact SH-SY5Y cells, sustained FAAH inhibition by URB597 (~75 %) led to accumulation of AEA, 2AG and PEA, but not OEA. Treatment with URB597, OL135 or PF750, three structurally and functionally distinct FAAH inhibitors, induced activation of endogenously expressed PPARs, while no activation was observed in FAAH-1 negative HeLa cells. Furthermore, exposure to URB597, OL135 or PF750 led to activation of over-expressed PPARs in SH-SY5Y cells. To rule out direct activation of PPARs by the FAAH inhibitors, cell-free binding assays showed that URB597, OL135 and PF750 could not bind to PPARα, PPARβ or PPARγ. Surprisingly, treatment with URB597 in HeLa cells led to intracellular accumulation of PEA but not AEA, OEA or 2AG. This might be due to inhibition of either FAAH-2 or NAAA, both of which are expressed in HeLa cells. Moreover, the presence of either URB597 or OL135 led to activation of PPARγ receptors over-expressed in HeLa cells. In conclusion, data in this study showed activation of PPAR nuclear receptors in vitro by inhibition of FAAH activity and subsequent augmentation of endocannabinoid tone. These data suggest that, at least in a model setup, it is possible to modulate the endocannabinoid tone without any previous external stimulus of their synthesis and trigger a functional effect.
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Kang, Ying. "Synthesis & evaluation of some anti-proliferative substances." Thesis, Nottingham Trent University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.396372.
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El-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.
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Clarke, 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.
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Hinze, Claudia. "Changes in endocytosis and trafficking during proliferative quiescence." Thesis, University College London (University of London), 2018. http://discovery.ucl.ac.uk/10060713/.
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A significant proportion of cells in the adult human body, including naïve lymphocytes, hepatocytes, stem cells and cancer stem cells, reside in an actively maintained state of proliferative quiescence (G0). Quiescent cells exit the cell cycle under certain conditions and resume proliferation upon appropriate stimuli, which distinguishes them from senescent or terminally differentiated cells. Little is known about how molecular processes, such as endocytosis, are regulated upon cell cycle exit. The aim of this study was to measure endocytic pathways during quiescence and study how their regulation contributes to quiescence maintenance. A quiescence induction protocol was optimised for hTERT-immortalised RPE1 (retina pigmented epithelial) cells to compare endocytosis between quiescent and proliferating RPE1 cells. A SILAC mass spectrometry screen comparing proteome and phosphoproteome between G0 and G1 RPE1 cells revealed changes in total protein levels and phosphorylation of endocytic proteins during G0. Confocal microscopy, Western blotting, flow cytometry and high throughput imaging techniques were used to measure clathrin-mediated (CME) and -independent endocytosis in quiescent and continuously proliferating RPE1 cells. Total levels of core proteins of the clathrin machinery were increased during G0, but uptake of the classical CME cargoes transferrin, EGF and LDL were decreased. CME activity during quiescence is cargo-specific, as could be shown for elevated Lamp1 endocytosis. Endocytosis of clathrin-independent cargoes such as oxidised LDL and Cholera toxin was highly active in quiescent cells, as was uptake of the acropinocytosis cargoes dextran and BSA. Elevated BSA uptake, however, did not promote mTORC1-mediated survival in a nutrient-(amino acid-) deprived environment. Moreover, BSA endocytosis was mediated by AP2. Finally, quiescence survival signalling via integrins was found to be dependent on endocytosis and recycling. Together, this study identified differentially regulated endocytic pathways and suggestd a role for integrin trafficking to maintain proliferative quiescence.
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Reyes, Gaige Andres Jose. "Invasion potential and colonization dynamics of Fusarium proliferatum." Diss., Kansas State University, 2016. http://hdl.handle.net/2097/32804.
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Doctor of PhilosophyDepartment 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.
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Lyndin, M. S. "Algorithmization diagnosis of proliferative processes of the breast." Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/33588.
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Decision support system (DSS) is used in various medical fields for over 20 years. The principle of the system is based on finding the participants in the program image in the presence of signs imposed on them. Expert systems (decision support) would facilitate the setting pathoanatomical diagnosis in doubtful cases.
The aim is to create a new method of diagnosing breast cancer as a result of histological analysis of biological objects and histograms obtained by histological study using light microscopy and development of information and software intellectual decision support system.
When you are citing the document, use the following link http://essuir.sumdu.edu.ua/handle/123456789/33588
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Heß, 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.
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Clifton-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.
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Romesser, Paul Bernard. "Differential proteomic characterization of B cell proliferative states." Thesis, Boston University, 2006. https://hdl.handle.net/2144/27753.
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Boston University. University Professors Program Senior theses.PLEASE 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.
2031-01-02
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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.
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Comalada, Vila Mónica. "Decisiones en los macrófagos: proliferar, activarse o morir." Doctoral thesis, Universitat de Barcelona, 2002. http://hdl.handle.net/10803/3004.
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El objetivo de esta Tesis ha consistido en estudiar diversos aspectos de la biología de los macrófagos, células clave en el desarrollo de la respuesta inmunitaria. Los macrófagos se caracterizan por ser células que en los tejidos se encuentran proliferando y manteniendo su viabilidad gracias a la presencia de factores de crecimiento. Sin embargo, cuando reciben un estímulo activador, ya sea el IFN-gamma, principal activador endógeno de los macrófagos o bien el LPS, componente de las bacterias Gram negativas, dejan de proliferar y pasan a activarse y a desarrollar sus funciones características, como son la expresión de citocinas proinflamatorias (como el TNF-alfa Il-1beta, IL-6), la producción de NO o bien la expresión de las moléculas del MHC II. En algunos casos, por ejemplo en ausencia de factores de crecimiento o bien estimulados con LPS, los macrófagos experimentan apoptosis o muerte celular. Este trabajo se ha centrado en estudiar las diferentes vías de señalización que participan en las distintas respuestas de los macrófagos (como proliferación, activación, supervivencia y apoptosis). En este sentido se ha demostrado que la vía de señalización de MEK/ERK es esencial para los procesos de proliferación y activación, aunque lo hace con una cinética distinta. Mientras que estímulos proliferativos generan un pico corto y rápido de activación, estímulos que inducen la activación de los macrófagos como por ejemplo el LPS, la cinética de activación de estas quinasas es más tardía. Esta cinética de activación de ERK diferencial nos permite discernir entre estímulos proliferativos y activadores. Además se ha demostrado que el IFN-gamma, aunque no activa a las quinasas ERK, induce un alargamiento en el tiempo de la activación de estas quinasas a través de la inhibición de la expresión de MKP-1 inducida por factores de crecimiento. El alargamiento de actividad de ERK, inhibe la expresión de c-myc, proteína indispensable para la progresión del ciclo celular y por tanto inhibe la proliferación de los macrófagos. Por otro lado, hemos demostrado que la vía de señalización de PI-3K/AKT es la responsable de la expresión de p21Waf1 y responsable de la respuesta de supervivencia de los macrófagos debida a factores de crecimiento y otros agentes. También hemos visto que la ciclosporina, un inmunosupresor ampliamente utilizado para evitar el rechazo de los transplantes, inhibe la actividad de ERK inducida por el M-CSF lo que produce un bloqueo de la proliferación. Este efecto es independiente de la fosfatasa Calcineurina, principal diana de la ciclosporina.Además, 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.
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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.
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Reynaud, Patrick. "Etude de la fraction proliferante tumorale apres incorporation in vivo de bromodesoxyuridine." Clermont-Ferrand 1, 1994. http://www.theses.fr/1994CLF1MS26.
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McGurk, 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.
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Proliferative kidney disease (PKD) poses a high financial burden upon the freshwater salmonid aquaculture industry of Europe and North America. The alternate hosts of the causative agent, Tetracapsuloides bryosalmonae (Myxozoa: Malacosporea), have been identified as freshwater bryozoans (Bryozoa: Phylactolaemata) within which spores capable of infecting salmonid fish develop. Currently, control of PKD relies upon complex management practices, with no licensed prophylaxis or treatment available. Assessment of the nutritional preferences of phylactolaemate bryozoans allowed development of an optimised laboratory culture system. Following laboratory maintenance, bryozoans collected from PKD-endemic sites were found to be infected with the malacosporean parasites T. bryosalmonae and Buddenbrockia plumatellae. Subsequent parasitic development was observed using light-, electron- and confocal-microscopy techniques. Methods of challenging rainbow trout with T. bryosalmonae spores were developed, with the minimum infective dose established. The presence of Thomsen-Friedenreich and Tn epitopes within the parasite was investigated, and experimental vaccine preparations based on either these specificities or T. bryosalmonae-infected bryozoans were efficacy tested in rainbow trout. In addition, salinomycin and amprolium were tested as prospective chemotherapeutants for PKD. Further insights into the development and subsequent release of malacosporean spores within their invertebrate hosts have been revealed. Long-term maintenance of T. bryosalmonae allowed controlled infection of rainbow trout previously vaccinated with experimental preparations. Findings of the project could potentially be utilised in future research into the development of control methods for PKD.
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Jones, 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.
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It has been widely demonstrated that mesenchymal stem cells (MSC) are capable of exerting powerful in vitro and in vivo suppressive effects on virtually all cells of the immune system. However, there is little information as to whether more mature mesenchymal stromal cells (SC) share the same property. To address this, I have characterised mature mesenchymal cells from a variety of tissues including articular cartilage, synovium, skin and lung and cOlTlpared them to MSC. The differentiation potential and surface phenotype of SC was evaluated, whilst the ability of SC from different human tissues to inhibit the proliferation of PBMC following polyclonal stimuli was also 'assessed. Irrespective of their differentiation potential and/or content of progenitor cells, SC from all tissues exhibited anti-proliferative functions. This' was in marked contrast to parenchymal cells from endodermal and ectodermal origins. Although' SC did not interfere with early T lymphocyte activation, they arrested stimulated T cells in the GJGt phase of the cell cycle and rescued them from apoptosis. In addition, IFNy and TNFa production were reduced. I observed that the inhibitory effect is ultimately mediated by soluble factors, the production of which requires SC to be 'licensed' in an inflammatory environment by cell contact. I conclude that the immunosuppressive effect of mesenchymal cells is not confined to multipotent stem cells but is a fundamental characteristic of all stroma. My data suggests that SC, appropriately licensed, regulate T cell homeostasis.
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Mehl, 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.
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Thesis (Ph. D.)--University of California, San Diego, 2007.Title from first page of PDF file (viewed April 4, 2007). Available via ProQuest Digital Dissertations. Vita. Includes bibliographical references.
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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.
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Morris, 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.
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Owens, 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.
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Banerjee, 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/.
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Proliferative vitreoretinopathy (PVR) is the most common cause of late anatomical failure of retinal detachment surgery. Efforts to modify this vitreoretinal scarring response have so far proved clinically unsuccessful, with surgical and visual outcomes remaining poor. This work is aimed at identifying strategies to improve outcomes in eyes at high risk of PVR development following open globe trauma (OGT), and those with established PVR disease. Two prospective clinical trials investigating the benefit of adjunctive corticosteroids in these two populations were conducted in a total of one hundred and eighty patients. Clinical and imaging data were collected over the course of approximately 3500 hospital attendances. The Adjunct in Ocular Trauma (AOT) Trial was a two year, pilot, single-centre prospective, participant and surgeon-masked randomized-controlled-clinical trial (RCT). Forty patients requiring vitrectomy surgery following OGT were randomized to either standard (control) or study treatment (adjuncts) in a 1:1 allocation ratio. Perioperatively, the adjunct group received intravitreal and subtenons triamcinolone acetonide, oral flurbiprofen and guttae prednisolone acetate 1%. The control group received standard care. Primary outcome was anatomical success at 6 months and showed similar results in anatomical success with 50% (10/20) in the adjunct group, compared to 47% (9/19) in the standard group (Odds Ratio 1.11, 95% Confidence Interval 0.316-3.904). Secondary outcomes included final visual acuity, occurrence of PVR, intraocular pressure (IOP) rise, number of operations and recruitment rate. Final median visual acuity was 31 ETDRS letters in the adjunct group compared to 25 ETDRS letters in the standard group. Other secondary outcomes were similar between the two groups. The hypothesis that an adjunctive slow-release dexamethasone implant (Ozurdex ®) could improve the outcomes of vitreoretinal surgery for established PVR was tested in the Ozurdex® in PVR Study. In this two year, single-centre prospective, participant and surgeon-masked RCT, 140 patients requiring vitrectomy surgery with silicone oil for retinal detachment with established PVR (Grade C) were randomized to either standard (control) or study treatment (adjunct) in a 1:1 allocation ratio. Intraoperatively, the adjunct group received an injection of 0.7mg of slow-release dexamethasone (Ozurdex) at the time of (a) vitrectomy surgery and (b) at silicone oil removal. The control group received standard care. Primary outcome measure was the proportion of patients with a stable retinal reattachment with removal of silicone oil without additional vitreoretinal surgical intervention at 6 months. Secondary outcomes included i) final visual acuity (median and ETDRS of 55 letters or better), ii) cystoid macular edema (CMO), foveal thickness and macular volume iii) development of overt PVR recurrence, iv) complete and posterior retinal reattachment, vi) tractional retinal detachment, vii) hypotony/raised IOP, viii) macula pucker/epiretinal membrane, ix) cataract, x) quality of life All 140 patients were recruited within 25 months of study commencement; 138 patients had primary outcome data. Primary outcome assessment showed similar results in anatomical success between the two groups (49.3% vs 46.3%, adjunct vs control, (Odds Ratio 0.89, 95% Confidence interval 0.46 – 1.74, p= 0.733). Mean visual acuity at 6 months was 38.3 ETDRS letters and 40.2 letters in the adjunct and control group respectively. Secondary anatomical outcomes (complete/posterior reattachment rates and PVR recurrence) were comparable between the two groups. Exploratory analysis suggested that the proportion of patients with cystoid macular oedema (CMO) or a foveal thickness of >300μm was lower in steroid-treated eyes compared to controls (42.7% and 47.6% vs 67.2% and 67.7%, respectively p= 0.004, p= 0.023). Cystoid macular oedema is a secondary cause of visual loss. At 6 months following successful surgery for PVR, eyes with evidence of external limiting membrane (ELM) disruption on Spectral Domain-Optical Coherence Tomography achieve a worse visual outcome than eyes where the ELM appears preserved (p=0.006). Provisional work using retinectomy specimens retrieved at the time of surgery in sixteen patients were studied aiming to isolate a population of Müller glia with stem cell characteristics (hMSC). This suggested that it is feasible to isolate a cell population of appropriate morphology of hMSCs, from eyes with advanced PVR. These cells survived up to ten weeks in culture but eventually terminally differentiate. The work in this thesis has shown that corticosteroids do not modify the vitreoretinal scarring response sufficiently to improve anatomical outcomes at 6 months. Further work is required to improve the outcome in eyes with PVR. Adopting visual acuity as a primary outcome, may be a plausible design in future vitreoretinal trials.
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Burghard, Alice [Verfasser]. "Einflussfaktoren auf proliferative Vorgänge nach Cochlea Implantation / Alice Burghard." Hannover : Bibliothek der Tierärztlichen Hochschule Hannover, 2013. http://d-nb.info/1046662295/34.
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Labbé, 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.
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A partir de tres obras de carácter objetual, esta tesis aborda las posibilidades metafóricas e la operación de recolección, contraponiendo el uso de material proliferante vegetal con distintos modelos de administración, como son el método de raíz científica, el eterminado por condiciones ambientales, y el regido por un sistema mecánico autónomo. Estos sistemas son puestos en tensión a través del uso de materiales inestables, los que en consecuencia acusan un proceso que permite la posibilidad de una apertura de sentidos en torno a las actividades productivas agrícolas y de jardinería.
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Welikala, Roshan Alex. "Automated detection of proliferative diabetic retinopathy from retinal images." Thesis, Kingston University, 2014. http://eprints.kingston.ac.uk/30591/.
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Diabetic retinopathy (DR) is a retinal vascular disease associated with diabetes and it is one of the most common causes of blindness worldwide. Diabetic patients regularly attend retinal screening in which digital retinal images are captured. These images undergo thorough analysis by trained individuals, which can be a very time consuming and costly task due to the large diabetic population. Therefore, this is a field that would greatly benefit from the introduction of automated detection systems. This project aims to automatically detect proliferative diabetic retinopathy (PDR), which is the most advanced stage of the disease and poses a high risk of severe visual impairment. The hallmark of PDR is neovascularisation, the growth of abnormal new vessels. Their tortuous, convoluted and obscure appearance can make them difficult to detect. In this thesis, we present a methodology based on the novel approach of creating two different segmented vessel maps. Segmentation methods include a standard line operator approach and a novel modified line operator approach. The former targets the accurate segmentation of new vessels and the latter targets the reduction of false responses to non-vessel edges. Both generated binary vessel maps hold vital information which is processed separately using a dual classification framework. Features are measured from each binary vessel map to produce two separate feature sets. Independent classification is performed for each feature set using a support vector machine (SVM) classifier. The system then combines these individual classification outcomes to produce a final decision. The proposed methodology, using a dataset of 60 images, achieves a sensitivity of 100.00% and a specificity of 92.50% on a per image basis and a sensitivity of 87.93% and a specificity of 94.40% on a per patch basis. The thesis also presents an investigation into the search for the most suitable features for the classification of PDR. This entails the expansion of the feature vector, followed by feature selection using a genetic algorithm based approach. This provides an improvement in results, which now stand at a sensitivity and specificity 3 of 100.00% and 97.50% respectively on a per image basis and 91.38% and 96.00% respectively on a per patch basis. A final extension to the project sees the framework of dual classification further explored, by comparing the results of dual SVM classification with dual ensemble classification. The results of the dual ensemble approach are deemed inferior, achieving a sensitivity and specificity of 100.00% and 95.00% respectively on a per image basis and 81.03% and 95.20% respectively on a per patch basis.
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Lorgat, Faizel. "Proliferative and cytotoxic cellular immune responses in human tuberculosis." Thesis, University of Cape Town, 1992. http://hdl.handle.net/11427/26373.
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Merritt, 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.
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Pandey, 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.
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Martins, 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.
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Mestrado em Biomedicina MolecularBreast 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.
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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.
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Molecular and Cellular PhysiologyPh.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
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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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