Дисертації з теми "Apoptosis/Necrosis"
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Schobesberger, Martina. "Oligodendroglial degeneration in distemper : apoptosis or necrosis? /." [S.l.] : [s.n.], 1998. http://www.ub.unibe.ch/content/bibliotheken_sammlungen/sondersammlungen/dissen_bestellformular/index_ger.html.
Повний текст джерелаDunlop, J. "Modulation of human neutrophil apoptosis by tumour necrosis factor-alpha." Thesis, University of Edinburgh, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.649799.
Повний текст джерелаMedan, Djordje. "Apoptosis-necrosis paradox implications to the pathogenesis of inflammatory disorders /." Morgantown, W. Va. : [West Virginia University Libraries], 2003. http://etd.wvu.edu/templates/showETD.cfm?recnum=2763.
Повний текст джерелаTitle from document title page. Document formatted into pages; contains ix, 75 p. : ill. (some col.) Vita. Includes abstract. Includes bibliographical reference.
Murray, Joanna. "Modulation of human neutrophil apoptosis by tumour necrosis factor-α". Thesis, University of Edinburgh, 1998. http://hdl.handle.net/1842/22514.
Повний текст джерелаAbdo, Michael A. "Tumour necrosis factor : alpha signal transduction in rat corpus luteum apoptosis." University of Western Australia. School of Anatomy and Human Biology, 2002. http://theses.library.uwa.edu.au/adt-WU2003.0024.
Повний текст джерелаAntoine, Daniel James. "Chemical and molecular markers of hepatic drug bioactivation, apoptosis and necrosis." Thesis, University of Liverpool, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.501593.
Повний текст джерелаSattiraju, Sandhya Ramani. "Apoptosis and necrosis drive muscle fiber loss in lipin1 deficient skeletal muscle." Wright State University / OhioLINK, 2020. http://rave.ohiolink.edu/etdc/view?acc_num=wright1598626794423032.
Повний текст джерелаLatif, Lubna Salah Eldin Abdel. "Assessment of Cell Death Parameters in Bovine Parvovirus-Infected EBTr Cells." BYU ScholarsArchive, 2005. https://scholarsarchive.byu.edu/etd/445.
Повний текст джерелаCrott, Jimmy. "Effect of vitamin C supplements on chromosome damage, apoptosis and necrosis ex vivo /." Title page and introduction only, 1997. http://web4.library.adelaide.edu.au/theses/09S.B/09s.bc9516.pdf.
Повний текст джерелаSpine title: Effect of vitamin C on chromosome damage, apoptosis and necrosis. Includes bibliographical references (leaves 30-34).
Pistilli, Emidio E. "The extrinsic apoptotic pathway in aged skeletal muscle roles of tumor necrosis factor-[alpha] and interleukin-15 /." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4912.
Повний текст джерелаTitle from document title page. Document formatted into pages; contains x, 189 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
Song, Haichen. "Functional studies of infectious pancreatic necrosis virus proteins and mechanism of virus-induced apoptosis." College Park, Md. : University of Maryland, 2003. http://hdl.handle.net/1903/144.
Повний текст джерелаThesis research directed by: Animal Sciences. Title from t.p. of PDF. Includes bibliographical references. Published by UMI Dissertation Services, Ann Arbor, Mich. Also available in paper.
Tan, Ping. "Migratory & functional properties of dendritic cells upon interactions with dying cells & after triggering by inflammatory stimuli /." View the Table of Contents & Abstract, 2006. http://sunzi.lib.hku.hk/hkuto/record/B36434024.
Повний текст джерелаTan, Ping, and 陳冰. "Migratory & functional properties of dendritic cells upon interactionswith dying cells & after triggering by inflammatory stimuli." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 2006. http://hub.hku.hk/bib/B45010961.
Повний текст джерелаHarrison, Moira Joan. "Growth factor modulation of cytokine-mediated cell death and Fas expression in insulin-containing cells." Thesis, University of Sussex, 2000. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.324191.
Повний текст джерелаColeman, Mikaela. "Developing an analytic platform to define the heterogeneity of cell death program." Thesis, The University of Sydney, 2021. https://hdl.handle.net/2123/24780.
Повний текст джерелаFischer, Stefan. "Dynamic changes in cell death after lung transplantation, apoptosis and necrosis in ischemia-reperfusion injury." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2000. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape4/PQDD_0015/MQ54136.pdf.
Повний текст джерелаMohamed, Ahmed A. A. "Cross-talk between kinases and proteases in tumour necrosis factor-#alpha# receptor subtype-induced apoptosis." Thesis, University of Aberdeen, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.274797.
Повний текст джерелаCaligtan, Marc J. "Ischemic Preconditioning Protects Adult Rat Cardiomyocytes Against Necrosis but not Apoptosis, via Activation of PKG." VCU Scholars Compass, 2005. http://scholarscompass.vcu.edu/etd/1442.
Повний текст джерелаYamashita, Kohei. "Caspases mediate tumor necrosis factor-α-induced neutrophil apoptosis snd downregulation of reactive oxygen production". Kyoto University, 2000. http://hdl.handle.net/2433/180864.
Повний текст джерелаSitu, Elaine Hua. "EVALUATION OF TUMOR NECROSIS FACTOR-RELATED APOPTOSIS-INDUCING LIGAND (TRAIL) EFFECTS ON REGULATORY T CELLS." Thesis, The University of Arizona, 2009. http://hdl.handle.net/10150/192990.
Повний текст джерелаLövborg, Henrik. "Cellular pharmacology of the novel antitumoural cyanoguanidine CHS 828 /." Uppsala : Acta Universitatis Upsaliensis : Univ.-bibl. [distributör], 2004. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-4088.
Повний текст джерелаYu, Zhengquan. "Proton trapping in the cellular acidic vacuolar compartment : lysosomal mechanisms in apoptosis/necrosis and iron chelation /." Linköping : Univ, 2003. http://www.bibl.liu.se/liupubl/disp/disp2003/med808s.pdf.
Повний текст джерелаWatt, Victoria. "The role of tumour necrosis factor-related apoptosis-inducing ligand in atherosclerosis and acute coronary syndromes." Thesis, University of Sheffield, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.443502.
Повний текст джерелаAlamu, Olufemi Akinyinka. "Differential toxicity of two murine endothelial cells to ROS duress: Understanding oxidative stress-induced blood-brain barrier dysfunction." University of the Western Cape, 2020. http://hdl.handle.net/11394/7876.
Повний текст джерелаThe blood-brain barrier (BBB) is a critical interface between the blood circulation and brain tissue which performs critical selection of circulating molecules that gain access to the brain tissue. Its unique ability to adjust to changes in the constituents of the blood circulation confer in the BBB a dynamic nature enabling changes in its properties to suit the homeostatic needs of the brain. Dysfunction of the BBB has been established to be pivotal to the initiation and/or maintenance of an array of neurological disorders, most of which involve the production of excess reactive oxygen species (ROS) and oxidative stress in their pathophysiology. Thus, clinical trials of exogenous antioxidant agents have been proposed and initiated, with most results being inconclusive. Extensive studies of the impact, capacity and plasticity of endogenous antioxidants in the cells that constitute the blood-brain barrier, especially the brain endothelial cells, therefore, became necessary for the rational choice, timing, and the mode of application of antioxidants in the management of oxidative stress-mediated neurological diseases.
Ennis, Maurice. "Tumour necrosis factor alpha and ultraviolet light activation of programmed cell death by apoptosis in D. melanogaster." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 2001. http://www.collectionscanada.ca/obj/s4/f2/dsk3/ftp05/MQ63107.pdf.
Повний текст джерелаVohra, Hunaid Ahmed. "Apoptosis and necrosis in ischaemia/reoxygenation injury of the human myocardium : mechanism of protection by ischaemic preconditioning." Thesis, University of Leicester, 2005. http://hdl.handle.net/2381/29881.
Повний текст джерелаJia, Zhenquan. "Pesticides and Pesticide Mixtures Induce Neurotoxicity: Potentiation of Apoptosis and Oxidative Stress." Diss., Virginia Tech, 2006. http://hdl.handle.net/10919/28381.
Повний текст джерелаPh. D.
Kim, Ji-Eun 1974. "Regulation of tumor necrosis factor-alpha induced apoptosis via posttranslational modifications in a human colon adenocarcinoma cell line." Thesis, Massachusetts Institute of Technology, 2004. http://hdl.handle.net/1721.1/28865.
Повний текст джерелаIncludes bibliographical references.
(cont.) phosphoproteomics technology, IMAC/LC/MS/MS, [approximately] 200 phosphosites were identified from HT-29 cells, some of which were detected only from insulin-treated cells. Our phosphoproteomics approach also enabled us to detect alteration of both known and unknown phosphorylation states of apoptosis-related proteins at two time points during early apoptosis induced by tumor necrosis factor-α
Apoptosis, a physiologically regulated cell death, plays critical roles in development and immune system by maintaining tissue homeostasis. The thesis project investigates regulations of apoptosis in a human colon adenocarcinoma cell line, HT-29, exposed to diverse cellular stimuli, focusing on a specific protein as well as global level of proteins. The first part of the thesis demonstrated S-nitrosation of procaspase-9. S-nitrosation is a novel protein modification to regulate protein-protein interaction or protein activity. This modification has been implied to inactivate caspases. We could visualize S-nitrosation of an initiator caspase, procaspase-9, by enriching low-abundant procaspase-9 with immunoprecipitation and stabilizing S-nitroso-cysteine with biotin labeling. Nitric oxide synthase inhibitors and tumor necrosis factor-α (TNF-α) reduced the S-nitrosation level of procaspase-9, suggesting that S-nitrosation may be regulated by a nitric oxide synthase and denitrosation is likely a mechanism of apoptosis. The second part of the thesis is to examine survival effects of insulin on cells undergoing TNF-α-induced apoptosis. Insulin decreased the TNF-α-induced cleavage of key apoptotic mediators, caspases, and their substrates as well as apoptosis, in part, depending on phosphatidylinositol-3 kinase (PI-3K)/Akt pathway. One of protective mechanisms by insulin is likely to decrease the TNF-α-induced dissociation of a potent inhibitor of caspases, X-chromosome linked inhibitor of apoptosis protein (XIAP), from procaspase-9 via PI-3K/Akt pathway. Lack of phosphoproteomics data in HT-29 cells led the third part of the thesis to focus on investigating global level regulation of phosphoproteins during apoptosis. With a
by Ji-Eun Kim.
Ph.D.
McManus, Stephen. "Modulation of tumor necrosis factor related apoptosis-inducing ligand (trail) receptors in a human osteoclast model in vitro." Mémoire, Université de Sherbrooke, 2010. http://savoirs.usherbrooke.ca/handle/11143/4077.
Повний текст джерелаHallam, Thomas M. "Shifting the balance of neuronal apoptosis and necrosis in the cerebral cortex is neuroprotective following traumatic brain injury /." For electronic version search Digital dissertations database. Restricted to UC campuses. Access is free to UC campus dissertations, 2003. http://uclibs.org/PID/11984.
Повний текст джерелаAhmadi, Ferogh Ali. "The mechanism of pesticide rotenone-induced cell death in models of Parkinson's disease /." Connect to full text via ProQuest. IP filtered, 2005.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 110-128). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Segovia, Pavez Raúl Emilio. "Efecto de las proteínas de virus Andes (Hantaviridae) sobre la apoptosis mediada por TRAIL." Tesis, Universidad de Chile, 2018. http://repositorio.uchile.cl/handle/2250/148887.
Повний текст джерелаEl virus Andes (ANDV) pertenece al género Orthohantavirus (familia Hantaviridae, orden Bunyavirales). En humanos la infección por ANDV produce el síndrome pulmonar asociado a hantavirus, el cual presenta una tasa de mortalidad de alrededor de un 35%. Estos virus se caracterizan por poseer una envoltura lipídica y un genoma de ARN de hebra simple tri-segmentado, de polaridad negativa que codifica para al menos 4 proteínas, entre ellas la proteína de nucleocápside (N) multifuncional y un precursor proteico denominado GPC, que tras ser procesado resulta en las glicoproteínas Gn y Gc que se encuentran ancladas en la envoltura viral. La apoptosis es una respuesta celular común frente a una infección viral. Sin embargo, en el ciclo replicativo de los hantavirus aún es controversial si inducen o inhiben apoptosis. La apoptosis celular puede ser inducida extrínsecamente mediante receptores de muerte específicos, que pueden ser activados por un ligando de la familia del factor de necrosis tumoral, como TRAIL (ligando inductor de apoptosis relacionado al factor de necrosis tumoral, por sus siglas en inglés) a través de una cascada de señalización, mediante un dominio de muerte. En este seminario de título, se buscó determinar si la expresión o localización del receptor de TRAIL, específicamente DR5 (receptor de muerte 5, por sus siglas en inglés) se ve alterada por la expresión de proteínas Gn, Gc y N de ANDV en células humanas, y si una posible variación podría afectar la tasa de apoptosis mediada por TRAIL. En primer lugar, se analizó la expresión de DR5 en distintos tipos celulares, y se determinó que éste receptor se expresa en mayor medida en células A549, por lo que para el resto de los análisis se continuó con esta línea celular. A continuación, se midió la expresión, tanto a nivel transcripcional como traduccional de DR5 en dependencia de ANDV Gn, Gc y N, frente a lo cual, no hubo una variación significativa en la expresión general de este receptor; sin embargo, en donde sí se encontró un incremento significativo fue en la localización de DR5 en la superficie de las células A549 en presencia de ANDV N. De todas formas, no se logró detectar inducción de apoptosis en células humanas transfectadas con ANDV N, lo cual no es posible interpretar debido a la carencia de un control positivo de apoptosis celular. En resumen, estos datos en conjunto muestran que a pesar de que la expresión de ANDV N indujo un aumento en la localización de DR5 en la superficie de células A549, sin embargo, queda por determinar si este aumento podría inducir apoptosis mediada por TRAIL.
Andes virus (ANDV) belongs to the Orthohantavirus genus (Hantaviridae family, Bunyavirales order). In humans ANDV infection causes hantavirus pulmonary syndrome, which has a fatality rate around 35%. These viruses are featured by a lipid envelope and a tri-segmented, single stranded, negative sense RNA genome, that encodes at least four proteins, among them, the multifunctional nucleocapsid protein (N) and a glycoprotein precursor termed GPC, which after being proteolytically cleaved, results in the mature glycoproteins Gn and Gc, which are anchored to the viral envelope. Apoptosis is a common cellular response against a viral infection. However, in the hantavirus replicative cycle, there is still controversy whether these viruses induce or rather block apoptosis. Apoptosis can be triggered extrinsically, through specific death receptors, that can be activated by a ligand belonging to the tumor necrosis factor family, such as TRAIL (tumor necrosis factor–related apoptosis inducing ligand), through a death domain mediated signaling cascade. During this degree seminary, we aimed to determine whether the expression or location of the TRAIL receptor DR5 (death receptor 5), is altered by ANDV Gc, Gn and N expression in human cells, and if any possible variation could affect TRAIL mediated apoptosis. First, we analyzed DR5 expression in different cell types and found that there is a higher extent of DR5 expression in A549 cells, that is why, for the rest of this seminary, we continued the work with this cell line. Next, we measured DR5 expression in these cells at a transcriptional and translational level, after being transfected with plasmids encoding ANDV Gc, Gn or N. We did not find any significant variation in the total amount of DR5 expression; nevertheless, we detected a significant increase in the location of DR5 on the surface of A549 cells in the presence of ANDV N. Although, we were unable to detect apoptosis in human cells transfected with ANDV N due to the lack of a positive control of apoptosis. Finally, all together, our results show that the expression of ANDV N induces an increase in DR5 on the surface of A549 cells, however, it has yet to be determined whether or not, this is enough to induce apoptosis mediated by TRAIL.
ELGENDY, HAMED MOHAMED SHERIF HAMED MOHAMED. "Augmented damage of islets by impaired exocrine acinar cells undergoing apoptosis that is possibly converted to necrosis during isolation." Kyoto University, 2011. http://hdl.handle.net/2433/147336.
Повний текст джерелаCatrina, Anca Irinel. "Studies of molecular mechanisms of action of TNF antagonists in rheumatoid arthritis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7140-102-4/.
Повний текст джерелаEmmanuel, Catherine. "Apoptotic And Morphometric Synergies Between Tumour Necrosis Factor-A And Transforming Growth Factor-B1 For Human Endothelial Cells." Thesis, The University of Sydney, 2006. http://hdl.handle.net/2123/4864.
Повний текст джерелаKerzic, Patrick James. "Inhibition of NF-[kappa]B by the benzene metabolite hydroquinone /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 121-141). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Wasfi, Yasmine S. "Apoptosis-related genetic polymorphisms in sarcoidosis /." Connect to full text via ProQuest. IP filtered, 2005.
Знайти повний текст джерелаSzczesny, Piotr Jan. "Patterns of cell death, apoptosis and necrosis and the question of recovery in light induced retinal degeneration in the rat." Thesis, City University London, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.307886.
Повний текст джерелаLo, Susan Z. Y. "NF-kB- and mitochondria-linked signaling events that contribute to TNFa action in deferring physiological and chemotherapeutic drug-induced apoptosis in macrophages." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0095.
Повний текст джерелаDias, Kássia de Carvalho. "Efeito das toxinas microbianas provenientes de biofilme simples ou misto de Staphylococcus aureus e Candida albicans sobre monoculturas ou culturas 3D de células da mucosa oral /." Araraquara, 2016. http://hdl.handle.net/11449/148693.
Повний текст джерелаResumo: Esta presente tese foi dividida em quatro estudos que tiveram como objetivos. 1. Validar um protocolo e comparar o efeito dos tampões RPMI/MOPS e RPMI/HEPES no desenvolvimento de biofilmes e na viabilidade celular de queratinócitos (NOK-si e HaCat); 2. Comparar o dano celular e a resposta inflamatória induzidos pelos metabólitos de biofilmes simples e misto de Staphylococcus aureus e Candida albicans; 3. Avaliar o tipo de morte celular (apoptose vs. necrose) e a ativação de caspases relacionadas aos metabólitos desses biofilmes e 4. Caracterizar um tecido oral reconstituído e analisar o dano tecidual causado pelo sobrenadante e biofilme propriamente dito desses microrganismos. No estudo 1, a viabilidade celular foi avaliada pelo método colorimétrico do MTT e por imagens da cultura após 12 horas em contato com os meios de cultura. Ambos os tampões permitiram similar crescimento do biofilme. Efeito citotóxico do MOPS foi verificado após 6 horas de crescimento de NOK-si e HaCat. Houve preservação da viabilidade e morfologia quando as células foram expostas a RPMI/HEPES. Conclui-se que RPMI/HEPES pode ser utilizado como um meio tamponamente viável para estudos que avaliam o efeito do biofilme em cultura de queratinócitos ao longo do tempo. No estudo 2, o sobrenadante dos biofilmes de 36 h de C. albicans e S. aureus, isolados ou em associação, foi colocado em contato com NOK-si, HaCat e macrófagos (J774A.1). O dano celular foi avaliado por meio de ensaios de viabilidade celular ... (Resumo completo, clicar acesso eletrônico abaixo)
The present thesis was divided into four studies with the following objectives. 1. Validate a protocol and compare the effect of RPMI/MOPS and RPMI/HEPES buffers on the development of biofilms and keratinocyte cell viability (NOK-si and HaCat); 2. Compare the cellular damage and the inflammatory response induced by the metabolites of simple and mixed biofilms of Staphylococcus aureus and Candida albicans; 3. Evaluate the type of cell death (apoptosis vs. necrosis) and the activation of caspases related to the metabolites of these biofilms and 4. Characterize the reconstituted oral tissue and analyze the tissue damage caused by the supernatant and biofilm of these microorganisms. In study 1, cell viability was evaluated by the MTT colorimetric method and by culture images after 12 hours in contact with the culture media. Both buffers permitted similar biofilm growth. The cytotoxic effect of MOPS was observed after six hours of NOK-si and HaCat growth. There was preservation of viability and morphology when cells were exposed to RPMI/HEPES. It was concluded that RPMI/HEPES can be used as a buffering medium for studies evaluating the effect of biofilm on keratinocyte culture over time. In study 2, the supernatant of the 36-hour biofilms of C. albicans and S. aureus, isolated or in combination, was placed in contact with NOK-si, HaCat and macrophages (J774A.1). Cell damage was assessed by cell viability assays (MTT) and LDH enzyme release. Cytokine production was analyzed by the ELISA method and evaluation of the type of cell death by the staining of the apoptotic cells with annexin V and the necrotic cells with propidium iodide. The mixed biofilm and biofilm of C. albicans were more cytotoxic, and the mixed biofilm caused greater cellular damage through the release of the LDH enzyme. S. aureus biofilm metabolites stimulated greater production of NO, IL-6 and TNF-α... (Complete abstract electronic access below)
Doutor
Hantak, Alison Marie. "Ginsenosides enhance the cytotoxicity of tumor necrosis factor-α in human MDA-MB 231 and MCF-7 breast cancer cells in a caspase-dependent manner". OpenSIUC, 2009. https://opensiuc.lib.siu.edu/theses/123.
Повний текст джерелаGomes, Andreia Ferreira de Castro. "Regulation of lymphocyte activation and apoptosis in the immune response in multiple sclerosis /." Stockholm, 2004. http://diss.kib.ki.se/2004/91-7349-910-2/.
Повний текст джерелаBeltran, Jackeline Soares de Oliveira. "Avaliação da participação dos processos apoptóticos, necróticos e autofágicos na hipoplasia medular de camundongos submetidos à desnutrição protéica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/9/9136/tde-04122013-151612/.
Повний текст джерелаMalnutrition can induce cell damage, compromising the mechanisms involved in proliferation, differentiation and cell death. Studies from our laboratory have demonstrated, in a murine model of protein malnutrition and protein-energy, marrow hypoplasia with histologic evidence of alteration of the extracellular matrix. Our objective was to evaluate the possible involvement of the processes of apoptosis, necrosis and autophagy in the development of bone marrow hypoplasia observed in this model. For this we used two groups of C57BL/6J adult male kept in metabolic gaioleiro. The control group (C) received normal protein diet containing 12% protein and undernourished group (D), fed low protein diet containing 2% protein. The protein source used was casein. The induction period of undernutrition was approximately five weeks, as defined by loss of 20 to 25% of body weight per part of group malnourished. After this period, the animals of both groups were anesthetized and held the collection of biological samples for nutritional assessment and hematology and bone marrow cells collected for evaluation of apoptosis, necrosis and autophagy. For assessment of apoptosis and necrosis of the cells were double labeled with Annexina V and PI caspase 3 were analyzed by flow cytometry. The expression of Bcl-2 was quantified by Western Blotting technique. The analysis revealed no statistical difference between the groups for these parameters. For evaluation of autophagy proteins extracted from bone marrow cells and evaluated the expression of proteins Akt and phosphorylated and total mTOR, complexes of mTOR (Raptor, and Rictor Gβl), Beclin-1 and LC3II. The results showed significant increase in overall mTOR, Raptor, and LC3II Beclin-1 and decreased phosphorylation of mTOR in cells derived from malnourished animals compared to the control group. Malnutrition did not modify the expression of Akt total, but decreased phosphorylation of Akt and decreased expression of the protein Rictor and Gβl cells analyzed. As apoptotic and autophagic processes can be difficult to detect in vivo, also redid the experiments in vitro, stimulating the cells with pro-apoptotic compounds (campotecina) and pro-autophagic (tamoxifen). In these experiments we observed that, when only stimulate cells with camptothecin malnourished, the same at 12 hours had a higher percentage of initial apoptosis compared to 0 hours, suggesting that there is a period in which cells are signaled to via malnourished being more susceptible to apoptotic stimuli. The animals starved cells stimulated after 12 h showed significant increase in apoptosis compared to control late stimulated, indicating that at that time there is an increase in apoptosis both in the initial process, both late process. Autophagy evaluated in kinetics of 0, 2, 6, 18 and 24 hours in vitro and observed a significant increase in autophagy in bone marrow cells of malnourished at 0 hours and after 18 hours stimulation with tamoxifen (20 microM) than the respective control, demonstrating that this period autophagy begins to be induced by stimulating more easily than the control. Autophagy is a major contributor to cellular metabolism, providing nutrients when they are unavailable, and therefore in our model of protein malnutrition in the marrow hypoplasia would autophagic process as a mechanism for survival and repair.
Bernardes, Mariana Furio Franco. "Avaliação da citotoxicidade, genotoxicidade e mutagenicidade dos herbicidas tebutiurom e trifluralina e de seus efeitos na expressão de genes de resposta ao estresse celular." Universidade de São Paulo, 2016. http://www.teses.usp.br/teses/disponiveis/60/60134/tde-07072016-151441/.
Повний текст джерелаHerbicides are used to control weeds in agriculture. The use of these chemicals makes possible an abundant and pest free supply of food. However, occupational and environmental exposure to these compounds can lead to health risks. Brazil is the largest consumer of pesticides since 2008, and herbicides match for 45% of the volume of these substances. The tebutiurom and trifluralin herbicides are widely used in sugarcane crops, and although they are described as selective in its mechanism of action, effects on non-target organisms, such as human cells, are are poorly known. The aim of this work was to evaluate the effects of tebuthiuron and trifluralin herbicides on non-target organisms. To this end, we used the cell line HepG2, and herbicides were tested at concentrations of 1 to 100 ?M and the exposure time ranged from 4 h to 14 days in accordance with the assay. We also used the strains TA100 TA98, TA97a and TA1535 of the bacterium S. typhimurium. In this case, the herbicide concentrations tested ranged from 0.1 to 5000 ?g / plate and the exposure time was 66 h. Analyzes indicated that the tebutiurom has no cytotoxic, genotoxic or mutagenic potential at tested conditions, highlighting its selectivity. Tests with the Trifluralin, however, showed that HepG2 had a decreased ability in forming clones when exposed to 100 ?M for 14 days, and a reduction in cell density when exposed to 50 and 100 ?M of the herbicide for 24, 48 and 72h. These effects occurred due a decrease in cell viability observed at 50 and 100 ?M by MTT assay, and due to a block in the cell cycle into S phase, as evidenced in 100 ?M, both at 24, 48 and 72h. The type of cell death detected first was apoptosis. It was observed by staining with annexin V in cells exposed to 100 ?M of trifluralin during 48 and 72 h, and through the nuclear condensation and fragmentation in exposure with 100 ?M during 24 and 48 h of exposure. At 72 h, necrosis was also observed in 100 ?M through the annexin V / PI and LDH assays. Cell death occurrence may be associated with decreased mitochondrial membrane potential observed in 50 and 100 ?M after 24, 48 and 72h of exposure, and also may be associated with incresed production of reactive species, observed in cells exposed to 100 ?M of trifluralin for 24 and 48 h. However, it was observed that the oxidative stress response pathway Keap1 / Nrf2-ARE was not activated within 24 hours. Furthermore, comet assay and micronucleus test indicated no potential of trifluralin in causing DNA damage of HepG2. In addition, the Ames test using S. typhimurium strains also showed no mutagenic potential of the herbicide. The analyzes showed that the trifluralin, despite not induce genotoxicity and mutagenicity, have cytotoxic potential in HepG2, indicating that can affect non-target organisms, such as human cells.
Freitas, Lucas Freitas de. "Ablação tumoral fototérmica in vivo utilizando nanobarras de ouro." Universidade de São Paulo, 2012. http://www.teses.usp.br/teses/disponiveis/82/82131/tde-15052012-105851/.
Повний текст джерелаLess invasive cancer treatments, likewise those based on magnetic fields or light, are in the most common aims of researchers nowadays. Regarding light based treatments, those in which metallic, plasmonic materials are highlighted in research field. Hiperthermic treatment fits this profile, once it already presents promising results with gold-coated silica nanoshells and with gold nanorods, although little is known about its action mechanism or about how cell death pathways are activated. The compound cetyltrimethylammonium bromide (CTAB) is necessary for the nanorods synthesis, but is known to be extremely cytotoxic, fact that instigates the modification of nanorods surface coating by a compatible biopolymer. Recent studies indicate that surface-adhered CTAB does not present significant cytotoxicity, but there are few evidences to confirm this hypothesis in the literature. This study aims to investigate the cell death pathway that can be activated, as well as to confirm the possibility of safe CTAB-coated nanoparticles use in antitumor in vivo treatments. For that, gold nanorods were synthesized by the seeding method and part of them were centrifuged and washed with deionized water to eliminate CTAB of the solution and the rest remained with CTAB. The particles were tested in vitro by [3-(4, 5-dimethythiazol-2-yl)-2,5-diphenyltetrazolium bromide] (MTT) cytotoxicity test, in HTC, HepG2, HT-29 and 786-O cancer cell lines, and investigated regarding their viability through time after their synthesis. After confirming that centrifuged and washed nanorods can be used in hiperthermic therapy without health risks, and after find out that seeds and nanorods must be used within 48 hours after their synthesis, those nanoparticles were used for in vivo hyperthermic Ehrlich tumor (induced on the back of mices) treatment. Four experimental groups were organized: L (mice did not receive nanoparticles, treated with laser at 808 nm), N (mice received nanoparticles, not treated with laser), and H (mice received nanoparticles and treated with laser at 808 nm) and Controls (mice did not receive nanoparticles and were not treated with laser). A tumor biopsy was taken after laser irradiation and was subjected to histological analysis, by a chemiluminescence assay to evaluate membrane lipoperoxidation, and by Total Radical-Trapping Antioxidant Parameter (TRAP) assay as well, to evaluate total antioxidant capacity. After irradiation with laser (intensities of 2 W/\'CM POT.2\' or 720 mW/\'CM POT.2\'), there was an evident tumor volume reduction in animals of H group treated with higher power laser, with a 47ºC rise in temperature (final temperature was 79ºC) observed locally. The damages in the tumors irradiated with lower power laser were less intense. The animals of L and H groups showed similar membrane lipoperoxidation, which was more intense than in N animals (statistically significant just in the animals treated with higher intensity of radiation). The antioxidant capacity of H animals tumor was elevated also in the animals treated with higher energy. Our results indicate that necrosis is the main activated cell death pathway in this case, and that nanorods treatment is worth it.
Chaisson, Michelle L. "The role of the transcription factor NF-kappa B in hepatocyte proliferation and apoptosis /." Thesis, Connect to this title online; UW restricted, 2001. http://hdl.handle.net/1773/6356.
Повний текст джерелаShiotani, Tomohiro. "Relocation of truncated Bid plays an important role in suppression of tumor necrosis factor α-induced apoptosis in hepatocytes isolated from transgenic mouse". Kyoto University, 2006. http://hdl.handle.net/2433/143864.
Повний текст джерелаJääskeläinen, M. (Minna). "Apoptosis-regulating factors in developing and adult ovaries." Doctoral thesis, Oulun yliopisto, 2010. http://urn.fi/urn:isbn:9789514263477.
Повний текст джерелаMcPhillips, Kathleen Ann. "The role of oxidants in the clearance of apoptotic cells /." Connect to full text via ProQuest. IP filtered, 2006.
Знайти повний текст джерелаTypescript. Includes bibliographical references (leaves 112-124). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
Imbeault, Emilie. "Le rôle du récepteur NOD-like, Nlrx1 dans la neuroprotection et la mort cellulaire." Mémoire, Université de Sherbrooke, 2015. http://hdl.handle.net/11143/6937.
Повний текст джерелаAbstract : Neuronal cell death is a phenomenon that occurs during brain development as well as in pathological diseases. Depending on the environment in which the cells are; a poptosis or necrosis can contribute to neuronal cell death. Necrosis produces an environment that promotes inflammation and cytotoxicity and apoptosis is a highly organized process that maintains tissue homeostasis. A recently discovered NOD receptor, Nlrx1, is thought to play a role in regulation of inflammation and cell death during infection. Therefore, we hypothesize that Nlrx1 plays a neuroprotective role by controlling cell death in neurons. To determine the protective mechanism of Nlrx1 in vitro, a Knock-Down, a Knock-In and a Scrambled control of Nlrx1 in N2a cells was generated. LDH assays for cell death detection with staurosporine or oxidative stress, such as rotenone, MPP+ or H[subscript 2]O[subscript 2], have been done. After 24h treatment of staurosporine, N2a Knock-In cells showed higher cell death than N2a Knock-Down and Scrambled. When cells were treated with rotenone or H[subscript 2]O[subscript 2], N2a Knock-In cells had less cell death than Scrambled cells. N2a Knock-Down cells resulted in more cell death than Scrambled cells when treated with rotenone or MPP+.Western Blotting of HSP90 and HMGB1 as well as flow cytometry of cell death demonstrated N2a Knock-In cells to have less necrotic cells when treated with rotenone compared to Scrambled. The ratio of necrotic cells on apoptotic cells was also higher in N2a Knock-Down cells compared to Scrambled cells. Electron microscopy of control cells showed that Knock-In cells contains more mitochondria than Knock-Down and Scrambled cells. These results were confirmed by mitotracker staining by flow cytometry. Western blotting showed that there was an increased in Knock-In cells of active phosphorylated-DRP1 protein, a protein implicated in mitochondrial fission. Thus, it could explain the increased number of mitochondria seen in Knock-In cells. Immunoprecipitation showed that Nlrx1 protein interacts with DRP1 as well as active phosphorylated-DRP1. Adding Mdivi, a mitochondrial fission inhibitor, to rotenone or H[subscript 2]O[subscript 2] treatments, cell death was increased in Knock-In cells compared to Scrambled. Also, necrosis was also augmented in Knock-In cells to levels comparable to Scramble and Knoc k-Down cells. These results suggest an implication for Nlrx1 in regulating the balance of necrosis to apoptosis, permitting cells to survive. Nlrx1 could serve as a neuroprotective molecule in diseases mediated by oxidative stress.