Tesis sobre el tema "Necrosis"
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Bridges, James. "Necrosis in colorectal cancer /". Leeds : University of Leeds, School of Computer Studies, 2008. http://www.comp.leeds.ac.uk/fyproj/reports/0708/Bridges.pdf.
Texto completoAlbataineh, Eman Mohammad. "Studies of tumour necrosis factor receptor-1 in tumour necrosis factor receptor associated periodic sysndrome (TRAPS)". Thesis, University of Nottingham, 2009. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.537655.
Texto completoDry, P. R. "Primary bud-axis necrosis of grapevines /". Title page, contents and summary only, 1986. http://web4.library.adelaide.edu.au/theses/09A/09ad798.pdf.
Texto completoNaylor, Michael Stuart. "Tumour necrosis factor and ovarian cancer". Thesis, Open University, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.332896.
Texto completoBraidwood, Luke Anthony. "Engineering resistance to maize lethal necrosis". Thesis, University of Cambridge, 2017. https://www.repository.cam.ac.uk/handle/1810/273678.
Texto completoBjörnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells". Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.
Texto completoGreen, Ian R. "Studies on ovine tumour necrosis factor alpha". Thesis, University of Edinburgh, 1994. http://hdl.handle.net/1842/29788.
Texto completoStewart, Victoria C. "Human renal lipoxygenases : implications for papillary necrosis". Thesis, University of Aberdeen, 1995. http://digitool.abdn.ac.uk/R?func=search-advanced-go&find_code1=WSN&request1=AAIU078660.
Texto completoSchobesberger, 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.
Texto completoJaramillo, Martinez Diana. "Epidemiology and pathogenesis of Nervous Necrosis Virus". Thesis, The University of Sydney, 2015. http://hdl.handle.net/2123/13088.
Texto completoDoerge, Thomas A., Deborah Young y Claire Owen. "Internal Bark Necrosis in Southeastern Arizona Apples". College of Agriculture, University of Arizona (Tucson, AZ), 1990. http://hdl.handle.net/10150/215718.
Texto completoMoriguti, Eny Kiyomi Uemura. "Efeito da L-alanil-L-glutamina na forma de dipeptídeo e L-glutamina-L-alanina na forma de aminoácido livre na evolução da necrose de lesão por queimaduras em ratos". Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17137/tde-10042018-143956/.
Texto completoIntroduction: The classification of burn severity is based on the relationship between the burned body surface (SCQ) and the depth of the lesion. Factors influencing the progression of necrosis in the stasis zone surrounding the area of necrosis (coagulation) may be related to perfusion, inflammation and oxidative stress. In the present study, we evaluated the effect of glutamine, as it has been shown to play an important role in the prevention of ischemia and reperfusion injury, inflammation and oxidative stress. Objective: to evaluate the effect of glutamine as a free amino acid and dipeptide on the progression of necrosis in the interspace (stasis zone) of the burn. Materials and Methods: Thirty male Wistar rats were used. In all animals a third degree burn injury was done with a metal comb containing four teeth and three interspaces preheated in water at 98ºC. Group 1- Control (n = 10) received 7,4 ml of 0.9% saline solution, Group 2- Dipeptide received 7.4 ml of dipeptide solution L-alanyl-L-glutamine (1g/k Lglutamine and 0.6g/k L-Alanine) and Group 3- Free AA received 1g/k L-glutamine and 0,6g/kg L-alanine as free amino acid, by gavage, for 7 days after burn injury. The analyzes evaluated were by means of photograph (in the time 48 hours and 7 days) and histopathology (on the 7th day after the injury), to evaluate the extent of necrosis, ischemic changes in the interspaces (stasis zone), besides the alteration of Glutathione . Results: In the photographic evaluation, there was a significant reduction of necrosis specifically in the 3-AA-free group between 48 hours and 7 days (P = 0.04). Histologically, there was a reduction in inflammation in Groups 2- Dipeptide and 3-AA-free when compared to Group 1-Control (p <0.01). Even in the treated groups there was a tendency to reduce necrosis in the interspaces dermis (Group 1-Control = 0.95, Group 2-Dipeptide = 0.73 and Group 3- AA-free = 0.8), but these differences were not significant. The treated groups also showed an increase in the number of fibroblasts when compared to Group 1- Control (p <0.05). In the dosage of Glutathione, a greater amount was found in Group 2 - Dipeptide (p <0.05) when compared to Group 1 - Control. Conclusion: The reduction of histological lesions, reduction of inflammation, maintenance of greater extension of the interspaces, the greater amount of fibroblasts and the increase of glutathione, with the administration of glutamine observed in the present study, may have benefited the maintenance or reduction of the evolution of necrosis of burn in rats.
Offei, Samuel K. "Molecular analysis of the tobacco necrosis virus genome". Thesis, Imperial College London, 1995. http://hdl.handle.net/10044/1/11319.
Texto completoJohnston, Julie Catherine. "In vitro translation of cucumber necrosis virus RNA". Thesis, University of British Columbia, 1989. http://hdl.handle.net/2429/28969.
Texto completoLand and Food Systems, Faculty of
Graduate
Molloy, Sally Dixon. "A DNA Vaccine Against Infectious Pancreatic Necrosis Virus". Fogler Library, University of Maine, 2007. http://www.library.umaine.edu/theses/pdf/MolloySD2007.pdf.
Texto completoEngelberts, Ingeborg. "Tumor necrosis factor during sepsis king of cytokines? /". Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6955.
Texto completoPérez, Lozano Alba Astril. "PATOGENIA DEL VIRUS DE LA NECROSIS PANCREÁTICA INFECCIOSA". Tesis de Licenciatura, Universidad Autónoma del Estado de México, 2018. http://hdl.handle.net/20.500.11799/95135.
Texto completoRESUMEN El virus de la necrosis pancreática infecciosa (VNPI) es el agente causal de la enfermedad conocida como necrosis pancreática infecciosa (NPI). De manera natural los salmónidos son los peces más susceptibles. El curso agudo de la enfermedad puede provocar una mortalidad hasta del 100% en salmónidos jóvenes. En las truchas, la susceptibilidad a la enfermedad disminuye con la edad. Los peces infectados transmiten el virus por vía horizontal y vertical, esto promueve que el virus se encuentre de forma continua en el agua y que infecte a otros peces. Al alcanzar los 1500 grados-día (valor que se obtiene multiplicando los días de edad de los peces, por el promedio de la temperatura en grados Celsius durante su esperanza de vida), los peces resisten más a la enfermedad. Los signos clínicos que presentan los peces afectados por el VNPI son: anorexia, ataxia, hiperventilación, obscurecimiento de piel (hiperpigmentación), hemorragias en áreas ventrales y aletas. Con base en ésto, un pez puede estar infectado mas no enfermo, y un pez enfermo sí está infectado. Por la complejidad del proceso salud - enfermedad, Casadevall y Pirofski propusieron una nueva teoría de la patogenia microbiana, empleando modelos de microorganismos patógenos en los humanos. Esto nos lleva a revisar los conceptos propuestos por estos autores, haciendo énfasis en modelos de patógenos importantes en el área de la Medicina Veterinaria. En nuestro país, el virus de la necrosis pancreática infecciosa fue reportado en 2002 y afecta principalmente a truchas jóvenes de unidades de producción intensiva. El virus ha sido aislado en unidades de producción trutícola de las siguientes entidades: México, Hidalgo, Morelos, Michoacán, Puebla, Chihuahua, Durango y Veracruz. Conocer la patogenia microbiana del único virus identificado y confirmado hasta ahora en la trutícultura nacional es de vital importancia. Palabras clave: patogenia microbiana, VNPI, trucha arcoíris.
“Serotificación y virulencia de aislados mexicanos del virus de la necrosis pancreática infecciosa”, financiado por CONACYT, CB-257781, con registro interno 4226/2016C; responsable técnico Dra. en C. Celene Salgado Miranda.
Brodowicz, Gary Ray. "Exercise training, indomethacin, and isoproterenol-induced myocardial necrosis /". The Ohio State University, 1986. http://rave.ohiolink.edu/etdc/view?acc_num=osu1487265555440899.
Texto completoKrugten, Michiel Volkert van. "Tumor necrosis factor gene polymorphisms and rheumatic diseases /". Leiden, 2003. http://catalogue.bnf.fr/ark:/12148/cb40223074h.
Texto completoOukacha, Khadija. "Perturbation chimique du transport de Tumor Necrosis Factor". Electronic Thesis or Diss., Université Paris sciences et lettres, 2023. http://www.theses.fr/2023UPSLS067.
Texto completoWhile it is essential to fight against pathogens, TNF (Tumor Necrosis factor) secreted in excess becomes harmful to the body as in the case of chronic inflammatory diseases (rheumatoid arthritis or Crohn's disease). Current therapies are based on recurrent injections of anti-TNF against which 30% of patients develop resistance. There is therefore a strong need for chemical compounds which reduce the secretion of TNF. We have exploited the diversity of secretory pathways dependent on the Golgi apparatus to identify molecules that specifically inhibit TNF secretion. The RUSH (Retention Using Selective Hooks) tool allowed the synchronization and analysis of TNF transport in HeLa cells. By combining the RUSH assay with a differential hight content screening of chemical libraries, 85 molecules inhibiting TNF transport were selected. The effects of certain molecules have been validated. Only molecules inhibiting at least 40% of TNF secretion were retained. The specificity of these molecules on the transport of other proteins, namely EGFP-GPI and IL-6 was evaluated. The 14 molecules rather specifically inhibiting the secretion of TNF were selected to continue their characterization in a physiological model.The effects of the molecules on the endogenous secretion of TNF and other cytokines were measured in human primary monocytes and macrophages obtained from blood donors after incubation with bacterial lipopolysaccharide (LPS). These experiments in physiological models have demonstrated three molecules capable of significantly inhibiting the endogenous secretion of TNF without affecting the secretion of IL-8. Dose-response experiments and the evaluation of the effects of molecules on the expression of TNF have been carried out to help in understanding the mode of action of these molecules.In conclusion, the chemical screening, the experiments in heterologous model then in physiological models made it possible to identify 3 molecules inhibiting the secretion of TNF. These results confirm that the diversity of secretory pathways is large enough to target the transport of a protein involved in a disease and could open the way to alternative or complementary treatments against inflammatory diseases
Helliwell, Timothy Richard. "Investigations into skeletal muscle damage and regeneration : a study of lectin-binding structures and desmin in skeletal muscle in vivo and in vitro". Thesis, University of Cambridge, 1992. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.327222.
Texto completoVaughan-Scott, Tarquin. "Serum concentrations of tumour necrosis factor in dogs naturally infected with Babesia Canis and its relation to severity of disease". Diss., University of Pretoria, 2002. http://hdl.handle.net/2263/29287.
Texto completoCanine babesiosis, caused by the tick-borne protozoan Babesia canis rossi, is an economically important and potentially fatal disease of dogs in South Africa. The host's response to many infectious diseases is mediated (at least in part) by intercellular messengers called cytokines. One of the most important cytokines released is tumour necrosis factor (TNF). A study was designed to measure serum concentrations of TNF in dogs naturally infected with canine babesiosis and to relate TNF concentrations to clinical severity, mortality, rectal temperature and parasitaemia. There was a statistically significant difference in TNF concentrations between groups of differing disease severity, with a general trend of increasing mean 10g(TNF) with increasing severity of disease. A noteworthy finding was that dogs with hypoglycaemia had very high TNF (mean 15.03 nglml compared to a mean of 2.32 nglml for other sick dogs without hypoglycaemia). When TNF values were compared between survival and non-survival groups, there was no significant difference. The rectal temperature of the dogs in this study did not show any statistically significant association with TNF concentrations. When parasitaemia and TNF were examined within groups of infected dogs, there was no significant relationship. However, when the sample size was increased by pooling all infected dogs and treating them as a single group, there was a highly significant positive correlation (p = 0.003) between parasitaemia and serum TNF concentrations. The results ofthis study were encouraging and indicate that canine babesiosis may share a similar pathophysiology with human malaria in terms ofTNF being associated with disease severity. One ofthe most significant findings in this study was the presence ofvery high TNF values in two ofthree dogs with hypoglycaemia. Hypoglycaemia has not been previously recorded in dogs with babesiosis and is a potentially important finding particularly in view ofthe hypoglycaemia associated with malaria in humans. Malarial hypoglycaemia is correlated with a higher mortality in humans, especially in pregnant women and children. If the findings ofthis study can be Vl confinned and expanded, they may lend further support to the use of canine babesiosis as a model for some ofthe problems encountered in human malaria research.
Dissertation (MMed Vet (Med))--University of Pretoria, 2001.
Companion Animal Clinical Studies
unrestricted
Barbara, Jeffrey A. J. "The mechanism of action of tumour necrosis factor-[alpha] /". Title page, contents and abstract only, 1995. http://web4.library.adelaide.edu.au/theses/09PH/09phb229.pdf.
Texto completoMahtani, Kamal Ram. "The post-transcriptional regulation of tumour necrosis factor alpha". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.271639.
Texto completoRayner, Sandra Anne. "Tumour necrosis factor and gene transfer in corneal transplantation". Thesis, Imperial College London, 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.248143.
Texto completoWilliams, Llinos. "Expression of tumour necrosis factors during chick lens development". Thesis, Cardiff University, 2008. http://orca.cf.ac.uk/54869/.
Texto completoLongin, Ondřej. "Construction of synthetic antibodies against tumour necrosis factor alpha". Thesis, University of Glasgow, 2018. http://theses.gla.ac.uk/39025/.
Texto completoBorg, Sebastian. "Synthetic bone grafts for treatment of femoral head necrosis". Thesis, Uppsala universitet, Oorganisk kemi, 2017. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-314857.
Texto completoGonzález, Aguirre Laura V. "Revascularización en dientes traumatizados, rizogénesis incompleta y necrosis pulpar". Trabajo final de especialización, Universidad Nacional de Cuyo. Facultad de Odontología, 2020. http://bdigital.uncu.edu.ar/15323.
Texto completoFil: González Aguirre, Laura V.. Universidad Nacional de Cuyo. Facultad de Odontología.
Willingham, Stephen B. Ting Jenny P. Y. "Microbial pathogen-induced necrosis mediated by NLRP3 and ASC". Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1712.
Texto completoTitle from electronic title page (viewed Sep. 16, 2008). "... in partial fulfillment of the requirements for the degree of Doctor of Philosophy in the Curriculum in Genetics & Molecular Biology." Discipline: Genetics and Molecular Biology; Department/School: Medicine.
Watts, Alan D. "The biological role of transmembrane tumour necrosis factor [alpha]". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27668.
Texto completoValbuena-Gonzalo, Carlos. "Identifying Genetic Causes of Hybrid Necrosis in Arrabidopsis lyrata". Thesis, Umeå universitet, Institutionen för ekologi, miljö och geovetenskap, 2019. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-163444.
Texto completoAtkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /". Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.
Texto completoFerreira, Juliana. ""Análise da necrose em tecidos normais fotossensibilizados pós terapia fotodinâmica - estudo in vivo"". Universidade de São Paulo, 2003. http://www.teses.usp.br/teses/disponiveis/17/17143/tde-17052004-144509/.
Texto completoThe PDT concept is the photo induction of the citotoxicity of proliferating cells involving a photosensitizer agent, a light source and oxygen. Despite being an efficient therapy on the treatment of several neoplasias, PDT presents some restrictions including the non-selectivity in hepatic tissue cells. This work evaluated the correlation between light penetration and necrosis, as well as the extension of such as function of the concentration of the photosensitizer used (Photogem) and three different doses of energy. The necrosed epithelium and healthy epithelium transition was performed after the irradiation of normal livers of previously photosensitized rats. The Photogem accumulation, intravenously administrated, on the liver was investigated through fluorescence spectroscopy. The light sources used for irradiation were: diode laser operating at 630 nm and a LEDs (Light Emitting Diode) device. We observe that the photosensitized normal hepatic tissue presents its optical characteristics altered, which was previously evidenced on the studies of light penetration and thermal alteration during the irradiation, altering the necrosis depth. We checked that the photosensitizer presence on the target tissue decreases the light penetration leading to a temperature increase, due to a large amount of energy absorbed by the photosensitizer, which is dissipated by means of heat. We noticed an abrupt necrosis delineation corresponding to the drop of the light intensity on the irradiated tissue. When the LED was used, the necrosis depth presented little variation, due to its spectral line being larger when compared to the lasers spectral line. Histological, the irradiated hepatic tissue presented coagulative necrosis, inflammatory infiltration neutrophilic and centrilobular vein necrosis in all experimental groups, we also observed a clear delimitation between normal epithelial tissue and photosensitized tissue. These results will be important to the development of strategies for a possible protocol for the PDT application on hepatic malign tumors.
Freitas, Vanessa Santana. "Investigação do efeito citotóxico do extrato metanólico de Bixa orellana L sobre células astrocíticas tumorais e astrócitos in vitro". reponame:Repositório Institucional da FIOCRUZ, 2011. https://www.arca.fiocruz.br/handle/icict/4320.
Texto completoMade available in DSpace on 2012-09-04T17:32:14Z (GMT). No. of bitstreams: 1 Vanessa Investigacao do efeito cititóxico....pdf: 1637760 bytes, checksum: 53a0a5f0c495bc04a29d54e8f4415870 (MD5) Previous issue date: 2011
Fundação Oswaldo Cruz. Centro de Pesquisas Gonçalo Moniz. Salvador, Bahia, Brasil
Investigar a capacidade antitumoral do extrato metanólico de Bixa orellana em células neoplásicas de Glioblastoma multiforme (GL-15) e Glioma murino (C6), sem toxicidadade para as células astrocitárias normais in vitro. Métodos e resultados: Caracterização do extrato por espectrofotometria por absorção de luz visível apresentou picos em 286, 363 e 435 nm. Determinou-se os teores de bixina e compostos fenólicos – 0,17 mg/mg e 0,05 mg por equivalência de pirogalol/mg de extrato seco, respectivamente. A citoxicidade foi investigada pelo teste de Brometo de 3-(4,5-dimetiltiazol-2-il)-2,5-difeniltetrazolium. A Mínima Concentração Citotóxica (MCC) para GL-15 foi 180 e 80 μg/mL para C6, para astrócitos foi 240 μg/mL, após 48 horas de tratamento. O teste de exclusão com azul tripan confirmou a EC50 para GL-15 após 24 horas. A análise morfológica foi realizada por microscopia de contrataste de fase e fluorescência. Comprovou-se a diminuição de células neoplásicas e alterações celulares na MCC em astrócitos. A capacidade de fluorescência foi comprovada em GL-15. A citotoxicidade não depletou GSH. Investigou-se alterações de ciclo celular e morte celular por citometria de fluxo. Alterações de ciclo celular não foram evidenciadas. O tipo de morte celular foi investigado com marcação para anexina V e Iodeto de Propídio comprovou morte por necrose em GL-15 e por apoptose tardia em C6, os astrócitos apresentaram valores pequenos de morte por apoptose tardia e necrose. Conclusão: Os dados indicam um potencial antitumoral das substâncias presentes neste extrato para células neoplásicas sem ser tóxico para células normais.
This work investigated the hypothesis that the methanol extract of Bixa orellana decreases the viability of GL-15 and C6 cells, without being toxic to normal astrocytes in vitro. Methods: The methanol extract of B. orellana seeds was obtained and characterized by UV-Vis spectrophotometry. The cytotoxic effects were assayed in vitro using the 3-(4,5-dimethylthiazol-2-yl)- 2,5-diphenyltetrazolium bromide method. The cell morphology was investigated by phase contrast and fluorescence microscopy. The depletion of reduced glutathione (GSH) was observed by fluorescence microscopy. The effects on cell cycle and the mode of cell death was studied by flow cytometry. Results: The contents of bixin and phenol were 0.17 mg/mg of extract and 0.05 mg of pyrogallol equivalent/mg of extract, respectively. Three peaks were observed at 286, 363, and 435 nm. The extract killed cells in a dose-dependent manner. The minimum cytotoxic concentrations in the two tumoral cells (GL-15 and C6) were respectively: 180 μg/mL and 80 μg/mL, meanwhile in astrocytes it was 240 μg/mL after 48 hours. The trypan blue assay confirmed the cytotoxic effect to GL-15 cells. Morphological degeneration of treated glioma cells was observed. The same was observed with astrocytes, but at a higher concentration. Treated cells became fluorescent, probably due to incorporation of bixin. The treatment neither depleted GSH, nor interfered on the cell cycle. The main kind of cell death was necrosis. Conclusions: Compounds present in B. orellana seeds are potentially cytotoxic to glioma cells, meanwhile primary astrocytes are more resistant.
Langton, Amy Jean. "The role of TRUSS in TNFα-TNFRI signalling : implications for inflammatory lung diseases". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608019.
Texto completoBond, Arden Lenore. "The production and characterization of a putative anti-idiotypic antibody to tumor necrosis factor-[alpha] /". This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042010-020132/.
Texto completoSaccon, Cassia Maria Toledo. "Alterações nas vias proteoliticas endogenas causados pela peçonha de Bothrops Jararacussu em musculo esqueletico". [s.n.], 2008. http://repositorio.unicamp.br/jspui/handle/REPOSIP/314699.
Texto completoDissertação (mestrado) - Universidade Estadual de Campinas, Instituto de Biologia
Made available in DSpace on 2018-08-11T19:23:03Z (GMT). No. of bitstreams: 1 Saccon_CassiaMariaToledo_M.pdf: 7279478 bytes, checksum: eb7fda24e7d486cd0267a344badc1b36 (MD5) Previous issue date: 2008
Resumo: O acidente causado por serpentes botrópicas produz intensa hemorragia e mionecrose local, com perda e degradação tecidual. Neste trabalho, investigamos as atividades do proteossomo (via seletiva da degradação protéica), catepsinas (proteases lisossomais) e calpaína (protease neutra dependente de cálcio) no envenenamento causado por peçonha de Bothrops jararacussu. Também analisamos a capacidade do MG-132, inibidor proteossômico, em atenuar os efeitos causados pela peçonha. A peçonha (25 µg e 75 µg) foi injetada em músculo gastrocnêmio de camundongos, que foram sacrificados 1, 3, 6, 12, 24, 48, 72 h e 7, 14, 21, 28 dias após o envenenamento. Os músculos tratados e contralaterais foram retirados e processados para histologia e para ensaios fluorimétricos e colorimétricos das enzimas e o sangue foi coletado para quantificação da creatina quinase (CK, indicador da mionecrose). A peçonha de B. jararacussu causou hemorragia e mionecrose (fase 1, até 6 h a 12 h pós-envenenamento - p.e.), a presença de infiltrado inflamatório e desencadeou a formação de miotubos e mioblastos (fase 2, de 12 h a 72 h p.e.) e o aparecimento de células regenerativas com maior deposição de colágeno ao redor dessas células (fase 3, 7-28 dias p.e.). De modo geral, as alterações mais marcantes ocorreram com a dose maior da peçonha. O dano tecidual agudo foi confirmado pelo aumento nos níveis plasmáticos de CK entre 1 h e 6 h p.e., com pico em 3 h. Houve redução na concentração de aminoácidos livres do músculo durante as primeiras 24 h, seguida por retorno a níveis normais. Também houve redução significativa na atividade proteossomal (até 48 h) nos músculos envenenados seguida por recuperação e aumento significativo em alguns períodos da regeneração. Nesses períodos de regeneração, houve aumento da expressão das subunidades 20Sa e 11S do proteossomo, principalmente com a dose maior da peçonha. O inibidor proteossômico diminuiu a atividade quimiotripsina e o número de células regenerativas, mas esses efeitos também foram observados no grupo que recebeu apenas o veículo do inibidor (DMSO). A calpaína foi ativada nas primeiras 6 h após o envenenamento somente com a dose maior da peçonha. As catepsinas (B e H) exibiram ativação significativa no período de regeneração (de 48 h até 28 dias) nas duas doses aplicadas. Esses resultados indicam que a peçonha de B. jararacussu afetou diferencialmente as vias proteolíticas estudadas. É possível que a calpaína esteja envolvida na fase 1 do dano tecidual e que as catepsinas estejam relacionadas à presença de infiltrado inflamatório (fase 2) ou à regeneração (fase 3). O proteossomo parece não estar relacionado à fase aguda de degradação tecidual, mas pode estar envolvido na regeneração muscular embora isso ainda precise ser confirmado
Abstract: Bites by Bothrops snakes produce intense local hemorrhage and myonecrosis, often with extensive tissue degradation. In this work, we investigated the activities of the proteasome (pathway for selective protein degradation), cathepsins (lysosomal proteinases) and calpains (neutral, calcium-dependent proteinases) in envenoming by Bothrops jararacussu. We also examined the ability of MG-132, a proteasome inhibitor, to attenuate the venom-induced effects. Mice were injected with venom (25 µg or 75 µg) in the left gastrocnemius muscle and then killed 1, 3, 6, 12, 24, 48, 72 h and 7, 14, 21 and 28 days post-venom. The venom-injected and contralateral muscles were removed and processed for histological analysis or enzymatic assays using fluorimetric or colorimetric substrates. Blood was also collected for the quantification of plasma creatine kinase (CK, an indicator of myonecrosis). Bothrops jararacussu venom caused hemorrhage and necrosis (phase 1, up to 6-12 h post-venom), an inflammatory cell infiltrate and it generated the formation of myotubes and myoblasts (phase 2, 12-72 h post-venom), and the appearance of regenerative cells with increase of collagen deposition around these cells (phase 3, 7-28 days post-venom). The alterations were generally more marked with the higher dose of venom. The early tissue damage was confirmed by an increase in plasma CK levels 1-6 h post-venom, with a peak at 3 h. The muscle content of free amino acids decreased during the first 24 h, followed by a return to normal levels. Proteasomal activity was significantly inhibited for up to 48 h post-venom, followed by recuperation and a significant increase during muscle regeneration. During regeneration, there was also an increase in the expression of the 20Sa and 11S proteasomal subunits, mainly with the highest dose of venom. The proteasomal inhibitor reduced the chymotrypsin activity of the proteasome and the number of regenerating cells, but these effects were also seen in mice that received vehicle (DMSO) alone. The highest dose of venom caused an increase in calpain activity in the first 6 h whereas both of the venom doses significantly increased the activities of cathepsins B and H during the regeneration phase (48 h¿28 days post-venom). These results indicate that B. jararacussu venom differentially affects the proteolytic activities studied. Calpain may be involved in phase 1 of tissue damage and cathepsin activity may be related to the presence of an inflammatory infiltrate (phase 2) and/or regeneration (phase 3). The lack of proteasomal activation in the early stages of envenoming suggests that this proteolytic pathway is not involved in early venom-induced muscle damage. However, the involvement of proteasomal activity during muscle regeneration remains to be established.
Mestrado
Bioquimica
Mestre em Biologia Funcional e Molecular
Higashi, Rosemeire Rosa. "Estudo da osteonecrose no processo de usinagem da cabeça do fêmur utilizando um dispositivo mecânico de furação". Universidade de São Paulo, 2014. http://www.teses.usp.br/teses/disponiveis/18/18146/tde-16122014-173014/.
Texto completoThe utilization of surgical implants for hip arthroplasty with a resurfacing prosthesis of the femoral head as a bone substitute have been conducted in 35% of osteoarthrosis cases in the USA. However, the friction of the drill and the increase in the temperature during the machining of the femoral head can possibly heat the bony tissue and provoke a thermal bone necrosis. The development of new tools and methodologies for minimizing the thermal damage of the friction has become fundamental. The present study analyzes the occurrence of bone necrosis in a procedure of bone drilling that uses an EQUITRON device, Mod. ES 2200, developed at the LTC-EESC-USP. Four samples of bovine ribs removed after the death of the animal were used for the tests. They were drilled by an 8mm stainless-steel drill (HSS-SKF) with no external irrigation, at 100, 1000, 1200 and 2500 RPM calibrated by a MINIPA, MDT-2238 digital photo/contact tachometer and whose 80mm/min. advance (EQUITORN device; MOD.ES 2200; RPM 2800; 0.30 Potency and 1,6Nm torque) was controlled. The initial temperatures of the drill and the sample and the final temperature of the sample were measured by a MEDISANA digital thermometer. After drilling, histological blades (HE) were produced from the bony tissue and prepared according to the adequate methodology for further qualification and quantification of the occurrence of thermal bone necrosis through images captured by optical microscopy (Olympus BX 41TF - made in Japan) and Motic Images Plus 2.0 program. The values of the temperatures measured in the sample after drilling showed a positive relation with the RPM utilized, i.e., the faster the rotation, the higher the temperature. Only the sample drilled at 2500RPM exceeded the reference temperature (47ºC) for the genesis of the thermal osteonecrosis. The histological analyses revealed a low predominance of picnotic cells and gaps, which suggest minor tissue damage. The results show the device (drilling machine) developed at the LTC-EESC-USP for the drilling in the bone samples in workbench tests is efficient to minimize the occurrence of thermal bone necrosis, even at temperatures above the physiological acceptable limit.
Maioli, Marcos Antonio. "Papel da mitocôndria na citoxicidade induzida pela abamectina em hepatócitos isolados de rato /". Araçatuba, 2012. http://hdl.handle.net/11449/92104.
Texto completoBanca: Cézar Rangel Pestana
Banca: Guilherme de Paula Nogueira
Resumo: Abamectina (ABA), pertencente à família das avermectinas é utilizada mundialmente como parasiticida, porém a intoxicação por ABA pode prejudicar o funcionamento hepático. Existem substâncias que quando metabolizadas exercem atividade tóxica, afetando a função de importantes organelas como a mitocôndria, responsável por uma variedade de processos bioquímicos, como a produção de ATP e morte celular. O objetivo desse estudo foi caracterizar o mecanismo de toxicidade da ABA em hepatócitos isolados de ratos e avaliar se esse efeito é dependente do seu metabolismo. A toxicidade da ABA foi avaliada monitorando o consumo de oxigênio e o potencial de membrana mitocondrial, concentração intracelular de ATP, viabilidade celular por meio da liberação das enzimas ALT e AST, homeostase intracelular Ca2+, liberação de citocromo c, atividade da caspase 3 e morte celular por necrose. A ABA reduz a respiração celular, tanto em células energizadas com glutamato mais malato quanto com succinato. O metabolismo da ABA reduz sua toxicidade, uma vez que hepatócitos previamente incubados com proadifen apresentam maior sensibilidade ao composto, sendo isto observado pelo rápido decréscimo da formação do potencial de membrana mitocondrial acompanhado pelas reduções das concentrações de ATP, viabilidade celular e ruptura da homeostase intracelular de Ca2+ com estabelecimento de necrose. Nossos resultados indicam que a toxicidade da ABA diminui com a sua biotransformação, e sua ação tóxica está relacionada com a inibição da atividade mitocondrial, levando à diminuição da síntese de ATP seguida pela morte da célula
Abstract: Abamectin (ABA), which belongs to the family of avermectinas, used worldwide as a parasiticide, but the ABA poisoning can impair the functioning liver. There are substances which exert toxic activity when metabolized, thus affecting the function of important organelles such as mitochondria, responsible for a variety of biochemical processes, such as ATP production and cell death. The aim of this study was to characterize the mechanism of toxicity of ABA in isolated rat hepatocytes and to evaluate whether this effect is dependent on your metabolism. The toxicity of ABA was assessed by monitoring oxygen consumption and mitochondrial membrane potential, intracellular concentration of ATP, cell viability by releasing enzymes ALT and AST, homeostasis intracellular Ca2+, release of cytochrome c, activity of caspase 3 and cell death necrosis. The ABA reduces cellular respiration, both in cells energized with glutamate and succinate over malate. The metabolism of ABA reduces its toxicity, since hepatocytes pre-incubated with proadifen are more sensitive to the compound, this being observed by the formation of rapidly decreasing mitochondrial membrane potential accompanied by reductions in concentrations of ATP, cell viability and rupture of the intracellular homeostasis Ca2+ with the establishment of necrosis. Our results indicate that the toxicity decreases as the ABA its biotransformed and its toxic action is related to the inhibition of mitochondrial activity, leading to decreased synthesis of ATP followed by cell death
Mestre
Dias, 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.
Texto completoResumo: 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
Han, Jiahuai. "Study of the regulation of cachectin/tumor necrosis factor expression". Doctoral thesis, Universite Libre de Bruxelles, 1990. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213139.
Texto completoJersmann, Hubertus Paul Anton. "Bacterial lipopolysaccharide and tumour necrosis factor- alpha synergism in inflammation". Title page, contents and abstract only, 2000. http://web4.library.adelaide.edu.au/theses/09PH/09phj56.pdf.
Texto completoHel, Zdenek. "Posttranscriptional regulation of tumor necrosis factor-Ã production in macrophages". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0010/NQ36980.pdf.
Texto completoMustapha, Shareef. "Signaling pathways of tumor necrosis factor à in ventricular myocytes". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ41751.pdf.
Texto completoMorris, Alison. "The role of tumour necrosis factor alpha (TNFđ) in obesity /". Title page, contents and abstract only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09phm8748.pdf.
Texto completoHel, Zdenĕk. "Posttranscriptional regulation of tumor necrosis factor-a production in macrophages". Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=34642.
Texto completoWe demonstrate that two distinct regions, located in a part of the 3 '-UTR of murine TNF-alpha mRNA previously shown to play a crucial role in the regulation of the stability and translatability, interact with macrophage nuclear and cytoplasmic proteins. The first protein binding region is located inside the AU-rich sequence 424 bp downstream of the end of the coding sequence, while the second protein binding region contains a single AUAUUUAU motif and is located 147 bp downstream of the first region. Six detectable protein species interact with the first protein binding region and seven proteins interact with the second binding region. Some of the RNA binding proteins mutually compete for the binding to both regions. TNF-alpha derived cRNA probes form complexes with proteins differentially distributed among the nuclear, cytosolic and particulate fractions of murine macrophages. Three of the TNF-alpha mRNA binding complexes cosediment in the polyribosomal fraction. The stimulation of macrophages with LPS, interferon-gamma, PMA or their combination significantly increases the stability and translational efficiency of TNF-alpha mRNA, yet does not alter the RNA binding activity nor the localization of TNF-alpha mRNA binding proteins, suggesting that regulation of gene expression by RNA-binding proteins may involve other mechanisms, such as posttranslational modification of these proteins or proteins interacting with them rather than global alteration of their amounts in particular cell compartements. The GA dinucleotide insertion inside the first protein binding region, found in NZW and several other strains of mice and associated with lowered ability of peritoneal macrophages to produce TNF-alpha, alters the formation of RNA-protein complexes, supporting their role in the posttranscriptional regulation of TNF-alpha production. Two candidate TNF-alpha mRNA binding proteins were cloned by direct screening of cDNA protein expression library using modified northwestern
Bain, Nicola. "Understanding host-pathogen interactions of infectious pancreatic necrosis virus (IPNV)". Thesis, University of Aberdeen, 2010. http://digitool.abdn.ac.uk:80/webclient/DeliveryManager?pid=158418.
Texto completoDunlop, 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.
Texto completoKnott, Rachel M. "The persistence of infectious pancreatic necrosis virus in Atlantic salmon". Thesis, University of Aberdeen, 1988. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.330104.
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