Дисертації з теми "Hemolytic uremic syndrome Prevention"
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Srimanote, Potjanee. "Analysis of putative virulence factors of a locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain." Title page, contents and abstract only, 2003. http://web4.library.adelaide.edu.au/theses/09PH/09php863.pdf.
Повний текст джерелаNoris, Marina. "Genetics of hemolytic uremic syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7591.
Повний текст джерелаMaga, Tara Kristen. "Unraveling the complex genetics of atypical hemolytic uremic syndrome." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/2935.
Повний текст джерелаEdwards, Kelly Katherine. "Bacterial factors contributing to the pathogenesis of the hemolytic uremic syndrome." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060096.
Повний текст джерелаBu, Fengxiao. "Exploring the genetics of a complex disease - atypical hemolytic uremic syndrome." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3055.
Повний текст джерелаKarpman, Diana O. "Studies of the pathogenesis of hemolytic uremic syndrome and thrombotic thrombocytopenic purpura." Lund : Lund University, 1997. http://catalog.hathitrust.org/api/volumes/oclc/68945090.html.
Повний текст джерелаValoti, Elisabetta. "Genetic factors associated with anti-factor H autoantibodies in atypical hemolytic uremic syndrome (aHUS)." Thesis, Open University, 2018. http://oro.open.ac.uk/55853/.
Повний текст джерелаMorigi, Marina. "Unravelling molecular and biochemical dysfunction by Shiga toxin: implication for thrombotic microangiopathy in Hemolytic Uremic Syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7590.
Повний текст джерелаMarinozzi, Maria Chiara. "Characterization of the complement hereditary and acquired abnormalities in atypical Hemolytic Uremic Syndrome and C3 Glomerulopathy." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB037/document.
Повний текст джерелаMcGannon, Colleen M. "Antibiotic Therapy in the Treatment of E. coli O157:H7." University of Cincinnati / OhioLINK, 2009. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1230919332.
Повний текст джерелаBollinger, Laurie M. "Factors affecting prevalence of Shiga toxin-producing Escherichia coli in cattle /." abstract and full text PDF (UNR users only), 2008. http://0-gateway.proquest.com.innopac.library.unr.edu/openurl?url_ver=Z39.88-2004&rft_val_fmt=info:ofi/fmt:kev:mtx:dissertation&res_dat=xri:pqdiss&rft_dat=xri:pqdiss:3329564.
Повний текст джерелаMiller, Rachel MD, Alex Yu, and Demetrio Rebano MD Macariola. "Virulent Bacteria in Appalachian Tennessee Waters." Digital Commons @ East Tennessee State University, 2018. https://dc.etsu.edu/asrf/2018/schedule/133.
Повний текст джерелаGomes, Priscila Aparecida Dal Pozo. "Desenvolvimento de uma nova estratégia vacinal contra síndrome hemolítica urêmica utilizando linhagens geneticamente modificadas de Bacillus subtilis capazes de expressar a toxina Stx2 de EHEC." Universidade de São Paulo, 2008. http://www.teses.usp.br/teses/disponiveis/42/42132/tde-04062008-102629/.
Повний текст джерелаThe Hemolytic Uremic Syndrome (HUS) is the main disease associated with infections with Shiga toxin (Stx) - producing Escherichia coli strain and no effective vaccine or treatment exist. The Stx toxin consist of an enzymatically active A subunit and a pentameric B subunit responsible toxin binding to host cells. In this work we propose the use of Bacillus subtilis, a harmless spore form bacteria as a vaccine vehicle for the expression atoxic forms of Stx2, under the control of stress inducible (PgsiB) promoter. BALB/c mice immunized with vegetative cells and spores of the B. subtilis vaccine strain using different immunization routes elicited low specific antibody levels at serum (IgG) or fecal extracts (IgA). We also investigated the immunogenic potencial of StxB purified from recombinant E. coli strain, but the induced anti-StxB antibodies did not neutralize the native toxin. The results indicate that alternative expression system or the incorporation of the adjuvants are required for the generation of vaccine formulation active against HUS.
Leeper, Molly Maitland. "Trends in Toxin Profiles of Human Shiga Toxin-Producing Escherichia Coli (STEC) O157 Strains, United States, 1996-2008." Atlanta, Ga. : Georgia State University, 2009. http://digitalarchive.gsu.edu/iph_theses/57/.
Повний текст джерелаTitle from file title page (Digital Archive@GSU, viewed June 16, 2010) Karen Giseker, committee chair; Peter Gerner-Smidt, committee member. Includes bibliographical references (p. 101-105).
Fogo, Verônica Simões. "Prevalência e caracterização de Escherichia coli O157:H7 e outras cepas produtoras de toxina de Shiga (STEC) na linha de abate de carne bovina destinada à exportação." Universidade de São Paulo, 2009. http://www.teses.usp.br/teses/disponiveis/9/9131/tde-27012017-123850/.
Повний текст джерелаEscherichia coli is a microorganism present in the intestinal tract of humans and warm-blood animals, being part of the normal microbiota and harmless to the host. However, some strains are able to cause human and animal infections. Shiga toxin-producing E. coli (STEC), regarded as foodborne pathogens, can cause since mild or severe and bloody diarrhea to major complications, such as hemorrhagic colitis (HC), hemolytic-uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP). Cattle are considered the main reservoir of this pathogen and the transmission to humans happens, most of the times, due to the consumption of contaminated food or water. The aim of the present research was to determine the prevalence of E. coli O157:H7 and other STEC on hide samples of beef cattle and on their corresponding carcasses, sampled prior to evisceration, and half-carcasses, sampled after evisceration; identity the genes that code for the virulence factors (stx1, stx2, eaeA e ehxA) of the isolates; detect E. coli O157:H7 strains using the gene uidA as epidemiological marker; identify the serotypes of the STEC isolates; verify the citotoxicity of the isolates in Vero cells and evaluate their resistance to different antibiotics. From 198 animals sampled, seven (3.5%) carried STEC strains. In six (3%) of them, STEC was detected on hide and in one (0.5%) it was isolated from half-carcass. The 23 strains isolated from hide presented the profile stx2, eaeA, uidA e ehxA, and were regarded as enterohemorrhagic Escherichia coli (EHEC), and the one isolated from half-carcass presented the profile stx2, uidA e ehxA. From the 24 isolated strains, 13 (54.2%) belonged to the serotype O157:H7. Besides this serotype, other strains belonging to serotypes that have been previously described and associated with severe human infections in Brazil and other countries, such as O174:H21 , O6:H49, ONT:H7, ONT:H8 and OR:H10, were isolated. From seven animals with strains harboring stx2, and ehxA, five (71.4%) presented verocytotoxigenic strains and one (14.2%) presented enterohemolisin producing strains. Regarding the antibiotics tested, four (16.7%) of the 24 isolated strains were resistant to some antibiotic, being three (12.5%) to streptomycin and one (4.2%) to streptomycin and ampicilin. Faced with these results, the production of enterohemolisin and the search of the genes ehxA and uidA can not be considered good epidemiological markers for the serotype O157:H7. The isolation of STEC strain from the half-carcass alerts for the need of surveillance on the presence of these microorganisms, since they may contaminate the final product, representing a risk to consumers health.
Iamashita, Priscila. "Estudo dinâmico da expressão gênica global durante a interação STEC-enterócito utilizando séries temporais." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5141/tde-20022018-131845/.
Повний текст джерелаShiga toxin-producing Escherichia coli (STEC) O113:H21 strains are associated with human diarrhea and some of these strains may cause hemolytic uremic syndrome (HUS). In Brazil O113:H21 strains are commonly found in cattle but, so far, were not isolated from HUS patients. Previously, our group conducted comparative gene co-expression network (GCN) analyses of two O113:H21 STEC strains: EH41, isolated from a HUS patient in Australia, and Ec472/01, isolated from bovine feces in Brazil. Differential transcriptome profiles for EH41 and Ec472/01 revealed a gene set exclusively expressed in EH41, which includes the dicA putative virulence factor regulator. GCN analysis showed that this set of genes constitutes an EH41 specific transcriptional module which may be associated to virulence factors. Therefore, in the present work a system biology approach was conducted to investigate the differential Caco-2 response - genomic and phenotypic - to EH41 (Caco-2/EH41) or to Ec472/01 (Caco- 2/Ec472) along enterocyte-bacteria interaction. The genomic analysis was based on temporal GCN data in order to gain a better understanding on the molecular mechanisms underlying the capacity to cause HUS. The phenotypic alterations in Caco-2 during enterocyte-bacteria interaction were assessed by scanning electronic microscopy (SEM). The genomic analysis showed that the molecular mechanism of Caco-2 response to EH41 or to Ec472/01 during enterocyte-bacteria interaction is clearly different. The GCN topological analyses for Caco-2/EH41 group revealed loss of the scale-free status after one hour of interaction, persistence of this condition along the second hour and establishment of a new gene hierarchy thereafter. These events resemble the network mechanism of health-disease transition. The new established network represents an adaptive cell response to the pathogen and not the return to a \"normal\" state. Conversely, the networks for Caco-2/Ec472 group showed a slow and progressive loss of the scale-free status without its restoration at the end of the time interval here studied. Through transcriptional module characterization it was possible to reveal the dynamic of the molecular mechanism involved in the Caco-2 differential responses to the STEC isolates. EH41 induces a rapid inflammatory and apoptotic response just after the first hour of enterocyte-bacteria interaction. Instead, the Caco-2 response to Ec472/01 is characterized by phagocytosis activation at the first hour, followed by the expression of immune response modulators after the second hour. SEM phenotypic analysis of Caco-2 cells along enterocyte-bacteria interaction showed more intense microvilli destruction in cells exposed to EH41, when compared to cells exposed to Ec472/01. The integration of genomic and phenotypic data allowed us to conclude that EH41, comparatively to Ec472/01, induces greater and precocious global gene expression alterations in Caco-2, what is related to excessive inflammatory and apoptotic responses. These responses are associated with the pronounced morphological alterations observed by SEM in Caco-2 cells exposed to EH41. Altogether, these results contribute for a better understanding of the molecular mechanism involved in STEC pathogenicity associated to HUS. Therefore, the future perspectives for the development of the present work should include the investigation of virulence factors and molecular pathways involved in the induction of immune responses leading to HUS
Mallick, Emily M. "A New Murine Model For Enterohemorrhagic Escherichia coli Infection Reveals That Actin Pedestal Formation Facilitates Mucosal Colonization and Lethal Disease: A Dissertation." eScholarship@UMMS, 2012. https://escholarship.umassmed.edu/gsbs_diss/601.
Повний текст джерелаOsório, Maria Clotilde Avides Moreira Pinto. "An overview on the treatment for atypical hemolytic uremic syndrome." Dissertação, 2018. https://repositorio-aberto.up.pt/handle/10216/112634.
Повний текст джерелаOsório, Maria Clotilde Avides Moreira Pinto. "An overview on the treatment for atypical hemolytic uremic syndrome." Master's thesis, 2018. https://hdl.handle.net/10216/112634.
Повний текст джерелаMotomochi, Amanda. "Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury." Thesis, 2014. https://hdl.handle.net/2144/14397.
Повний текст джерелаMalva, Jéssica Filipa Pires. "Study of VTN, PLG and other coagulation genes in atypical Hemolytic Uremic Syndrome (aHUS)." Master's thesis, 2020. http://hdl.handle.net/10773/30449.
Повний текст джерелаIntrodução: A síndrome hemolítica urémica atípica é uma variante rara de microangiopatia trombótica caracterizada por anemia hemolítica microangiopática, trombocitopenia e, por vezes, insuficiência renal aguda. Esta patologia é frequentemente idiopática, podendo também ser secundária a outras patologias ou devida a causas genéticas – variantes nos genes do complemento (C3, CFB, CFH, CFI, MCP, THBD). Estas alterações, na maioria dos casos, originam a hiperativação da via alternativa do complemento e consequentemente resultam em formação de trombos microvasculares que afetam, principalmente, a função renal. No entanto, recentemente surgiram outras possíveis causas genéticas desta patologia, em genes não relacionados com o complemento, VTN, PLG, entre outros genes de coagulação. Objetivos e Métodos: Com o objetivo de analisar a correlação genótipo/fenótipo em pacientes com SHUa, analisámos 45 genes em 50 pacientes, utilizando a sequenciação Sanger para o gene VTN e um painel de genes personalizado de sequenciação de próxima geração (NGS) para o PLG e outros genes de coagulação. Resultados: No total, foram identificadas 53 variantes raras diferentes em VTN, PLG, ADAMTS13, ANKRD26, F5, F7, F8, F10, F13A1, FGA, FGB, FGG, GP6, ITGA2B, ITGB3, NBEAL2, PLAT, PROC, PROS1, SERPINC1, SERPINE1, SERPINF2, TUBB1 e VWF. Das quais, identificámos 8 variantes patogénicas, 11 provavelmente patogénicas, 14 de significado incerto e 20 provavelmente benignas. Conclusões: Este estudo não implicou os genes VTN e PLG, em particular, como importantes contribuintes para SHUa. Contudo, encontrámos variantes em vários genes que poderão constituir uma predisposição genética nestes doentes, e ter um efeito cumulativo em ambos os sistemas - coagulação e complemento.
Mestrado em Bioquímica
Psotka, Mitchell Adam. "The pathophysiology of renal failure in a shiga toxin plus lipopolysaccharide induced murine model of hemolytic uremic syndrome." 2008. http://proquest.umi.com/pqdweb?did=1805440271&sid=3&Fmt=2&clientId=3507&RQT=309&VName=PQD.
Повний текст джерелаKeepers, Tiffany Rae. "Renal inflammation in a shiga toxin plus lipopolysaccharide induced murine model of hemolytic uremic syndrome." 2007. http://proquest.umi.com/pqdweb?did=1801471441&sid=4&Fmt=2&clientId=3507&RQT=309&VName=PQD.
Повний текст джерелаThompson, Morgan Paige. "Changes in tissue expression of coagulation-related molecules after challenge with coagulopathic Shiga toxin-2." Thesis, 2017. https://hdl.handle.net/2144/23879.
Повний текст джерелаNiu, Shuo. "Regulation Of Innate Immune Cell Response Under Sub-acute/Chronic Inflammatory Conditions." 2017. http://scholarworks.gsu.edu/biology_diss/191.
Повний текст джерелаMayer, Chad. "Shiga toxins and damage-associated molecular patterns leading to endothelial dysfunction." Thesis, 2016. https://hdl.handle.net/2144/15270.
Повний текст джерелаRogers, Trisha Jayne. "CXC chemokine responses of intestinal epithelial cells to Shiga-toxigenic Escherichia coli." 2004. http://hdl.handle.net/2440/37966.
Повний текст джерелаThesis (Ph.D.)--School of Molecular and Biomedical Science, 2004.
Parello, Caitlin Suzanne Leibowitz. "Investigating the contributions of leukocyte responses and kidney cell stress on Shiga- toxin pathogenesis." Thesis, 2015. https://hdl.handle.net/2144/15616.
Повний текст джерелаPage, Andrea Vaughn. "Angiopoietin-1 and -2 in Infectious Diseases associated with Endothelial Cell Dysfunction." Thesis, 2012. http://hdl.handle.net/1807/32274.
Повний текст джерела