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Relevant bibliographies by topics / Hemolytic uremic syndrome Prevention / Dissertations / Theses

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Dissertations / Theses on the topic 'Hemolytic uremic syndrome Prevention'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

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.

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"February 2003." Addendum and corrigenda inserted at back Includes bibliographical references (leaves 249-272) Aims to identify and characterise potential virulence-associated factors from the locus of enterocyte effacement-negative shiga-toxigenic Escherichia coli O113:H21 strain 98NK2 which was responsible for an outbreak of haemolytic uremic syndrome. Particular attention was focused on putative virulence genes encoded on the megaplasmid of this strain.

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2

Noris, Marina. "Genetics of hemolytic uremic syndrome." Maastricht : Maastricht : Universiteit Maastricht ; University Library, Maastricht University [Host], 2006. http://arno.unimaas.nl/show.cgi?fid=7591.

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3

Maga, Tara Kristen. "Unraveling the complex genetics of atypical hemolytic uremic syndrome." Diss., University of Iowa, 2012. https://ir.uiowa.edu/etd/2935.

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Atypical hemolytic uremic syndrome (aHUS) is characterized by acute renal failure, thrombocytopenia, and microangiopathic hemolytic anemia. aHUS is far less common and more severe than typical HUS, which is caused by E. coli infection and manifests as diarrheal illness. The pathogenesis of the disease is linked to dysregulation of the alternative pathway of the complement cascade. Mutations in the complement regulators factor H (CFH), membrane cofactor protein (MCP), factor B (CFB), and factor I (CFI) have been implicated

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4

Edwards, Kelly Katherine. "Bacterial factors contributing to the pathogenesis of the hemolytic uremic syndrome." MU has:, 2002. http://wwwlib.umi.com/cr/mo/fullcit?p3060096.

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5

Bu, Fengxiao. "Exploring the genetics of a complex disease - atypical hemolytic uremic syndrome." Diss., University of Iowa, 2016. https://ir.uiowa.edu/etd/3055.

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Atypical hemolytic uremic syndrome (aHUS) is a rare renal disorder characterized by thrombotic microangiopathy, thrombocytopenia, and acute kidney injury. Its pathogenesis has been attributed to a ‘triggering' event that leads to dysregulation of the complement cascade at the level of the endothelial cell surface. Consistent with this understanding of the disease, mutations in complement genes have been definitively implicated in aHUS. However, the existence of other genetic contributors is supported by two observations. First, in ~50% of cases, disease-causing variants are not identified in c

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6

Karpman, 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.

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7

Valoti, 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/.

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Atypical hemolytic uremic syndrome (aHUS) is a rare form of thrombotic microangiopathy characterized by renal failure and determined by genetic and acquired defects of alternative pathway (AP) of the complement system. Autoantibodies against factor H (anti-FHs), a regulator of the AP, were reported in 10% of patients, and are associated with the deficiency of factor H related 1 (FHR1), a FH homologous protein. The aim of this thesis was to evaluate the contribution of genetics to the development of anti-FHs in aHUS. Thirty patients affected by aHUS resulted positive for anti-FHs (9.8%) and FHR

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8

Morigi, 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.

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9

Marinozzi, 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.

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10

McGannon, 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.

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11

Bollinger, 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.

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12

Miller, 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.

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BACKGROUND: Over the past 5 years, 634 cases of Shigatoxin E. coli (STEC) infection were reported to Tennessee Health Department 1. At our local children’s hospital, 4-5 children are hospitalized with STEC infection each year. Some of these children had no history of ingesting food items that could have placed them at risk to develop STEC infection; however, there are other ways that humans could get infected, such as exposure to contaminated water from cattle farms 2. GOALS: To determine if bodies of water in the city are contaminated with STEC. METHODS: Fifty (50) ml of water samples were co

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13

Gomes, 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/.

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A Síndrome Hemolítica Urêmica (SHU) é a principal doença associada à infecção com linhagens de Escherichia coli produtoras de toxina de Shiga (Stx), doença para qual não há uma vacina ou tratamento específico. A toxina Stx é formada por uma subunidade A enzimaticamente ativa e uma B pentamérica responsável pela ligação da toxina na célula hospedeira. Neste trabalho propomos o uso de Bacillus subtilis, uma bactéria não patogênica e formadora de esporos, como veículo vacinal para a expressão de formas atóxicas da Stx2, sob o controle de um promotor induzível por estresse (PgsiB). Camundongos BAL

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14

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/.

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Thesis (M.P.H.)--Georgia State University, 2009.<br>Title 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).

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15

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/.

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Escherichia coli é um microrganismo presente no trato intestinal do homem e de animais de sangue quente, fazendo parte da microbiota, coexistindo sem causar danos ao hospedeiro. No entanto, algumas linhagens desse microrganismo podem ser patogênicas e causar doenças tanto ao homem como aos animais. E. coli produtoras de toxina de Shiga (STEC), consideradas patógenos de origem alimentar, podem causar desde diarréias brandas até severas e sanguinolentas a complicações graves, como colite hemorrágica (HC), síndrome urêmica hemolítica (HUS) e púrpura trombótica trombocitopênica (TTP). O gado é con

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16

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/.

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As Escherichia coli produtoras da toxina Shiga (STEC) são importantes patógenos humanos, causando desde diarréias até a síndrome hemolítica urêmica (SHU). Há diversos sorotipos associados a SHU, tais como O157:H7 e O113:H21. No Brasil o sorotipo O113:H21 ainda não aparece associado a SHU, embora seja frequentemente isolado de carcaças e fezes bovinas. Nosso grupo já investigou comparativamente as redes de coexpressão gênica (RCG) de STEC EH41 (associado à SHU) e Ec472/01 (isolado de fezes bovinas). A análise comparativa do perfil transcricional de EH41 e Ec472/01 revelou que somente EH41 expre

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17

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.

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Enterohemorrhagic Escherichia coli (EHEC) colonizes the intestine and produces the phage-encoded Shiga toxin (Stx) which is absorbed systemically and can lead to hemolytic uremic syndrome (HUS) characterized by hemolytic anemia, thrombocytopenia, and renal failure. EHEC, and two related pathogens, Enteropathogenic E. coli (EPEC), and the murine pathogen, Citrobacter rodentium, are attaching and effacing (AE) pathogens that intimately adhere to enterocytes and form actin “pedestals” beneath bound bacteria. The actin pedestal, because it is a unique characteristic of AE pathogens, has been the s

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18

Osório, 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.

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19

Osório, 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.

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20

Motomochi, Amanda. "Cell stress markers during development of hemolytic uremic syndrome and acute kidney injury." Thesis, 2014. https://hdl.handle.net/2144/14397.

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Enterohemorrhagic E. coli (EHEC) infections are a leading cause of foodborne illness in the United States. Shiga-like toxins are produced that can cause hemorrhagic colitis and can lead to dangerous complications, such as acute kidney injury and hemolytic uremic syndrome (HUS). There are currently no specific treatments for HUS, and therefore more research into EHEC and HUS needs to be done. Our study focuses on Shiga-like toxin induction of endoplasmic reticulum (ER) stress in in vitro and in vivo systems, using human monocyte-like THP-1 cells and a non-human primate model of HUS. We used

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21

Malva, 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.

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Background: Atypical hemolytic uremic syndrome is a rare variant of thrombotic microangiopathy characterized by microangiopathic hemolytic anemia, thrombocytopenia and, occasionally, acute renal failure. This condition is often idiopathic and may also be secondary to other pathologies or due to genetic causes - variants in the complement genes (C3, CFB, CFH, CFI, MCP, THBD). These changes, in most cases, lead to hyperactivation of the pathway complement and consequently result in the formation of microvascular thrombi that affect, mainly, the renal function. However, other possible genetic cau

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22

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.

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23

Keepers, 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.

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24

Thompson, 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.

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Typical Hemolytic Uremic Syndrome (HUS) presents as a complication of infection with Shiga-toxin producing E. coli (STEC). While there are many animal models for infection, few show true signs of HUS. Additionally, these models differ greatly from the clinical presentation that affects small children and elderly populations. Immunohistochemical assays of tissues from a known HUS model may provide insight into molecular changes associated with the condition, particularly as it pertains to clotting factors. In this study, tissue factor (TF) was investigated in the kidneys of non-human primates

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25

Niu, Shuo. "Regulation Of Innate Immune Cell Response Under Sub-acute/Chronic Inflammatory Conditions." 2017. http://scholarworks.gsu.edu/biology_diss/191.

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Sub-acute/chronic inflammatory diseases are often associated with altered inflammatory response, leading to increased host vulnerability to secondary inflammatory challenges. In the first study, by employing streptozotocin (STZ)-induced diabetes in mice, we further investigate mechanisms leading to enhanced polymorphonuclear leukocytes (PMN) response under hyperglycemia. We show that existence of a proinflammatory state associated with broad increases of macrophages in various organs plays a dominant role in promoting PMN response in diabetic mice. Studies of PMN infiltration during zymosan-in

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26

Mayer, Chad. "Shiga toxins and damage-associated molecular patterns leading to endothelial dysfunction." Thesis, 2016. https://hdl.handle.net/2144/15270.

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Enterohemorrhagic E. coli (EHEC) infection is a leading cause of acute kidney failure in otherwise healthy children, and a leading cause of foodborne illness with an outsized economic impact from outbreaks. EHEC secrete two Shiga-like toxins (Stx1 and Stx2) which are AB5 holotoxins that inhibit protein synthesis in cells expressing the toxin receptor Gb3. Infection with EHEC typically begins with a diarrheal prodrome that can progress in 5-15% of cases to hemolytic uremic syndrome (HUS), a clinical diagnosis characterized by thrombocytopenia, hemolytic anemia, and thrombotic microa

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27

Rogers, Trisha Jayne. "CXC chemokine responses of intestinal epithelial cells to Shiga-toxigenic Escherichia coli." 2004. http://hdl.handle.net/2440/37966.

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Since Shiga-toxigenic Escherichia coli (STEC) strains are not considered to be enteroinvasive, the mechanism(s) by which Shiga toxin (Stx) gains access to the circulation and to target tissues expressing its target receptor Gb3 is crucial to the disease process. There is increasing evidence that by facilitating translocation of Stx across the intestinal epithelium and by transporting bound toxin to remote sites such as the renal endothelium, polymorphonuclear leucocytes (PMNs) play a key role in the pathogenesis of serious STEC disease. Plasma levels of PMN-attracting CXC chemokines such as IL

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28

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.

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BACKGROUND: Shiga toxin (Stx)-producing enterohemorrhagic Escherichia coli (EHEC) are emerging food- and water- borne pathogens and a leading cause of acute renal failure in otherwise healthy children. Ribotoxic Shiga toxins are the primary virulence factors and are responsible for the potentially lethal EHEC complication of hemolytic uremic syndrome (HUS). HUS, defined clinically by microangiopathic hemolytic anemia, thrombocytopenia and thrombotic microangiopathy which contribute to acute kidney injury or renal failure, is associated with significant patient morbidity. No pathogen- or toxin-

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29

Page, Andrea Vaughn. "Angiopoietin-1 and -2 in Infectious Diseases associated with Endothelial Cell Dysfunction." Thesis, 2012. http://hdl.handle.net/1807/32274.

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Normal endothelial cell function is controlled in part by a tightly regulated balance between angiopoietin-1 and -2 (Ang-1 and Ang-2). Angiopoietin dysregulation (decreased Ang-1 and increased Ang-2) leads to an activated endothelium that is contractile, adhesive, and prothrombotic. Since an activated endothelial phenotype is seen in invasive group A streptococcal infection, E. coli O157:H7-induced hemolytic-uremic syndrome (HUS), and sepsis, we hypothesized that angiopoietin dysregulation might also be present in these syndromes, and to that end, measured angiopoietin levels in several well-c

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