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Dissertations / Theses on the topic 'Hemolytic Disease'

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Published: 4 June 2021

Last updated: 26 July 2025

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1

Fashola, Bola. "The Effect of Sodium Chloride on Beta-Hemolytic Streptococci." TopSCHOLAR®, 1987. https://digitalcommons.wku.edu/theses/2321.

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The drug of choice for the treatment of Stieptococcal pharyngitis is penicillin G. However, a common home remedy prescribes the use of salt-water solutions for gargling. Members of Beta -hemolytic streptococcal groups A, B, and C were isolated from the upper -respiratory tracts of patients diagnosed as having streptococcal pharyngitis. These cultures we:e obtained from HCA Greenview Hospital (Bowling Green, Kentucky) and used to study the effects of sodium chloride on the isolates. The minimum inhibitory concentration of sodium chloride was determined for each of eight hospital isolates. Croup

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2

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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3

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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4

Kuruthukulangare, Joseph Sebastian. "Prevention of Rh-hemolytic disease of the newborn : an evaluation of competing strategies." Thesis, McGill University, 1995. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=28806.

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Rh hemolytic disease of the newborn, once a major cause of perinatal mortality and long-term disability, is rarely seen in developed countries today. This drastic reduction in the frequency of disease occurrence has followed the widespread postpartum use of Rh immunoglobulin. However, more than half the world's population does not have access to this health care technology.<br>The objective of this thesis was to study the epidemiology of Rh disease in developed country settings and specifically to quantify the magnitude of Rh disease reduction that occurred secondary to Rh prophylaxis, and to

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5

Maranho, Caroline Klein. "Prevalência de anticorpos irregulares em gestantes atendidas em serviços públicos da hemorrede de Santa Catarina." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/17/17155/tde-07062017-145049/.

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A doença hemolítica perinatal (DHPN) é caracterizada pela destruição das hemácias fetais por anticorpos da classe IgG presentes na circulação materna. Esses anticorpos, dirigidos contra antígenos eritrocitários presentes nas hemácias do feto, atravessam a barreira placentária e promovem a hemólise prematura dos eritrócitos, podendo levar à anemia fetal. O presente trabalho teve como objetivo principal determinar a prevalência dos anticorpos irregulares em gestantes atendidas em maternidades públicas da hemorrede de Santa Catarina por meio de um estudo observacional, com coorte retrospectiva, e

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6

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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7

Sá, Cynthia Amaral Moura. "Doença hemolítica perinatal pelo fator Rh: experiência de 10 anos do Instituto Fernandes Figueira." Instituto Fernandes Figueira, 2006. https://www.arca.fiocruz.br/handle/icict/7361.

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Made available in DSpace on 2014-02-26T19:13:30Z (GMT). No. of bitstreams: 2 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) 56122.pdf: 943164 bytes, checksum: 31ab7a412fa0e24ec2743d0b364e47f6 (MD5) Previous issue date: 2013-07-22<br>Fundação Oswaldo Cruz. Instituto Fernandes Figueira. Departamento de Ensino. Programa de Pós-Graduação em Saúde da Criança e da Mulher. Rio de Janeiro, RJ, Brasil.<br>Introdução: a Doença Hemolítica Perinatal pelo fator Rh é causada pela incompatibilidade entre o sangue da mãe e do recém-nascido, levando a destruição de hemácias feta

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8

Cavalcante, Francimary de Oliveira. "Presença de Aloanticorpos Eritrocitários em gestantes Rh negativo, atendidas na Fundação de Hematologia e Hemoterapia do Amazonas (Hemoam)." Universidade Federal do Amazonas, 2005. http://tede.ufam.edu.br/handle/tede/2236.

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Made available in DSpace on 2015-04-11T13:38:35Z (GMT). No. of bitstreams: 1 Dissertacao Francimary.pdf: 640225 bytes, checksum: 1eebacf1e67b120750607e8d1a1c46d2 (MD5) Previous issue date: 2005-10-26<br>Conselho Nacional de Desenvolvimento Científico e Tecnológico<br>The presence of G class irregular erythrocyte alloantibodies in the blood circulation during pregnancy may cause a series of consequences to the newborn. The alloimmunization can occur under different situations, such as: blood incompatibility during delivery, miscarriage, amniocentese, blood transfusion, among others, all

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9

Mohamed, Bashir. "NGS-baserad metod för fetal blodgruppstypning." Thesis, Linnéuniversitetet, Institutionen för kemi och biomedicin (KOB), 2021. http://urn.kb.se/resolve?urn=urn:nbn:se:lnu:diva-106208.

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Hemolytic disease of fetus or newborn (HDFN) är en komplikation där foster eller nyföddas erytrocyter förstörs för tidigt. HDFN uppstår när det föreligger blodgruppsinkompatibilitet mellan moder och barnet. Komplikationerna/ symptomen kan variera allt från mildare symptom till fosterdöd. HDFN orsakas framförallt av antikropp D (RhD-immunisering) och på grund av detta utförs det typning av fetalt RhD i maternell plasma. Utöver RhD-immuniseringar kan svåra fall av HDFN ibland orsakas av andra blodgruppssystem som c (Rh) och K (Kell). Fetal RhD-typning görs idag som screening på alla RhD-negativa

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10

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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11

Merle, Nicolas. "Mechanisms of complement activation under hemolytic conditions." Thesis, Sorbonne Paris Cité, 2017. http://www.theses.fr/2017USPCB076/document.

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Le système du complément est une cascade de défense immunitaire complexe et étroitement régulée, conduisant à des dommages tissulaires lorsqu’il est suractivé. L’hème, un motif moléculaire de danger dérivant de l’hémolyse, est capable d’activer le complément dans le sérum et à la surface des cellules endothéliales (CE) in vitro, suggérant un rationel pour examiner l’impact de l’activation du complément dans les maladies hémolytiques. L’objectif de ce projet était d’étudier si et comment l’hémolyse intravasculaire active le complément in vivo, et de comprendre les mécanismes sous-jacent conduis

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12

Seidl, Valeria. "Doença hemolítica perinatal: fatores de risco e abordagem terepêutica." reponame:Repositório Institucional da FIOCRUZ, 2013. https://www.arca.fiocruz.br/handle/icict/8313.

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Made available in DSpace on 2014-09-09T12:22:45Z (GMT). No. of bitstreams: 2 license.txt: 1748 bytes, checksum: 8a4605be74aa9ea9d79846c1fba20a33 (MD5) 69594.pdf: 1287197 bytes, checksum: 097f898f1364f075660a2a3257570c38 (MD5) Previous issue date: 2013<br>Fundação Oswaldo Cruz. Instituto Nacional de Saúde da Mulher, da Criança e do Adolescente Fernandes Figueira. Departamento de Ensino. Programa de Pós-Graduação em Saúde da Criança e da Mulher. Rio de Janeiro, RJ, Brasil.<br>Objetivo: Identificar fatores de risco associados à necessidade de exsanguíneotransfusão (EXT) em gestações acometidas

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13

Laurentino, MarÃlia Rocha. "Relationship between gene polymorphisms at BCL11A and hemolysis markers in patients with sickle cell disease." Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16437.

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CoordenaÃÃo de AperfeÃoamento de Pessoal de NÃvel Superior<br>Sickle cell disease (SCD) is a hematological disease caused by a point mutation in the β-globin gene. Sickle hemoglobin (HbS) is generated due to fragile mutation that decreases the red blood cell lifetime due to its chronic destruction, being the main responsible for the signs and symptoms of the disease. The use of hydroxyurea (HU) and genetic polymorphisms on modulates fetal hemoglobin (HbF), the main inhibitor of HbS polymerization, reducing hemolysis and vaso-occlusion. This study aimed to evaluate the association of polym

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14

Thompson, James Russell. "Imaging the assembly of the Staphylococcal pore-forming toxin alpha-Hemolysin." Thesis, University of Oxford, 2009. http://ora.ox.ac.uk/objects/uuid:e320004a-6118-4dac-af2a-eca6e90be7ac.

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Alpha-hemolysin is a pore-forming toxin secreted by pathogenic Staphylococcus aureus. Its spontaneous oligomerization and assembly into a trans-bilayer beta-barrel pore is a model for the assembly of many other pore-forming toxins. It is studied here in vitro as a means to probe general membrane protein oligomerization and lipid bilayer insertion. This thesis details the results of experiments to develop and implement a novel in vitro lipid bilayer system, Droplet-on-Hydrogel Bilayers (DHBs) for the single-molecule imaging of alpha-hemolysin assembly. Chapter 2 describes the development of DHB

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15

Lévy, Eva. "Identification de causes génétiques du syndrome d’Evans pédiatrique." Thesis, Sorbonne Paris Cité, 2016. http://www.theses.fr/2016USPCB017/document.

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Le syndrome d'Evans est défini par l'existence concomitante ou séquentielle de cytopénies auto-immunes, le plus souvent, anémie hémolytique et thrombopénie immunologique. Chez l'enfant, il peut être secondaire à une infection, une maladie auto-immune systémique ou un déficit immunitaire primitif. Alternativement, chez une grande partie des patients, l'étiologie n'est pas clairement identifiée. Les patients atteints de syndrome d'Evans présentent parfois d'autres atteintes, telles une auto-immunité d'organe, une lymphoprolifération bénigne ou un déficit immunitaire. L'objectif de ce travail éta

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16

Ma, Jianneng. "Purification, serology and pathogenic role of the 110 kilodalton rtx hemolysins of Actinobacillus pleuropneumoniae." Diss., Virginia Tech, 1991. http://hdl.handle.net/10919/39935.

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<i>Actinobacillus pleuropneumoniae</i> is the etiological agent of contagious swine pleuropneumonia, an economically important disease of the swine industry worldwide. Improved control of this disease requires enhanced understanding of the factors contributing to pathogenesis. The objectives of this study were to investigate the immune response and virulence properties of the 110-kilodalton (110-KDa) hemolysins [hemolysin I (HlyI) and hemolysin II (HlyII)] of <i>A. pleuropneumoniae</i>. Several monoclonal antibodies (MAb) to the hemolysins were developed. An IgGl. MAb (8C2) specific for HlyII,

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17

Baltyde, Kizzy-Clara. "Implication de la voie adénosine/adénosine récepteur A2B dans les mécanismes physiopathologiques de deux manifestations drépanocytaires : l'hémolyse et le priapisme." Thesis, Antilles, 2016. http://www.theses.fr/2016ANTI0039/document.

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La drépanocytose résulte d’une mutation du gène β-globine entrainant la synthèse d’une hémoglobine anormale, l’HBS, qui polymérise en condition désoxygénée. Le globule rouge deviendra plus rigide et plus fragile, donnant lieu a deux conséquences majeures : l’hémolyse accrue et l’occlusion vasculaire.Récemment, un nouvel acteur moléculaire, l’adénosine, a été identifie. Ce nucléoside présente des effets bénéfiques sur les atteintes pulmonaires en inhibant l’activation des cellules « tueur naturel t inductibles », mais aussi délétères en favorisant la polymérisation de l’HBS et la survenue du pr

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18

Lizarralde, Iragorri Maria. "Impact of mechanical and oxidative stress on red blood cell properties in sickle cell disease." Thesis, Sorbonne Paris Cité, 2018. http://www.theses.fr/2018USPCC324.

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Le globule rouge est une cellule simple avec l’une des fonctions les plus importantes de l’organisme : participer aux échanges gazeux et fournir l’oxygène aux tissus. C'est un disque biconcave hautement élastique grâce à un réseau de protéines du cytosquelette et de protéines membranaires spécifiques. La fonction, ainsi que la structure des globules rouges sont altérées dans plusieurs pathologies humaines telles que les hémoglobinopathies et les anomalies de membrane. La drépanocytose est une maladie héréditaire génétique caractérisée par une hémoglobine anormale qui polymérise en conditions h

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19

Assunção, Renata Almeida de. "Índice de performance miocárdica fetal na doença hemolítica perinatal." Universidade de São Paulo, 2015. http://www.teses.usp.br/teses/disponiveis/5/5139/tde-24022016-094707/.

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A hemólise decorrente da doença aloimune desencadeia mecanismos adaptativos hematológicos e hemodinâmicos fetais, com intuito de garantir o suprimento adequado de oxigênio para todos os tecidos e órgãos. Na anemia grave, a sobrecarga imposta ao coração fetal, devido ao fluxo hiperdinâmico, tem sido considerada responsável pela insuficiencia cardiaca, e posterior desenvolvimento de hidropisia fetal. No entanto, a literatura médica ainda apresenta controvérsias acerca da integridade da função cardiaca nesta doença. O índice de performance miocárdico (IPM) é uma ferramenta propedêutica não invasi

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20

Zhao, Jun. "Multi-scale Molecular Dynamics Simulations of Membrane-associated Peptides." University of Akron / OhioLINK, 2013. http://rave.ohiolink.edu/etdc/view?acc_num=akron1377265339.

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21

Shahcheraghi, Ali. "The pathophysiology of anti-Kell "hemolytic disease of newborn."." 2005. http://link.library.utoronto.ca/eir/EIRdetail.cfm?Resources__ID=362534&T=F.

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22

Martins, Susana Gomes Rodrigues. "A protective role for ataxia-telangiectasia mutated in hemolytic conditions." Master's thesis, 2019. http://hdl.handle.net/10362/90764.

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Ataxia-telangiectasia mutated (ATM) is a kinase that plays key roles in DNA repair signaling pathways and oxidative stress response, among others. ATM mutations lead to ataxia-telangiectasia (A-T), a disease characterized for example by ataxia, immunodeficiencies and redox potential dysregulation. Malaria is characterized by excessive hemolysis with hemoglobin and heme being accumulated in plasma, causing tissue damage. Unpublished data from the host laboratory showed that: i) mice without Atm are more susceptible to malaria than controls, revealing a new disease where the presence of Atm is

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23

Seto, Eva. "The Inhibitory Effect of Kell Blood Group Antibodies on Erythroid Progenitor Cell Growth." Thesis, 2008. http://hdl.handle.net/1807/17221.

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The clinical manifestations of hemolytic disease of the fetus and newborn mediated by anti-K, an antibody of the Kell blood group system, are distinguishable from the classical form of the disease. Affected fetuses have low numbers of circulating reticulocytes and antibody titers and bilirubin levels are not reliable predictors of anemia. These observations suggest that antibodies to Kell glycoprotein lead to anemia through suppression of erythropoiesis. This study established a liquid erythroid progenitor cell culture model in which to perform analyses on the mechanism of the suppressive g

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24

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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25

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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26

Brinc, Davor. "IgG-mediated Immune Suppression: the Effect on the Host Immune System." Thesis, 2008. http://hdl.handle.net/1807/11184.

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One of the most effective immunological interventions for human disease prevention is the administration of anti-red blood cell (RBC) IgG, more specifically, anti-D IgG, for prevention of hemolytic disease of the fetus and newborn (HDN), a serious and potentially fatal condition caused by the maternal immune response against the Rhesus (Rh) blood group system D antigen on fetal RBC. Despite its widespread clinical use, the mechanism of the suppressive anti-RBC IgG effect is not fully understood. In a murine model of immunity to foreign RBCs, transfusion of mice with IgG-opsonized RBCs strongly

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27

Allison, Health Elizabeth. "Cloning and characterization of a Prevotella melaninogenica hemolysin." 1997. http://catalog.hathitrust.org/api/volumes/oclc/48229226.html.

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28

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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29

Lin, Men-Chieng, and 林孟謙. "Hemolysis Phenotype and Genetic Analysis of Streptococcus agalactiae Isolated from Diseased Fish in Taiwan." Thesis, 2015. http://ndltd.ncl.edu.tw/handle/97641293827910831627.

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碩士<br>國立臺灣大學<br>獸醫學研究所<br>104<br>Streptococcus agalactiae are Gram positive cocci, also known as Group B Streptococcus (GBS). S. agalactiae can infect numerous fish species, including tilapia, rainbow trout, mullet, and hybrid striped seabass, and cause economic losses during cultivation. From 2009 to 2014, it was found that all S. agalactiae strains isolated from cultured fishes, such as tilapia and seabass, had different hemolytic phenotypes including α, β and γ. GBS hemolysin is responsible for hemolysis, and it is encoded by cyl operon. cyl operon is mainly regulated by the two-component r

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Gusmão, Sofia Vargas Nobre de. "Cerebral vasculopathy in children with sickle cell disease A study of genetic modulators of the disease." Master's thesis, 2015. http://hdl.handle.net/10362/16333.

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Sickle cell disease (SCD) is a genetic disorder with recessive transmission, caused by the mutation HBB:c.20A>T. It originates hemoglobin S that forms polymers inside the erythrocyte, upon deoxygenation, deforming it and ultimately leading to premature hemolysis. The disease presents with high heterogeneity of clinical manifestations, the most devastating of which, ischemic stroke, occurs in 11% of patients until 20 years of age. In this study, we tried to identify genetic modifiers of risk and episodes of stroke by studying 66 children with SCD, grouped according to the degree of cerebral va

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