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  • About
  • The Global ETD Search service is a free service for researchers to find electronic theses and dissertations. This service is provided by the Networked Digital Library of Theses and Dissertations.
    Our metadata is collected from universities around the world. If you manage a university/consortium/country archive and want to be added, details can be found on the NDLTD website.
51

Factores clinicos asociados a ulcera peptica en pacientes atendidos en el servicio de gastroenterologia del hospital vitarte en el año 2015

Bonzano Díaz, luisa January 2017 (has links)
Objetivo: Determinar la asociación entre factores clínicos y desarrollo de úlcera péptica en pacientes atendidos en el servicio de gastroenterología del hospital vitarte en el año 2015. Material y métodos: Es un estudio observacional, analítico, retrospectivo. Se incluyó 144 pacientes a los que se les realizó examen endoscópico en el año 2015 en el servicio de gastroenterología del Hospital Vitarte. Se excluyó a aquellos con historias clínicas incompletas y con comorbilidades que alteren el resultado histopatológico. Para el análisis de asociación se utilizó la prueba Chi2 y se estimaron los ORs. Para el procesamiento de datos se utilizó el programa estadístico IBM SPSS v21. Resultados: la prevalencia de úlcera péptica fue de 37.5%, la frecuencia de infección por Helicobacter pylori fue 37.5% (OR= 5.4 IC 95% 2,6 - 11,2) demostrando que es un factor clínico asociado a úlcera péptica. El 27.7% de pacientes consumía Antiinflamatorios no esteroideos (AINES) (OR= 5.9 IC 95% 2,7 - 13,1). Solo el 2,8% de pacientes consumía corticoides (OR =1.7 IC 95% 0,2 - 12,4). Respecto a factores sociales, la frecuencia de consumo de tabaco fue 8,3% (OR= 5.8 IC 95% 1,5 - 22,5). En cuanto a los factores demográficos, se observó que los varones presentaron una mayor frecuencia de úlcera péptica 59.3% (OR= 2.5 IC 95% 1.3 - 5.0). Se observó una mayor frecuencia de úlcera péptica en el grupo de pacientes menores a 51 años (OR= 1,6 IC 95% 0.8 - 3,1). Conclusiones: existe asociación significativa entre los factores clínicos como Helicobacter pylori y consumo de AINES con la presencia de úlcera péptica.
52

Estudo da influencia da acidez gastrica na farmacocinetica da furazolidona : implicações terapeuticas para a erradicação do Helicobacter pylori

Ortiz, Rodrigo Agustin Mas 03 January 2001 (has links)
Orientador: Jose Pedrazzoli Junior / Dissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciencias Medicas / Made available in DSpace on 2018-08-04T01:27:58Z (GMT). No. of bitstreams: 1 Ortiz_RodrigoAgustinMas_M.pdf: 16210694 bytes, checksum: 03121c038a931fbadbc8007c72aeda35 (MD5) Previous issue date: 2001 / Resumo: o objetivo deste estudo foi investigar os efeitos da administração de cinco dias de omeprazol na farmacocinética da furazolidona. Dezoito voluntários saudáveis (9 homens e 9 mulheres) foram selecionados. O estudo teve um perfil de dois períodos, com randomização aberta, e um período de washout de 21 dias entre as fases. As concentrações séricas de furazolidona foram medidas por HPLC de fase reversa, com detecção em ultravioleta. A administração de omeprazol causou uma redução significativa de Cmax (0.343 :t 0.042 vs. 0.244 :t 0.046), e uma redução não significativa de T1/2 (4.87:t 1.06 vs. 3.90 :t 0.85). A Furazolidona foi bem absorvida após a administração oral. O tratamento, a curto prazo, com omeprazol alterou a farmacocinética desta droga. A redução observada em sua biodisponibilidade, induzida pelo bloqueio ácido sugere uma interferência com a dinâmica de absorção ou com o metabolismo de primeira passagem da furazolidona / Abstract: Background: The administration of omeprazole may interfere with the absorption of orally administered drugs by reducing gastric pH and thus tablets dissolution.The aim of this study was to investigate the effects of a tive day administration of omeprazole on furazolidone pharmacokinetics. Methods: Eighteen healthy (male, female) volunteers were selected. The study had an open randomized two-period crossover design with a 21 day washout period between the phases. Plasma concentrations of furazolidone were measured by reversed-phase HPLC with ultraviolet detection. Results: Administration of omeprazole caused a signiticant reduction of Cmax (0.3426 .:t0.042 vs. 0.2440 .:t 0.046) and a not significant reduction of T1/2(4.869.:t 1.06 vs. 3.904 .:t 0.85 ) but did not interfere with other pharmacokinetic parameters of orally administered furazolidone. Conclusion: Our results indicate that furazolidone is well absorbed afier oral administration. Short-term treatment with omeprazole does not alter the bioavailablitity of furazolidone. The observed reduction in Cmaxand T1/2induced by acid blockade suggests a possible interference with the absorption kinetics of the drug / Mestrado / Farmacologia / Mestre em Farmacologia
53

Helicobacter pylori and peptic ulcer disease, with special reference to the Western Cape

Louw, Jacob Albertus 25 July 2017 (has links)
No description available.
54

Genetic characterization and molecular evolution of the CAG pathogenicity island of Helicobacter pylori

Kouri, Kimberly. January 1999 (has links)
No description available.
55

Expression von Chemokinrezeptoren auf Magenepithelien und neutrophilen Granulozyten während der Helicobacter pylori Infektion / Expression of chemokinereceptors on gastric epithelia and neutrophil granulocytes during the infection with helicobacter pylori

Endrich, Simon January 2010 (has links) (PDF)
Bekanntermaßen führt die H.pylori Infektion des Magens über eine komplexe Modulation des Chemokinsystems zur Ausbildung der H.pylori Gastritis. Die Chemokinrezeptorexpression in der H.pylori Gastritis ist jedoch bisher noch fast nicht untersucht. Das Ziel der Arbeit war die Charakterisierung der Chemokinrezeptorexpression im Magen und die Testung eines Einfluss von H.pylori auf die Expression von Chemokinrezeptoren. In vitro führt die Inkubation von neutrophilen Granulozyten mit H. pylori zu einer schnellen Herunterregulation von CXCR1 und CXCR2 auf Proteinebene durch Rezeptorinternalisation und intrazellulären Abbau. Der Effekt ist unabhängig vom cag Status von H. pylori, sowie von TNF-α- oder IL-8. Als möglicher Signaltransduktionsmechanismus für diesen Effekt wäre die direkte Interaktion von H. pylori mit „toll-like receptors“ (TLRs) denkbar. Auf mRNA Ebene kommt es in vitro bei der Inkubation von neutrophilen Granulozyten mit H. pylori zu einer Herunterregulation von CXCR1 und CXCR2 mRNA nach 3 Stunden. Dieser Effekt tritt bei Inkubation mit einem cag positiven H. pylori Stamm verstärkt auf und könnte bedingt sein durch autokrine Herunterregulation der Expression von CXCR1 und CXCR2 durch IL-8. In vivo exprimieren neutrophile Granulozyten in der H. pylori Gastritis in den Krypten ebenfalls vermindert CXCR1 und CXCR2. Sowohl die Expression der Chemokine als auch der korrespondierenden Chemokinrezeptoren wird somit durch H.pylori beeinflusst. Es lässt sich somit der folgende Pathomechanismus postulieren: Nach dem Eintritt der neutrophilen Granulozyten in die Schleimhaut, kommt es über den direkten Kontakt mit H.pylori zum Verlust der Chemokinrezeptoren. Die neutrophilen Granulozyten können somit nicht mehr auf Chemokinsignale reagieren und werden in der Magenschleimhaut immobilisiert. Dort setzen sie reaktive Sauerstoffradikale, proinflammatorische Zytokine und Chemokine frei, die zur Schleimhautschädigung führen. Magenkarzinome exprimieren die Chemokinrezeptoren CXCR4 und CCR7. Die Expression wird mit der Neigung zur Metastasierung und einer schlechten klinischen Prognose assoziiert. In unseren Untersuchungen wird CXCR4 in vivo während des Prozess der Karzinogenese im Magen ab dem Stadium der intestinalen Metaplasie exprimiert. Bei Inkubation der Zelllinien mit cagA positiven und cagA negativen H. pylori – Stämmen, kommt es zu keiner Änderung der Expression von CXCR4. Die Infektion mit H. pylori ist zwar die Voraussetzung für die Genese der intestinalen Metaplasie, scheint jedoch nicht ursächlich an der Expression von CXCR4 beteiligt zu sein. CCR7 tritt in vivo auf den Magenepithelien der H. pylori Gastritis, der intestinalen Metaplasie, Dysplasie und Magenkarzinomen auf. In vitro führt die Koinkubation von CCR7 tragenden Magenzelllinien mit H. pylori zur Hochregulation von CCR7 kommt. Die Expression von CCR7 auf Karzinomzellen wird ebenfalls möglicherweise durch eine begleitende Infektion mit H. pylori begünstigt. Der Effekt der CCR7 Induktion durch H. pylori in vitro ist unabhängig vom cag Status des für die Infektion verwendeten H. pylori Stammes. Die Hochregulation von CCR7 ist möglicherweise bedingt durch die intrazelluläre Aktivierung von NFκB infolge der H. pylori Infektion. Denkbar wäre auch eine Induktion der Expression von CCR7 in den Magenepithelzellen in TLR abhängiger Weise, äquivalent zu Mechanismen, die in dendritischen Zellen beschrieben wurden. Es lässt sich abschließend feststellen, dass die H.pylori Infektion nicht nur die Freisetzung von Chemokinen, sondern auch die Expression von Chemokinrezeptoren wesentlich beeinflusst. Neutrophile Granulozyten verlieren in direktem Kontakt zu H.pylori die Chemokinrezeptoren CXCR1 und CXCR2. Auf Epithelzellen führt der direkte Kontakt zu H.pylori zur vermehrten Expression von CCR7. Die direkte Regulation von Chemokinrezeptoren durch H.pylori scheint also sowohl bei der H.pylori Gastritis, als auch bei der Entstehung und Progression von Magenkarzinomen eine Rolle zu spielen. / It is known that the infection with helicobacter pylori leads by a complex modulation of the chemokine system to the helicobacter pylori gastritis. Interestingly, the expression of chemokinereceptors in the helicobacter pylori gastritis is nearly not investigated now. The aim of this study was to characterize the expression of chemokinereceptors in the stomach and to test if there in an influece of helicobacter pylori. In vitro, the coincubation of neutrophils leads to a rapid downregulation of CXCR1 and CXCR2 proteine via internalisation of the receptor and proteolytic digestion. The effect is independant of the cag status of the infecting helicobacter pylori, as well as of TNF-α or IL-8. A possible mechanism could be an interaction with toll like receptors. The mRNA aof CXCR1 and CXCR2 is downregulated during the incubation of neutrophils with h.pylori after 3 hours. This effect is stronger using a cag positve helcobacter strain and could be an autocrine effect of IL-8. In vivo, neutrophils also express CXCR1 and CXCR2 in a lower level in the gastric crypts. So the expression of the chemokines, as well as of the corresponding chemokine receptors are under the influence of helicobacter pylori. It is possible to postulate the following pathomechanism: After the entrance of neutrophils in the gastric epithelia, the contact to helicobacter pylori leads to al loss of their chemokinreceptors. They can nomore react to chemotaktic signals and are immobilised in the epithelia. The release of oxigen radicals and proinflammatory cytokines leads to a progressive demolition of the epithelia. Gastric carcinoma express the chemokinreceptors CXCR4 and CCR7. The expression is associated with metastasis and a poor prognosis. In our study, CXCR4 is expressed in vivo during the carcinogenesis at the point of intestinal metaplasia. The Infection of gastric epithelial cell lines with H. pylori however has no influence on the expression of the chemokine receptors. In our study, CCR7 is expressed in a higher level in vivo during the carcinogenesis at the point of the helicbacter gastritis. In vivo it comes to a upregulation of CCR7 on gastric epithelial cell lines when infected with helicobacter pylori. Possibly toll like receptors are involved in thee mechanism. So the direct regulation of chemoikne receptors seems to play a role in the carcinogenesis of gastric carcinoma, as well as in the helicobacter pylori gastritis.
56

Clinical effectiveness of helicobacter pylori screening in Chinese population

Jiao, Yang, Peter., 焦洋. January 2011 (has links)
published_or_final_version / Public Health / Master / Master of Public Health
57

The pathology, diagnosis and treatment of helicobacter pylori infection

Wong, Wai-man, Raymond, 王衛民 January 2001 (has links)
published_or_final_version / abstract / toc / Medicine / Master / Doctor of Medicine
58

RNAseq Analysis of Gastric Bacteria in Helicobacter pylori-Associated Carcinogenesis

Liu, Oscar H. January 2014 (has links)
Helicobacter pylori infects more than half of the world's population, and is known to be involved in several diseases including gastric cancer. Its close interactions with the stomach and host immune system serves as a good model to study the co-adaptation and co-evolution of the organisms in the stomach micro-environment. In this project, we utilized RNA-seq and data analysis tools to investigate differentially expressed genes by H. pylori in patients at different stages of early gastric cancer development. We also investigated the abundance and diversity of bacterial genera other than H. pylori, and looked for correlations with H. pylori presence and number. For differential gene expression of H. pylori, one gene was differentially expressed between samples of corpus atrophy without metaplasia vs. samples of antrum gastritis, and eight genes were found to be differentially expressed between samples of corpus atrophy with metaplasia vs. samples with pan-gastritis. When samples were clustered into different groups based on the expression data, 52 genes (shared or unique to the specific comparison groups) were found to be differentially expressed, but no apparent patterns were observed that could be explained by medical or sample collection data. For bacterial diversity and abundances, we found several genera colonizing the stomach, of which some have been previously identified. While most of these bacteria colonize regardless of the presence of H. pylori, the abundance of three genera, Wolinella, Campylobacter, and Veillonella, seem to be correlated with the presence of H. pylori.
59

Diversity and persistence of Helicobacter pylori /

Lundin, Annelie, January 2004 (has links)
Diss. (sammanfattning) Stockholm : Karol. inst., 2004. / Härtill 5 uppsatser.
60

The discovery and pathology of H pylori /

Warren, John Robin. January 1999 (has links) (PDF)
Thesis (M.D.) -- University of Adelaide, Dept. of Medicine, 2000. / Includes bibliographical references.

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