No description available.

Diss. (sammanfattning) Göteborg : Göteborgs universitet, 2007. / Härtill 4 uppsatser.

Thesis (Ph. D.)--University of Wisconsin--Madison, 1959. / Typescript. Abstracted in Dissertation abstracts, v. 20 (1959) no. 3, p. 1108-1109. Vita. eContent provider-neutral record in process. Description based on print version record. Includes bibliographical references.

Thesis (Ph.D.)--Cleveland State University, 2008. / Abstract. Title from PDF t.p. (viewed on Mar. 4, 2009). Includes bibliographical references. Available online via the OhioLINK ETD Center. Also available in print.

Call number: LD2668 .T4 1978 A35 / Master of Science

No description available.

Objetivos: 1) Determinar la prevalencia de incremento de eosinófilos en mucosa colónica en pacientes con colitis linfocítica (CL). 2) Determinar la coexistencia de colitis eosinofílica (CE) en pacientes con CL. Materiales y métodos: Las biopsias colónicas de pacientes adultos con diarrea crónica diagnosticados como CL en el hospital Daniel A. Carrión durante octubre 2009 a marzo 2012 fueron revisadas de forma independiente por 2 patólogos. Microscópicamente, se investigó y cuantificó la presencia de eosinófilos en mucosa colónica. Resultados: Se incluyeron 68 casos de CL, de los cuales 76,5% tuvieron eosinófilos elevados en la mucosa colónica y en 51,4% se pudo hacer el diagnóstico de CE según los criterios establecidos. Conclusión: Tres de cuatro pacientes con CL presentan eosinófilos elevados y 1 de cada 2 pacientes con CL cumple criterios para CE. / Objectives: 1) To determine the prevalence of increased number of eosinophils in colonic mucosa of patients with lymphocytic colitis (LC). 2) To determine the coexistence of eosinophilic colitis (EC) in patients with lymphocytic colitis. Materials and methods: slides of adult patients with cronic diarrhea with diagnosis of LC were reviewed between October 2009 and March 2012. The number of eosinophils was quantified. Results: Sixty eight patients with LC were included. Elevated eosinophils were found in 76.5 and in 51.4% a diagnosis of EC was established. Conclusion: 3 out of 4 patients with LC had elevated eosinophils and 1 of 2 patients with LC had criteria for EC.

Zhang Jiping. / Thesis (Ph.D.)--Chinese University of Hong Kong, 2001. / Includes bibliographical references (p. 157-179). / Electronic reproduction. Hong Kong : Chinese University of Hong Kong, [2012] System requirements: Adobe Acrobat Reader. Available via World Wide Web. / Mode of access: World Wide Web. / Abstracts in English and Chinese.

Diss. (sammanfattning) Stockholm : Karolinska institutet, 2006. / Härtill 4 uppsatser.

Eosinophils are end-point effectors of inflammation that contribute to the clinical severity of asthma. Eosinophil homing to the asthmatic lung is primarily guided by eotaxin-1, which is an eosinophil-selective chemokine. The mechanism by which eotaxin-1 augments intracellular calcium during cell migration is incompletely understood but is integral to the extravasation of eosinophils at sites of inflammation. We consequently report here that fluid shear stress, like eotaxin-1, unexpectedly activates human eosinophils in a calcium-dependent manner. We used confocal fluorescence microscopy to study calcium-handling in purified human eosinophils. Application of eotaxin-1 augmented the [Ca2+]i in a concentration-dependent manner. Pre-treatment of cells with ryanodine (10 μM) completely abolished the eotaxin-mediated calcium response, indicating that this phenomenon is dependent on Ca2+-release from the ER. Several SOCC blockers (2-APB, 100 μM; Gd3+, 10 μM; SKF-96365, 100 μM) attenuated SOCE, suggesting that these channels may directly contribute towards the eotaxin-1 calcium response in human eosinophils. In the presence of fluid-perfusion, eosinophils displayed a robust perfusion-induced calcium response (PICR) demonstrating that eosinophils are mechanically sensitive. The PICR rapidly induced adhesion and non-directional migration in eosinophils, suggesting that some hitherto unknown molecular mechanosensor permits these cells to detect and respond to changes in shear-stress. Pre-treatment of eosinophils with the non-selective tripeptide integrin receptor blocker, Arg-Gly-Asp (RGD), abrogated the PICR. The highly selective, dual α4β7/α4β1 integrin receptor blocker, CDP-323, was used to ascertain whether these highly expressed integrin subtypes mediate the PICR in eosinophils. Pre-treatment of cells with CDP-323 completely abolished the PICR, in addition to the eotaxin-mediated calcium response in a shear-dependent manner. Taken together, our results support a novel role for the α4β7/α4β1 integrin receptors as mechanosensors that directly modulate [Ca2+]i, adhesion and migration in human eosinophils. On-going experiments will seek to quantify the shear-response thresholds at which eosinophils activate and the time-course of the associated calcium response. This study suggests that the recruitment and activation of eosinophils are regulated by chemical and mechanical stimuli via overlapping, calcium-dependent signal transduction cascades. Given that the PICR is mediated by the eosinophil-specific α4β7/α4β1 integrin receptors, we conclude that integrin receptors are molecular mechanosensors that may facilitate eosinophil activation, adhesion and non-directional migration independently of, or in conjunction with, chemokine signaling. / Thesis / Master of Science in Medical Sciences (MSMS)