Relevant bibliographies by topics / Eosinophil

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  1. Journal articles
  2. Dissertations / Theses
  3. Books
  4. Book chapters
  5. Conference papers
  6. Reports

Academic literature on the topic 'Eosinophil'

Author: Grafiati
Published: 4 June 2021
Last updated: 6 September 2023

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Journal articles on the topic "Eosinophil"

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Cantarini, L., N. Volpi, P. Carbotti, G. Greco, M. Aglianò, F. Bellisai, F. Giannini, C. Alessandrini, G. Grasso, and M. Galeazzi. "Eosinophilia-associated muscle disorders: an immunohistological study with tissue localisation of major basic protein in distinct clinicopathological forms." Journal of Clinical Pathology 62, no. 5 (January 12, 2009): 442–47. http://dx.doi.org/10.1136/jcp.2008.060616.

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Aims:(a) To evaluate tissue eosinophil density, location of eosinophil cytotoxic products, histopathological muscle changes and inflammatory cell types in different eosinophilia-associated myopathies that are clinicopathologically heterogeneous. (b) To determine the immunohistological range of tissue eosinophil density in non-eosinophilic inflammatory myopathies.Methods:Muscle biopsy specimens from seven patients with blood and/or tissue eosinophilia and clinicolaboratory myopathic signs (five chronic course myopathies, one subacute onset fasciitis/myositis, one acute myositis), and from 18 non-eosinophilic inflammatory myopathies, underwent routine staining, inflammatory infiltrate immunophenotyping, immunostaining for eosinophil major basic protein (MBP) and transmission electron microscopy examination. Eosinophil and total inflammatory cell counts were statistically analysed.Results:Histological examination showed occasional or no infiltrating eosinophils in all cases. MBP staining showed that tissue eosinophil density and percentages in eosinophilia-associated myopathies were significantly higher than in idiopathic myositides. Extracellular MBP diffusion, the hallmark of eosinophil cytotoxicity, was recurrent on sarcolemma and endothelium. Electron microscopy showed eosinophils close to sarcolemma, abundant mast cells, and capillary endothelial swelling. Immunostaining detected a higher mean eosinophil density in idiopathic myositides than previously assessed histologically.Conclusions:MBP immunohistology on skeletal muscle, previously performed only for acute eosinophilic polymyositis, suggests that eosinophil-mediated injury of muscle cells may occur in a wider spectrum of less aggressive eosinophilia-associated myopathies than previously thought. As conventional histology is likely to underestimate this leucocyte subset, MBP staining may be a useful tool in the analysis of tissue infiltration of eosinophils as a possible treatment target.
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Oliver, Brian, Katrina Tonga, David Darley, Sandra Rutting, Xin Zhang, Hui Chen, and Gang Wang. "COPD treatment choices based on blood eosinophils: are we there yet?" Breathe 15, no. 4 (December 2019): 318–23. http://dx.doi.org/10.1183/20734735.0254-2019.

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Eosinophils are increasingly being recognised as an important characteristic feature of COPD. Patients with COPD and eosinophilic inflammation tend to respond to steroid therapy; however, many questions remain regarding the optimum measurement. Eosinophilic inflammation may be defined based on various sampling techniques, including eosinophil levels in blood, sputum, bronchoalveolar lavage or biopsy, which leads to inconsistencies in its definition. Blood eosinophils may increase in conjunction with sputum eosinophils during COPD exacerbations and therefore may be a good surrogate marker of airway eosinophilic inflammation. However, the timing of the blood eosinophil measurement, the stability of the eosinophil count and the threshold used in different studies are variable. The use of blood eosinophil count to direct biological therapies in COPD has also had variable outcomes. Eosinophilic inflammation has an important role in COPD management; however, its use as the optimum biomarker still needs further investigation.Key pointsEosinophilia may play a significant role in the pathogenesis of COPD.Eosinophilic inflammation in COPD can be steroid responsive; however, eosinophilic inflammation is variable, and caution needs to be taken with measurements and the thresholds used.The long-term effects of reducing eosinophil levels in COPD is unclear.Educational aimsTo explore current knowledge of eosinophils in COPD.To explore the relationship between eosinophilia and corticosteroid use.To understand the limitations of assessing and using eosinophilia in COPD.
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Desreumaux, P., A. Janin, S. Dubucquoi, MC Copin, G. Torpier, A. Capron, M. Capron, and L. Prin. "Synthesis of interleukin-5 by activated eosinophils in patients with eosinophilic heart diseases." Blood 82, no. 5 (September 1, 1993): 1553–60. http://dx.doi.org/10.1182/blood.v82.5.1553.1553.

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Abstract Eosinophilic endomyocardial disease represents a major evolutive risk in chronic eosinophilia-associated disorders. Eosinophil granule proteins appear to be involved in cardiac injury, but the mechanisms leading to eosinophil infiltration and degranulation are not clear. Interleukin-5 (IL-5) has been recently shown to be produced by eosinophils and might play a role in both chemoattraction and degranulation of eosinophils. In four cases of eosinophilic diseases with severe cardiac failure, we evaluated the proportion of eosinophil phenotypes and the serum levels of eosinophil cationic protein (ECP) and soluble IL-2 receptor (sIL-2R), markers of disease activity in the hypereosinophilic syndromes. All four patients showed a markedly increased proportion of hypodense eosinophils with elevated serum ECP and sIL-2R levels. In all four patients, extracellular deposition of eosinophil granule proteins and features of eosinophil activation were observed in cardiac tissues. The synthesis of IL-5 by eosinophils was detected in myocardial sections and blood cells by in situ hybridization and by immunostaining with a monoclonal antibody against human IL-5. Sixty percent to 90% of tissue eosinophils expressed IL-5 mRNA and IL-5 protein. These data suggest that IL-5 can be produced by eosinophils at the sites of myocardial tissue damage and might participate in local eosinophil activation.
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Desreumaux, P., A. Janin, S. Dubucquoi, MC Copin, G. Torpier, A. Capron, M. Capron, and L. Prin. "Synthesis of interleukin-5 by activated eosinophils in patients with eosinophilic heart diseases." Blood 82, no. 5 (September 1, 1993): 1553–60. http://dx.doi.org/10.1182/blood.v82.5.1553.bloodjournal8251553.

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Eosinophilic endomyocardial disease represents a major evolutive risk in chronic eosinophilia-associated disorders. Eosinophil granule proteins appear to be involved in cardiac injury, but the mechanisms leading to eosinophil infiltration and degranulation are not clear. Interleukin-5 (IL-5) has been recently shown to be produced by eosinophils and might play a role in both chemoattraction and degranulation of eosinophils. In four cases of eosinophilic diseases with severe cardiac failure, we evaluated the proportion of eosinophil phenotypes and the serum levels of eosinophil cationic protein (ECP) and soluble IL-2 receptor (sIL-2R), markers of disease activity in the hypereosinophilic syndromes. All four patients showed a markedly increased proportion of hypodense eosinophils with elevated serum ECP and sIL-2R levels. In all four patients, extracellular deposition of eosinophil granule proteins and features of eosinophil activation were observed in cardiac tissues. The synthesis of IL-5 by eosinophils was detected in myocardial sections and blood cells by in situ hybridization and by immunostaining with a monoclonal antibody against human IL-5. Sixty percent to 90% of tissue eosinophils expressed IL-5 mRNA and IL-5 protein. These data suggest that IL-5 can be produced by eosinophils at the sites of myocardial tissue damage and might participate in local eosinophil activation.
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Bates, Alan W. H. "Diagnosing Eosinophilic Colitis: Histopathological Pattern or Nosological Entity?" Scientifica 2012 (2012): 1–9. http://dx.doi.org/10.6064/2012/682576.

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Reports of “eosinophilic colitis”—raised colonic mucosal eosinophil density in patients with lower gastrointestinal symptoms—have increased markedly over the last fifteen years, though it remains a rarity. There is no consensus over its diagnosis and management, and uncertainty is compounded by the use of the same term to describe an idiopathic increase in colonic eosinophils and an eosinophilic inflammatory reaction to known aetiological agents such as parasites or drugs. In patients with histologically proven colonic eosinophilia, it is important to seek out underlying causes and careful clinicopathological correlation is advised. Because of the variability of eosinophil density in the normal colon, it is recommended that histological reports of colonic eosinophilia include a quantitative morphometric assessment of eosinophil density, preferably across several sites. Few reported cases of “eosinophilic colitis” meet these criteria. As no correlation has been shown between colonic eosinophil density and symptoms in older children or adults, it is suggested that treatment should be directed towards alleviation of symptoms and response to treatment assessed clinically rather than by histological estimates of intramucosal eosinophils.
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Van Hulst, Glenn, Fabrice Bureau, and Christophe J. Desmet. "Eosinophils as Drivers of Severe Eosinophilic Asthma: Endotypes or Plasticity?" International Journal of Molecular Sciences 22, no. 18 (September 21, 2021): 10150. http://dx.doi.org/10.3390/ijms221810150.

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Asthma is now recognized as a heterogeneous disease, encompassing different phenotypes driven by distinct pathophysiological mechanisms called endotypes. Common phenotypes of asthma, referred to as eosinophilic asthma, are characterized by the presence of eosinophilia. Eosinophils are usually considered invariant, terminally differentiated effector cells and have become a primary therapeutic target in severe eosinophilic asthma (SEA) and other eosinophil-associated diseases (EADs). Biological treatments that target eosinophils reveal an unexpectedly complex role of eosinophils in asthma, including in SEA, suggesting that “not all eosinophils are equal”. In this review, we address our current understanding of the role of eosinophils in asthma with regard to asthma phenotypes and endotypes. We further address the possibility that different SEA phenotypes may involve differences in eosinophil biology. We discuss how these differences could arise through eosinophil “endotyping”, viz. adaptations of eosinophil function imprinted during their development, or through tissue-induced plasticity, viz. local adaptations of eosinophil function through interaction with their lung tissue niches. In doing so, we also discuss opportunities, technical challenges, and open questions that, if addressed, might provide considerable benefits in guiding the choice of the most efficient precision therapies of SEA and, by extension, other EADs.
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Shigemoto, Emi, Masashi Mizuno, Yasuhiro Suzuki, Kazuma Kobayashi, Fumiko Sakata, Tetsuyoshi Kariya, Takayuki Katsuno, Shoichi Maruyama, and Yasuhiko Ito. "Increase of Eosinophil in Dialysate during Induction of Peritoneal Dialysis." Peritoneal Dialysis International: Journal of the International Society for Peritoneal Dialysis 39, no. 1 (January 2019): 90–92. http://dx.doi.org/10.3747/pdi.2017.00205.

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As a rare complication in patients on peritoneal dialysis (PD), increase of eosinophil (peritoneal dialysate fluid [PDF] eosinophilia), including eosinophilic peritonitis, was observed in PDF. The majority of eosinophilic peritonitis cases are detected during the early phase of PD induction. However, the frequency of and mechanisms underlying PDF eosinophilia remain unclear. We therefore investigated the frequency of PDF eosinophilia and what mechanisms, specifically complement activation, might contribute to its occurrence. In 48 patients, eosinophil counts and concentrations of complement activation products, such as C3a, C5a, and sC5b-9, interleukin (IL)-5, and IL-6 in PDF were evaluated on days 1, 2, and 4 after starting PD therapy. We focused on the relationships between patient background characteristics and eosinophil counts and levels of C3a, C5a, and sC5b-9 as complement activation products in PDF. In 33.3% of PD patients, increased PDF eosinophils were observed on day 1. Eosinophil counts correlated with PDF levels of C3a on days 1 and 2, IL-5 on days 1, 2, and 4, and IL-6 on day 1. In terms of background characteristics, only the duration the PD catheter was left in place differed significantly between PDF eosinophilia and non-PDF eosinophilia. Notably, PDF levels of C3a differed significantly between patients with and without eosinophilia, suggesting that C3a might be a candidate for induction of increased eosinophil. PDF eosinophilia was frequently observed during PD initiation. Our results suggest that PD catheter insertion and complement activation might be related to increases in eosinophils in PDF during PD initiation.
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Mycroft, Katarzyna, Magdalena Paplińska-Goryca, Małgorzata Proboszcz, Patrycja Nejman-Gryz, Rafał Krenke, and Katarzyna Górska. "Blood and Sputum Eosinophils of COPD Patients Are Differently Polarized than in Asthma." Cells 12, no. 12 (June 15, 2023): 1631. http://dx.doi.org/10.3390/cells12121631.

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Different eosinophil subpopulations have been identified in asthma and other eosinophilic disorders. However, there is a paucity of data on eosinophil subpopulations in patients with chronic obstructive pulmonary disease (COPD). The aim of this study was to compare eosinophil phenotypes in blood and induced sputum in patients with COPD, asthma and controls. Stable patients with mild-to-moderate COPD (n = 15) and asthma (n = 14) with documented blood eosinophilia ≥100 cells/µL in the year prior to the study and the control group (n = 11) were included to the study. The blood and sputum eosinophil phenotypes were analyzed by flow cytometry. IL-5, IL-13, CCL5 and eotaxin-3 levels were measured in the induced sputum. The marker expression on blood eosinophils was similar among control, asthma and COPD groups. The expressions of CD125, CD193, CD14 and CD62L were higher on blood than on sputum eosinophils in all three groups. We found increased levels of CD193+ and CD66b+ sputum eosinophils from COPD patients, and an elevated level of CD11b+ sputum eosinophils in asthma compared to COPD patients. The results of our study suggest that the profile of marker expression on COPD sputum eosinophils differed from other groups, suggesting a distinct phenotype of eosinophils of COPD patients than in asthma or healthy subjects.
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Kiani, Arda, Fatemehsadat Rahimi, Siamak Afaghi, Maryam Paat, Mohammad Varharam, Mehdi Kazempour Dizaji, Maryam Dastoorpoor, and Atefeh Abedini. "Association of Upon-Diagnosis Blood Eosinophilic Count with Frequency and Severity of Annual Exacerbation in Chronic Obstructive Pulmonary Disease: A Prospective Longitudinal Analysis." Canadian Respiratory Journal 2023 (April 26, 2023): 1–11. http://dx.doi.org/10.1155/2023/8678702.

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Introduction. There is a controversy regarding the relationship between blood eosinophil count and COPD exacerbation. We aimed to determine whether peripheral eosinophils upon COPD diagnosis could affect the frequency and severity of annual acute exacerbation of COPD (AECOPD). Methods. This prospective study was conducted on 973 newly diagnosed COPD patients who were under 1-year follow-up in a pulmonology center in Iran. The Cox proportional model, polynomial regression, and receiver operator characteristic curves were conducted to evaluate the impact of the eosinophil levels on AECOPD. A linear regression model was conducted to evaluate the continuous association of eosinophilic count with AECOPDs. Results. Patients with eosinophil >200 cells/microliter were higher pack-year smokers with more pulmonary hypertension prevalence compared to COPD patients with <200 cells/microliter. There was a positive correlation between the eosinophilic count and the frequency of AECOPDs. Eosinophil >900 cells/microliter and eosinophil >600 cells/microliter had a sensitivity of 71.1% and 64.3%, respectively, in predicting the occurrence of more than one AECOPD. Eosinophilic count cutoff of 800 cells/microliter had the highest Youden index with sensitivity and specificity of 80.2% and 76.6%, respectively, for incident AECOPD in newly diagnosed patients. Using a linear model, increasing 180 cells/microliter in serum eosinophils was associated with further exacerbation. Evaluating gender, BMI, smoking pack-year, FEV1/FVC, CAT score, GOLD score, pulmonary hypertension, annual influenza, pneumococcal vaccinations, leukocytosis, and blood eosinophils, only blood eosinophils (hazard ratio (HR) = 1.44; 95% confidence interval = 1.33–2.15; p value = 0.03) and GOLD score (HR = 1.19; 95% CI = 1.30–1.52; p value = 0.03) were found as independent risk factors of AECOPD >3 episodes/year. Requirement for ICU admission, invasive ventilation, and mortality rate due to AECOPDs was similar between eosinophilic and noneosinophilic groups. Conclusion. Eosinophilia upon COPD diagnosis is a factor of recurrent AECOPDs. To reduce the risk of AECOPDs and the burden of disease, clinicians may consider inhaler corticosteroids and domiciliary oxygen with a lower threshold for eosinophilic-COPD patients regardless of their clinical status.
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Aldebert, D., B. Lamkhioued, C. Desaint, AS Gounni, M. Goldman, A. Capron, L. Prin, and M. Capron. "Eosinophils express a functional receptor for interferon alpha: inhibitory role of interferon alpha on the release of mediators." Blood 87, no. 6 (March 15, 1996): 2354–60. http://dx.doi.org/10.1182/blood.v87.6.2354.bloodjournal8762354.

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Recent reports describe the beneficial use of alpha interferon (IFNalpha) for the treatment of idiopathic hypereosinophilic syndrome (HES) unresponsive to conventional therapy. A clinical improvement associated with a rapid decrease of peripheral blood eosinophilia suggested possible direct effects of IFNalpha on eosinophils through the presence of IFNalpha receptors (IFNalphaR). Reverse transcriptase- polymerase chain reaction (RT-PCR) and cytochemistry were used respectively to detect the presence and define the distribution of IFNalphaR on enriched eosinophil preparations purified from blood cells. IFNalphaR was found on eosinophils collected from patients with various eosinophilic disorders. In addition, IFNalpha inhibited the release of eosinophil granule proteins such as eosinophil cationic protein (ECP), neurotoxin (EDN, or interleukin-5 (IL-5). Moreover, antiparasite cytotoxicity was also strongly reduced in a dose-dependent manner by IFNalpha. These results provide the first evidence that human eosinophils express a functional receptor for IFNalpha and represent a potential basis for the beneficial effects of IFNalpha in patients with hypereosinophilic syndromes.
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Dissertations / Theses on the topic "Eosinophil"

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Konikoff, Michael R. "Non-Invasive Biomarkers of Eosinophilic Esophagitis: Blood Eosinophil Level, Eosinophil-Derived Neurotoxin, and Eotaxin-3." Cincinnati, Ohio : University of Cincinnati, 2006. http://www.ohiolink.edu/etd/view.cgi?acc_num=ucin1148043525.

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Thesis (M.S.)--University of Cincinnati, 2006.
Advisor: Dr. James E. Heubi. Title from electronic thesis title page (viewed June 3, 2009). Includes abstract. Keywords: Eosinophilic esophagitis; biomarker; eosinophil; eosinophil-derived neurotoxin; eotaxin-3. Includes bibliographical references.
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Seton, Kristina. "Eosinophil Apoptosis." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2003. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-3427.

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Apoptosis or programmed cell death is crucial for the resolution of inflammation, and phagocytosis of apoptotic cells initiates the release of actively anti-inflammatory responses from the phagocytes. Eosinophils are one of the most potent inflammatory cells in the body and is involved in a number of diseases, most commonly associated with parasitic infections and allergic diseases. Apoptosis in eosinophils is therefore one of the most important systems to avoid inflammation. This aim of the present investigation was to examine the mechanisms behind, and the consequences of this process in eosinophils. Apoptotic eosinophils have a unique surface receptor expression that indicates abilities to communicate with T-, B- and antigen presenting cells. They have a novel expression of CD49f, indicating an importance for binding to laminin or unknown functions of the VLA-6 receptor, possibly in the concept of phagocytosis of the apoptotic cell.

In apoptotic eosinophils the granules are translocated to the periphery of the cell, probably through a disruption of the cytoskeleton. This translocation makes the granules easily accessible and the apoptotic eosinophil can release considerable amounts of granule proteins in response to specific stimuli. The spontaneous release however, is decreased as compared with living cells.

Furthermore, the survival of eosinophils in response to an allergen challenge is increased in healthy subjects, but not in allergic patients. Mechanistically, this needs further investigation, but one theory is that it is due to the presence of specific IgE in patients in combination with differences in the response from the epithelial cells.

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Dewson, Grant. "Regulation of human eosinophil apoptosis." Thesis, University of Leicester, 2001. http://hdl.handle.net/2381/29380.

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Eosinophils play a pivotal role in the pathogenesis of asthma and allergic disease. The accumulation and persistence of eosinophils at sites of inflammation are mediated at least in part by the extended survival of eosinophils in response to circulating hematopoietins IL-3, IL-5 and GM-CSF. The apoptosis and subsequent clearance of eosinophils without histotoxic mediator release is thought to be crucial in the resolution of airway inflammation in asthma. This study characterised the morphological and biochemical events of human eosinophil apoptosis in vitro and investigated the mechanism by which IL-5 induces eosinophil survival. Peripheral blood eosinophils have a distinct expression profile of Bcl-2 homologues, critical regulators of apoptosis, with detectable expression of pro-apoptotic family homologues Bax, Bcl-xs, Bim, Bak, Bid, and Bad, and anti-apoptotic homologue Bcl-xL, with little or no detectable Bcl-2 expression. Stimulation with IL-5 induced modest upregulation of Bcl-2 mRNA and protein, with no significant modulation of the other Bcl-2 homologues examined. Caspases are the conserved executioners of the apoptosis. Eosinophils endogenously expressed 'initiator' caspase-8 and -9, and 'effector' caspase-3, -6, and -7. Spontaneous eosinophil apoptosis involved caspase-independent translocation of Bax to the mitochondria, resulting in perturbation of the mitochondrial membrane, cytochrome c release, and subsequent activation of caspase-3, -6, -7, -8, and -9. IL-5 inhibited constitutive eosinophil apoptosis at a site upstream of Bax translocation to the mitochondria, thereby preventing cytochrome c release and caspase activation. Eosinophils constitutively expressed the conformationally active form of Bax diffusely in the cytosol, but predominantly in the nucleus. Apoptosis induced by Fas receptor ligation involved detectable activation of caspase-3 and -8, and caspase-dependent Bax translocation to the mitochondria, supporting classification of eosinophils as a Type II cell in terms of apoptotic control. The data implicate Bax and mitochondria as pivotal regulators of eosinophil apoptosis in response to diverse stimuli.
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Al-Khabuli, Jumaʾ. "Role of eosinophil in oral squamous cell carcinoma and traumatic ulcerative granuloma with stromal eosinophilia." Thesis, University of Leeds, 2005. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.418167.

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Humbles, Alison Anita. "The relationship between the generation of an eosinophil-selective chemoattractant, ecotoxin and eosinophil accumulation in vivo." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.267879.

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Byström, Jonas. "Eosinophil Cationic Protein : Expression Levels and Polymorphisms." Doctoral thesis, Uppsala University, Department of Medical Sciences, 2002. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-2059.

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The eosinophil cationic protein (ECP) is usually associated with the eosinophil granulocyte. In this thesis the presence and production of this protein has been studied in two other cells. The circulating monocyte was found to contain ECP mRNA and small amounts of ECP, one thousand times less than that found in the eosinophil. The production decreased by differentiation of the myelomonoblastic cell line U937 into a macrophage phenotype. Submucosal lung macrophages did not stain for ECP and alveolar macrophages did not contain ECP mRNA. The circulating neutrophil contains ECP at a level hundred fold less than the eosinophil. We found that the protein is located to the primary granules of the neutrophil but could detect no ECP mRNA in the cell. It was shown in vitro that the protein was taken up by the cell and partly transported to the primary granules. The uptake did not seem to be receptor mediated. Upon stimulation of the neutrophils, ECP previously taken up, was re-secreted.

The ECP protein is heterogeneous both to molecular characteristics and to function. To evaluate if a genetic component is involved, the ECP gene was analysed in 70 individuals. Three single nucleotide polymorphisms (SNP´s) were found, denoted 277(C>T), 434(G>C) and 562(G>C). The two first were located to the mature peptide-coding region and would change the amino acids, arg45cys and arg97thr. The prevalence of the most common SNP, 434, was evaluated in two eosinophil-related diseases, allergy/asthma and Hodgkin Lymphoma (HL). Forty-three HL patients were evaluated and it was found that the 434GG was significantly more prevalent in patients having nodular sclerosis (NS) as compared to other histologies (p=0.03). Erythrocyte sedimentation rate was also related to the 434GG genotype (p=0.009). In 209 medical students 434GG was more common (p=0.002) in those who indicated allergy. The genotype was unrelated to the production of IgE antibodies to allergens. In analysis of 76 subjects with asthma it was found that the 434GG genotype was significantly more common among allergic asthmatics (p=0.04). Asthma and HL-NS are characterized by fibrosis and eosinophils and ECP has been suggested in fibrosis development.

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Admiraal, Claudia Johanna. "Eosinophil degranulation as an allergy activation marker." [S.l. : Amsterdam : s.n.] ; Universiteit van Amsterdam [Host], 2001. http://dare.uva.nl/document/59048.

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Sandig, Hilary. "CRTH2 and its ligands in eosinophil biology." Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.430475.

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Hallsworth, Matthew Pearce. "GM-CSF and eosinophil survival in asthma." Thesis, King's College London (University of London), 1999. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.341883.

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Flemmig, Jörg, Johannes Remmler, Josefin Zschaler, and Jürgen Arnhold. "Detection of the halogenating activity of heme peroxidases in leukocytes by aminophenyl fluorescein." Universitätsbibliothek Leipzig, 2016. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-201836.

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The formation of hypochlorous and hypobromous acids by heme peroxidases is a key property of certain immune cells. These products are not only involved in defense against pathogenic microorganisms and in regulation of inflammatory processes, but contribute also to tissue damage in certain pathologies. After a short introduction about experimental approaches for the assessment of the halogenating activity in vitro and in cell suspensions, we are focusing on novel applications of fluorescent dye systems to detect the formation of hypochlorous acid (HOCl) in leukocytes. Special attention is directed to properties and applications of the non-fluorescent dye aminophenyl fluorescein that is converted by HOCl, HOBr, and other strong oxidants to fluorescein. This dye allows the detection of the halogenating activity in samples containing free myeloperoxidase and eosinophil peroxidase as well as in intact granulocytes using fluorescence spectroscopy and flow cytometry, respectively.
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Books on the topic "Eosinophil"

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Eosinophils: A comprehensive review and guide to the scientific and medical literature. Oxford: Oxford University Press, 1988.

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Sohei, Makino, and Fukuda Takeshi, eds. Eosinophils: Biological and clinical aspects. Boca Raton: CRC Press, 1993.

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Sc, Smith Harry D., and Cook R. M, eds. Immunopharmacology of eosinophils. London ; San Diego: Academic Press, 1993.

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Powell, Mark D. Morphological description of a possible nerve-eosinophilic granule cell relationship in the rainbow trout small intestine. Charlottetown: University of Prince Edward Island, 1991.

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Powell, Mark D. Morphological description of a possible nerve-eosinophilic granule cell relationship in the rainbow trout small intestine. Ottawa: National Library of Canada, 1991.

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Walsh, Garry M. Eosinophils: Structure, biological properties, and role in disease. Hauppauge, N.Y: Nova Science Publisher's, Inc., 2011.

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Eosinophils: Methods and protocols. New York: Humana Press, 2014.

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Craddock, Rachel. Molecular mechanisms of spontaneous neutrophil and eosinophil apoptosis. Birmingham: University of Birmingham, 2003.

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Warren, David John. Studies on an eosinophil differentiation factor produced by a T-hybrid line. Uxbridge: Brunel University, 1985.

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Lilliehook, Inger. Studies of blood eosinophil and neutrophil granulocytes in health and diseased dogs. Uppsala: Sveriges Lantbruksuniversitet, 1999.

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Book chapters on the topic "Eosinophil"

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Butterfield, Joseph H. "The Eosinophil and Eosinophilia." In Primary Hematology, 161–71. Totowa, NJ: Humana Press, 2001. http://dx.doi.org/10.1007/978-1-59259-228-9_12.

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Tiñana, Adrienne, Larry Borish, and John W. Steinke. "Eosinophil." In Nasal Polyposis, 35–43. Berlin, Heidelberg: Springer Berlin Heidelberg, 2010. http://dx.doi.org/10.1007/978-3-642-11412-0_5.

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Gooch, Jan W. "Eosinophil." In Encyclopedic Dictionary of Polymers, 891. New York, NY: Springer New York, 2011. http://dx.doi.org/10.1007/978-1-4419-6247-8_13679.

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Dent, Gordon. "Eosinophil Chemotaxis." In Methods in Molecular Biology, 101–10. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4939-1016-8_10.

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Yousefi, Shida, and Hans-Uwe Simon. "Eosinophil Recruitment." In Encyclopedia of Medical Immunology, 270–71. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9194-1_88.

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Yousefi, Shida, and Hans-Uwe Simon. "Eosinophil Activation." In Encyclopedia of Medical Immunology, 265–67. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9194-1_89.

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Lacy, P., and R. Moqbel. "Eosinophil Cytokines." In Chemical Immunology and Allergy, 134–55. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058782.

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Moy, James N. "The Eosinophil." In Atlas of Allergic Diseases, 43–47. London: Current Medicine Group, 2002. http://dx.doi.org/10.1007/978-1-4615-6481-2_6.

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Ward, Tony Milford. "Eosinophil Cationic Protein." In Proteins and Tumour Markers May 1995, 1175–76. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0681-8_32.

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Ward, Tony Milford. "Eosinophil Protein X." In Proteins and Tumour Markers May 1995, 1176. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0681-8_33.

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Conference papers on the topic "Eosinophil"

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Koranteng, J. B., S. L. Lai, K. L. Raby, P. Dixey, K. F. Chung, C. Michaeloudes, and P. K. Bhavsar. "Role of Eosinophil Mitochondrial Function in Severe Eosinophilic Asthma." In American Thoracic Society 2023 International Conference, May 19-24, 2023 - Washington, DC. American Thoracic Society, 2023. http://dx.doi.org/10.1164/ajrccm-conference.2023.207.1_meetingabstracts.a2541.

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Schmid, Johannes, Bjarke Hviid-Vyff, Tina Skjold, and Hans Juergen Hoffmann. "The usefulness of blood eosinophil count and FeNO to predict sputum eosinophilia in the diagnosis of severe eosinophilic asthma." In ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.oa2150.

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Kang, H., C. K. Rhee, and H. K. Yoon. "The Prediction of Eosinophilic Exacerbation by Eosinophil Levels Stratified in Stable COPD." In American Thoracic Society 2020 International Conference, May 15-20, 2020 - Philadelphia, PA. American Thoracic Society, 2020. http://dx.doi.org/10.1164/ajrccm-conference.2020.201.1_meetingabstracts.a5041.

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Griesbaum, Lena, Julie Petry, Admar Verschoor, and Barbara Wollenberg. "Untersuchung der Eosinophil Plättchen Interaktionen in vitro mittels einer standardisierten Eosinophil artigen Zelllinie." In 94. Jahresversammlung Deutsche Gesellschaft für Hals-Nasen-Ohren-Heilkunde, Kopf- und Hals-Chirurgie e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1766443.

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Imaoka, M. "Eosinophil as a Determinant of Airway Hyperresponsiveness in Allergic Asthma with Elevated Blood Eosinophils." In American Thoracic Society 2022 International Conference, May 13-18, 2022 - San Francisco, CA. American Thoracic Society, 2022. http://dx.doi.org/10.1164/ajrccm-conference.2022.205.1_meetingabstracts.a1247.

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Griesbaum, Lena, Julie Petry, Admar Verschoor, and Barbara Wollenberg. "Study of eosinophil-platelet interactions in vitro using a standardized eosinophilic cell line." In 94th Annual Meeting German Society of Oto-Rhino-Laryngology, Head and Neck Surgery e.V., Bonn. Georg Thieme Verlag, 2023. http://dx.doi.org/10.1055/s-0043-1767030.

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Farahi, Neda, Alison M. Condliffe, Sarah Heard, Nanak R. Singh, Rosalind P. Simmonds, Katrin Eitel, Mamta Baxi, et al. "Measuring Eosinophil Kinetics In Humans." In American Thoracic Society 2011 International Conference, May 13-18, 2011 • Denver Colorado. American Thoracic Society, 2011. http://dx.doi.org/10.1164/ajrccm-conference.2011.183.1_meetingabstracts.a4355.

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Southworth, Thomas, Gussie Beech, Umme Kolsum, and Dave Singh. "Reproducibility of COPD blood eosinophil counts." In ERS International Congress 2018 abstracts. European Respiratory Society, 2018. http://dx.doi.org/10.1183/13993003.congress-2018.pa4395.

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Konya, Viktoria, Eva M. Sturm, Petra Luschnig-Schratl, and Akos Heinemann. "Endothelial Prostaglandin I2 Restrains Eosinophil Trafficking." In American Thoracic Society 2010 International Conference, May 14-19, 2010 • New Orleans. American Thoracic Society, 2010. http://dx.doi.org/10.1164/ajrccm-conference.2010.181.1_meetingabstracts.a6401.

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Davies, Benjamin, Sue Frost, Satish Rao, David Thickett, Sejal Saglani, and Prasad Nagakumar. "Accuracy of blood eosinophil count in predicting sputum eosinophils in children with problematic severe asthma (PSA)." In ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.1212.

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Reports on the topic "Eosinophil"

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Furbert-Harris, Paulette. Eosinophil Granular Protein(s) Modulate Tumor Metastasis Marker Gene Expression. Fort Belvoir, VA: Defense Technical Information Center, May 2007. http://dx.doi.org/10.21236/ada473779.

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Furbert-Harris, Paulette M. Eosinophil Cell Lines in a Tri-Cell Multicellular Tumor Spheroid (MTS)/Endothelium Complex: Down Regulation of Adhesion and Integrin Molecules-Implications of Metastasis Inhibition. Fort Belvoir, VA: Defense Technical Information Center, October 2003. http://dx.doi.org/10.21236/ada442676.

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Rothenberg, Marc. Genetics of Eosinophilic Esophagitis. Fort Belvoir, VA: Defense Technical Information Center, March 2012. http://dx.doi.org/10.21236/ada567625.

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Rothenberg, Marc E. Genetics of Eosinophilic Esophagitis. Fort Belvoir, VA: Defense Technical Information Center, March 2011. http://dx.doi.org/10.21236/ada567626.

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Trocha, Steven D. The Great Imposture: Eosinophilic Cholangitis. Science Repository Oü, November 2018. http://dx.doi.org/10.31487/j.scr.2018.03.013.

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Broide, David. Genes Associated with Food Allergy and Eosinophilic Esophagitis. Fort Belvoir, VA: Defense Technical Information Center, November 2013. http://dx.doi.org/10.21236/ada601820.

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Kliewer, Kara, Qin Sun, Lin Fei, J. Pablo Abonia, Seema Aceves, Dan Atkins, Peter Bonis, et al. Comparing Two Restrictive Diets for Treating Eosinophilic Esophagitis in Children. Patient-Centered Outcomes Research Institute (PCORI), April 2020. http://dx.doi.org/10.25302/04.2020.cer.140311593.

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Viksna, Ludmila, Oksana Kolesova, Aleksandrs Kolesovs, Ieva Vanaga, and Seda Arutjunana. Clinical characteristics of COVID-19 patients (Latvia, Spring 2020). Rīga Stradiņš University, December 2020. http://dx.doi.org/10.25143/fk2/hnmlhh.

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Abstract:
Data include following variables: Demographics, epidemiological history, comorbidities, diagnosis, complications, and symptoms on admission to the hospital. Also, body’s temperature and SpO2. Blood cells: white cells count (WBC), neutrophils (Neu), lymphocytes (Ly), eosinophils (Eo) and monocytes (Mo), percentages of segmented and banded neutrophils, erythrocytes (RBC), platelet count (PLT), hemoglobin (Hb), and hematocrit (HCT); Inflammatory indicators: erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP); Tissue damage indicators: alanine aminotransferase (ALT), lactate dehydrogenase (LDH), and troponin T (TnT); Electrolytes: potassium and sodium concentration; Renal function indicators: creatinine and glomerular filtration rate (GFR); Coagulation tests: D-dimer, prothrombin time, and prothrombin index on admission to the hospital.
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Deng, Xuemei, Jesus Arango, Kadir Kizilkaya, Jian Zeng, Weiguo Cai, Janet Fulton, Neil O'Sullivan, and Jack C. M. Dekkers. Whole Genome Association Analysis of Idiopathic Eosinophilic Enteritis in Brown Egg Layers. Ames (Iowa): Iowa State University, January 2011. http://dx.doi.org/10.31274/ans_air-180814-77.

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Furbert-Harris, Paulette. Growth Inhibition of Breast Tumor Cells by Hypodense and Normodense Eosinophilic Cell Lines. Fort Belvoir, VA: Defense Technical Information Center, July 2000. http://dx.doi.org/10.21236/ada394003.

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