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Artykuły w czasopismach na temat "Eotaxin"
Varlamov, E. E., T. V. Vinogradova, A. A. Chuslyaeva, T. S. Okuneva i A. N. Pampura. "BIOMARKERS ALLERGIC INFLAMATION AND SEVERITY OF ATOPIC DERMATITIS AT CHILDREN". Russian Journal of Allergy 9, nr 5 (15.12.2012): 31–35. http://dx.doi.org/10.36691/rja694.
Pełny tekst źródłaBadewa, A. P., C. E. Hudson i A. S. Heiman. "Regulatory Effects of Eotaxin, Eotaxin-2, and Eotaxin-3 on Eosinophil Degranulation and Superoxide Anion Generation1". Experimental Biology and Medicine 227, nr 8 (wrzesień 2002): 645–51. http://dx.doi.org/10.1177/153537020222700814.
Pełny tekst źródłaHaley, Kathleen J., Mary E. Sunday, Yolanda Porrata, Colleen Kelley, Anne Twomey, Aliakbar Shahsafaei, Benjamin Galper, Larry A. Sonna i Craig M. Lilly. "Ontogeny of the eotaxins in human lung". American Journal of Physiology-Lung Cellular and Molecular Physiology 294, nr 2 (luty 2008): L214—L224. http://dx.doi.org/10.1152/ajplung.00086.2007.
Pełny tekst źródłaVarlamov, E. E., O. G. Elisyutina, T. V. Vinogradova, E. S. Fedenko i A. N. Pampura. "AGE-RELATED PATHOGENTIC SPECIFICITY OF CYTOKINE PROFILE IN ATOPIC DERMATITIS PATIENTS". Russian Journal of Allergy 13, nr 4-5 (15.12.2016): 37–42. http://dx.doi.org/10.36691/rja358.
Pełny tekst źródłaDiny, Nicola, Xuezhou Hou, Jobert G. Barin, Monica V. Talor, Noel R. Rose i Daniela Cihakova. "The eotaxin-CCR3 pathway is required for eosinophil trafficking to the heart in eosinophilic myocarditis". Journal of Immunology 196, nr 1_Supplement (1.05.2016): 117.10. http://dx.doi.org/10.4049/jimmunol.196.supp.117.10.
Pełny tekst źródłaRothenberg, Marc E. "Eotaxin". American Journal of Respiratory Cell and Molecular Biology 21, nr 3 (wrzesień 1999): 291–95. http://dx.doi.org/10.1165/ajrcmb.21.3.f160.
Pełny tekst źródłaJo, Jung Hyun, Yong-Tae Kim, Ho Soon Choi, Ho Gak Kim, Hong Sik Lee, Young Woo Choi, Dong Uk Kim i in. "KG 4/2015: A randomized, controlled, multicenter, open-label phase III clinical trial of GV1001 with gemcitabine/capecitabine in previous untreated, eotaxin-high patients with advanced pancreatic ductal adenocarcinoma." Journal of Clinical Oncology 39, nr 15_suppl (20.05.2021): 4020. http://dx.doi.org/10.1200/jco.2021.39.15_suppl.4020.
Pełny tekst źródłaBeal, Dominic R., David M. Stepien, Sudha Natarajan, Jiyoun Kim i Daniel G. Remick. "Reduction of eotaxin production and eosinophil recruitment by pulmonary autologous macrophage transfer in a cockroach allergen-induced asthma model". American Journal of Physiology-Lung Cellular and Molecular Physiology 305, nr 11 (1.12.2013): L866—L877. http://dx.doi.org/10.1152/ajplung.00120.2013.
Pełny tekst źródłaForssmann, Ulf, Mariagrazia Uguccioni, Pius Loetscher, Clemens A. Dahinden, Hanno Langen, Marcus Thelen i Marco Baggiolini. "Eotaxin-2, a Novel CC Chemokine that Is Selective for the Chemokine Receptor CCR3, and Acts Like Eotaxin on Human Eosinophil and Basophil Leukocytes". Journal of Experimental Medicine 185, nr 12 (16.06.1997): 2171–76. http://dx.doi.org/10.1084/jem.185.12.2171.
Pełny tekst źródłaStruyf, Sofie, Paul Proost, Dominique Schols, Erik De Clercq, Ghislain Opdenakker, Jean-Pierre Lenaerts, Michel Detheux i in. "CD26/Dipeptidyl-Peptidase IV Down-Regulates the Eosinophil Chemotactic Potency, But Not the Anti-HIV Activity of Human Eotaxin by Affecting Its Interaction with CC Chemokine Receptor 3". Journal of Immunology 162, nr 8 (15.04.1999): 4903–9. http://dx.doi.org/10.4049/jimmunol.162.8.4903.
Pełny tekst źródłaRozprawy doktorskie na temat "Eotaxin"
Pope, Samuel M. "Specific Role of Eotaxin-1 and Eotaxin-2 in Allergic Pulmonary Eosinophilia". Cincinnati, Ohio : University of Cincinnati, 2004. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=ucin1098472372.
Pełny tekst źródłaBenarafa, Charaf. "Equine eotaxin : cloning, expression and biological activity". Thesis, Royal Veterinary College (University of London), 2001. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.394942.
Pełny tekst źródłaWatanabe, Kimiko. "Eotaxin -1, -2 and -3 generation by different cell types". Thesis, Imperial College London, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.404880.
Pełny tekst źródłaMariano, Nadia Sabrina. "Estudo da resposta inflamatoria pulmonar alergica em ratos expostos a enterotoxina estafilococica do tipo A (SEA)". [s.n.], 2009. http://repositorio.unicamp.br/jspui/handle/REPOSIP/308954.
Pełny tekst źródłaDissertação (mestrado) - Universidade Estadual de Campinas, Faculdade de Ciências Médicas
Made available in DSpace on 2018-08-14T02:35:58Z (GMT). No. of bitstreams: 1 Mariano_NadiaSabrina_M.pdf: 621386 bytes, checksum: b01cd4d186fa15a5e8ea3c7657df604a (MD5) Previous issue date: 2009
Resumo: O Staphylococcus aureus é um tipo de bactéria gram-positiva que produz e secreta uma série de enterotoxinas com propriedade imunomoduladoras. Entretanto, pouco é conhecido sobre os mecanismos envolvidos na exacerbação do influxo celular observado em indivíduos asmáticos expostos a enterotoxinas estafilocócicas. O objetivo desse trabalho é investigar os efeitos da exposição das vias aéreas à enterotoxina estafilocócica do tipo A (SEA) sobre o recrutamento de leucócitos para o pulmão de ratos sensibilizados e desafiados com ovalbumina (OVA). Em nossos protocolos experimentais, ratos foram expostos à SEA 4 h antes ou 4 h após o desafio antigênico com OVA. O lavado broncoalveolar (LBA), a medula óssea e o tecido pulmonar foram obtidos 24 h após o desafio com OVA. A pré-exposição à SEA aumentou significativamente o número de eosinófilos no LBA e no tecido pulmonar de ratos desafiados com OVA, enquanto que o número de neutrófilos e células mononucleares não foi significativamente alterado. Na medula óssea, a pré-exposição à SEA isoladamente aumentou significativamente o número de eosinófilos, sendo esse aumento potencializado em ratos desafiados com OVA. Por outro lado, a pós-exposição à SEA não afetou o número de eosinófilos, neutrófilos ou células mononucleares observadas no LBA. A pré-exposição ao LPS em animais desafiados com OVA aumentou somente o número de neutrófilos no LBA. No LBA de ratos pré-expostos à SEA e desafiados com OVA, notamos uma elevação significativa nos níveis de TNF-? e eotaxina, mas não de IL-10. Os níveis de eotaxina presentes em sobrenadante de cultura de macrófagos alveolares tratados com SEA in vitro aumentaram cerca de 3 vezes em relação a macrófagos não estimulados com SEA. Concluímos que a pré-exposição (mas não a pós-exposição) das vias aéreas de ratos à SEA aumenta seletivamente o número de eosinófilos presente no LBA, tecido pulmonar e medula óssea de ratos desafiados com OVA por mecanismos que envolvem o aumento na síntese de TNF-? e eotaxina
Abstract: Gram-positive Staphylococcus aureus releases classical enterotoxins which aggravates allergic airway diseases. However, little is known about the mechanisms underlying the cell influx exacerbation in asthmatic individuals under exposure to Staphylococcal enterotoxins. We therefore aimed to investigate the effects of airways exposure to Staphylococcal enterotoxin A (SEA) to pulmonary leukocyte recruitment in rats sensitized and challenged with ovalbumin (OVA). Rats were exposed to SEA at 4 h prior to OVA challenge or at 4 h post-OVA challenge. Bronchoalveolar lavage (BAL) fluid, bone marrow and lung tissue were obtained at 24 h after OVA challenge. Preexposure to SEA markedly enhanced the eosinophil counts in both BAL fluid and pulmonary tissue in OVA-challenged rats, whereas neutrophil and mononuclear cell counts remained unchanged. In bone marrow, pre-exposure to SEA alone significantly increased the number of eosinophils, and that was further increased in OVA-challenged rats. Exposure to SEA post-OVA challenge did not affect the number of eosinophils, neutrophils and mononuclear cells in BAL fluid. Pre-exposure to the endotoxin lipopolyssacharide (LPS) in OVA-challenged animals rather enhanced the neutrophil number in BAL fluid. In rats pre-exposed to SEA and OVA-challenged, a marked elevation in the levels of TNF-? and eotaxin (but not of IL-10) in BAL fluid was observed. The eotaxin levels increased by about of 3-fold in alveolar macrophages treated with SEA in vitro. In conclusion, airways pre-exposure to SEA (but not the postexposition) causes a selective increase in eosinophil number in BAL fluid, lung tissue and bone marrow of OVA-challenged rats by mechanisms involving enhancement of TNF-? and eotaxin synthesis
Mestrado
Farmacologia
Mestre em Farmacologia
Bodman, Lee Graham. "The effect of glycosylation on the biological activity of eotaxin and related chemokines". Thesis, Imperial College London, 2004. http://hdl.handle.net/10044/1/11889.
Pełny tekst źródłaGhaffar, Omar. "Constitutive and cytokine-stimulated expression of eotaxin by human airway smooth muscle cells". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1998. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape11/PQDD_0024/MQ50776.pdf.
Pełny tekst źródłaMenzies-Gow, Andrew Neil. "The roles of interleukin-5 and eotaxin in oesinophil recruitment, maturation and activation". Thesis, Imperial College London, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.429161.
Pełny tekst źródłaKirchem, Antje. "Investigation of the signalling pathways coupled to the eotaxin receptor CCR3 in human eosinophils". Thesis, Imperial College London, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.406094.
Pełny tekst źródłaKonikoff, 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.
Pełny tekst źródłaAdvisor: 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.
Lieschke, Simone [Verfasser]. "Untersuchung der Rolle von Eotaxin-1 nach ischämischem Schlaganfall im Mausmodell: Neuroprotektion, Neuroregeneration oder destruktiv-proinflammatorische Rolle? / Simone Lieschke". Göttingen : Niedersächsische Staats- und Universitätsbibliothek Göttingen, 2021. http://d-nb.info/1232492825/34.
Pełny tekst źródłaCzęści książek na temat "Eotaxin"
Conroy, Dolores M., i Timothy J. Williams. "Eotaxin in Disease". W Chemokines in Disease, 123–38. Totowa, NJ: Humana Press, 1999. http://dx.doi.org/10.1007/978-1-59259-706-2_8.
Pełny tekst źródłaWilliams, T. J., i P. J. Jose. "Role of Eotaxin and Related CC Chemokines in Allergy and Asthma". W Immunological Mechanisms in Asthma and Allergic Diseases, 166–77. Basel: KARGER, 2000. http://dx.doi.org/10.1159/000058825.
Pełny tekst źródłaMitchell, Tracey J., i Timothy J. Williams. "The role of eotaxin and related CC-chemokines in asthma and allergy". W Inflammatory Processes: Molecular Mechanisms and Therapeutic Opportunities, 1–12. Basel: Birkhäuser Basel, 2000. http://dx.doi.org/10.1007/978-3-0348-8468-6_1.
Pełny tekst źródłaWilliams, Timothy John, i James Edward Pease. "Eotaxins (CCL11, CCL24, CCL26)". W Encyclopedia of Signaling Molecules, 1554–58. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101627.
Pełny tekst źródłaWilliams, Timothy John, i James Edward Pease. "Eotaxins (CCL11, CCL24, CCL26)". W Encyclopedia of Signaling Molecules, 1–5. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_101627-1.
Pełny tekst źródła"Eotaxin". W Encyclopedia of Genetics, Genomics, Proteomics and Informatics, 617. Dordrecht: Springer Netherlands, 2008. http://dx.doi.org/10.1007/978-1-4020-6754-9_5409.
Pełny tekst źródła"Eotaxin". W Encyclopedia of Immunotoxicology, 298. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_200451.
Pełny tekst źródłaEnna, S. J., i David B. Bylund. "Eotaxin". W xPharm: The Comprehensive Pharmacology Reference, 1. Elsevier, 2007. http://dx.doi.org/10.1016/b978-008055232-3.61690-3.
Pełny tekst źródłaVaddi, Krishna, Margaret Keller i Robert C. Newton. "Eotaxin". W The Chemokine FactsBook, 135–37. Elsevier, 1997. http://dx.doi.org/10.1016/b978-012709905-7/50024-5.
Pełny tekst źródła"Eotaxin-1". W Encyclopedia of Signaling Molecules, 1553. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101126.
Pełny tekst źródłaStreszczenia konferencji na temat "Eotaxin"
Murphy, GE, NI Pitman, M. Kurowska-Stolarska, P. Kewin, D. Xu, C. McSharry, NC Thomson i MC Shepherd. "Murine Airway Eosinophilia Following IL-33 Administration Is Eotaxin Dependent." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a4253.
Pełny tekst źródłaFarghly, Saher, Atef Farouk El-Karn, Mahmoud Farouk Sherif, Mohamed Ismail Seddik, Safaa Abdelgayed i Mohammed Abdelghany. "Serum periostin and eotaxin-2 as promising biomarkers in asthmatic smokers". W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa1135.
Pełny tekst źródłaLababidi, RR, JL Cane i M. Bafadhel. "P54 Eosinophil migration is enhanced towards il-5 and eotaxin in copd". W British Thoracic Society Winter Meeting 2017, QEII Centre Broad Sanctuary Westminster London SW1P 3EE, 6 to 8 December 2017, Programme and Abstracts. BMJ Publishing Group Ltd and British Thoracic Society, 2017. http://dx.doi.org/10.1136/thoraxjnl-2017-210983.196.
Pełny tekst źródłaGela, Anele, Gopinath Kasetty, Sandra Jovic, Maria Ekoff, Gunnar Nilsson, Sven Kjellstrom, James Pease i Arne Egesten. "Eotaxin-3 exerts innate host defense activities that are modulated by mast cell proteases". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.pa4032.
Pełny tekst źródłaYocum, G. T., J. J. Hwang i C. W. Emala. "6-shogaol, A Component of Ginger, Inhibits Human Airway Smooth Muscle Eotaxin Expression In Vitro". W 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.a4399.
Pełny tekst źródłaLee, AH, SE Wenzel, JB Trudeau i AT Mustovich. "Increased Eotaxin-2 mRNA in Asthmatic Bronchial Epithelial Cells Ex Vivo: Correlations with Clinical/Inflammatory Parameters." W American Thoracic Society 2009 International Conference, May 15-20, 2009 • San Diego, California. American Thoracic Society, 2009. http://dx.doi.org/10.1164/ajrccm-conference.2009.179.1_meetingabstracts.a5412.
Pełny tekst źródłaSmith, Steven G., Haruki Imoaka, Karen J. Howie, Rick Watson, Roma Sehmi i Gail M. Gauvreau. "The Effects Of Low Dose Peroxisome Proliferator-Activated Receptor (PPAR) Agonists On Eotaxin-Induced Eosinophil Chemotaxis". W 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.a4356.
Pełny tekst źródłaCouillard, Simon, James Melhorn, Akul Singhania, Daniel Horowitz, Ratko Djukanović, Christpher H. Woelk i Timothy S. C. Hinks. "Correlation of eotaxin-3 gene expression and other IL-13-induced genes in patients with asthma". W ERS International Congress 2021 abstracts. European Respiratory Society, 2021. http://dx.doi.org/10.1183/13993003.congress-2021.pa825.
Pełny tekst źródłaNaik, Chetan, John Trudeau, Sally E. Wenzel i Amy Lee. "Increased Expression Of Eotaxin-2 In The Airway Epithelium Correlates With Airway Eosinophilia And Severity Of Asthma". W 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.a4443.
Pełny tekst źródłaHuang, M., J. Zhang i Z. Chen. "Exposure to Ambient Particles Amplifies the Eotaxin-1 Release from Alternatively Activated Macrophages in Allergen-Sensitized Mice". W American Thoracic Society 2019 International Conference, May 17-22, 2019 - Dallas, TX. American Thoracic Society, 2019. http://dx.doi.org/10.1164/ajrccm-conference.2019.199.1_meetingabstracts.a3797.
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