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Artykuły w czasopismach na temat "CCR3"
Korbecki, Jan, Klaudyna Kojder, Katarzyna Barczak, Donata Simińska, Izabela Gutowska, Dariusz Chlubek i Irena Baranowska-Bosiacka. "Hypoxia Alters the Expression of CC Chemokines and CC Chemokine Receptors in a Tumor–A Literature Review". International Journal of Molecular Sciences 21, nr 16 (6.08.2020): 5647. http://dx.doi.org/10.3390/ijms21165647.
Pełny tekst źródłaPrincen, Katrien, Sigrid Hatse, Kurt Vermeire, Stefano Aquaro, Erik De Clercq, Lars-Ole Gerlach, Mette Rosenkilde i in. "Inhibition of Human Immunodeficiency Virus Replication by a Dual CCR5/CXCR4 Antagonist". Journal of Virology 78, nr 23 (1.12.2004): 12996–3006. http://dx.doi.org/10.1128/jvi.78.23.12996-13006.2004.
Pełny tekst źródłaZvejniece, Laura, Svetlana Kozireva, Zanna Rudevica, Ainars Leonciks, Barbro Ehlin-Henriksson, Elena Kashuba i Irina Kholodnyuk. "Expression of the Chemokine Receptor CCR1 in Burkitt Lymphoma Cell Lines Is Linked to the CD10-Negative Cell Phenotype and Co-Expression of the EBV Latent Genes EBNA2, LMP1, and LMP2". International Journal of Molecular Sciences 23, nr 7 (22.03.2022): 3434. http://dx.doi.org/10.3390/ijms23073434.
Pełny tekst źródłaWenzl, Kerstin, Katharina Troppan, Alexander JA Deutsch, Werner Linkesch, Peter Neumeister i Christine Beham-Schmid. "Distinct Chemokine Receptor Profile In Chronic Lymphocytic Leukaemia and Richter Transformed Diffuse Large B Cell Lymphomas Compared To Germinal Center B Cells and De Novo Diffuse Large B Cell Lymphomas". Blood 122, nr 21 (15.11.2013): 4852. http://dx.doi.org/10.1182/blood.v122.21.4852.4852.
Pełny tekst źródłaZhang, Yi-jun, Tatjana Dragic, Yunzhen Cao, Leondios Kostrikis, Douglas S. Kwon, Dan R. Littman, Vineet N. KewalRamani i John P. Moore. "Use of Coreceptors Other Than CCR5 by Non-Syncytium-Inducing Adult and Pediatric Isolates of Human Immunodeficiency Virus Type 1 Is Rare In Vitro". Journal of Virology 72, nr 11 (1.11.1998): 9337–44. http://dx.doi.org/10.1128/jvi.72.11.9337-9344.1998.
Pełny tekst źródłaMazur, Grzegorz, Emilia Jaskula, Ilona Kryczek, Dorota Dlubek, Tomasz Wrobel, Aleksandra Butrym, Andrzej Lange i Kazimierz Kuliczkowski. "Gene Expression for Chemokine Receptors Influences Survival of Non-Hodgkin Lymphoma Patients". Blood 116, nr 21 (19.11.2010): 3103. http://dx.doi.org/10.1182/blood.v116.21.3103.3103.
Pełny tekst źródłaTiffany, H. Lee, Ghalib Alkhatib, Christophe Combadiere, Edward A. Berger i Philip M. Murphy. "CC Chemokine Receptors 1 and 3 Are Differentially Regulated by IL-5 During Maturation of Eosinophilic HL-60 Cells". Journal of Immunology 160, nr 3 (1.02.1998): 1385–92. http://dx.doi.org/10.4049/jimmunol.160.3.1385.
Pełny tekst źródłaOrtega Moreno, L., S. Fernández Tomé, M. Chaparro, A. Marin, I. Mora Gutiérrez, C. Santander, M. Baldán, J. Gisbert i D. Bernardo. "P045 Profiling of human circulating dendritic cells and monocytes subsets discriminates type and mucosal status in patients with inflammatory bowel disease". Journal of Crohn's and Colitis 14, Supplement_1 (styczeń 2020): S155—S156. http://dx.doi.org/10.1093/ecco-jcc/jjz203.174.
Pełny tekst źródłaSallusto, Federica, Danielle Lenig, Charles R. Mackay i Antonio Lanzavecchia. "Flexible Programs of Chemokine Receptor Expression on Human Polarized T Helper 1 and 2 Lymphocytes". Journal of Experimental Medicine 187, nr 6 (16.03.1998): 875–83. http://dx.doi.org/10.1084/jem.187.6.875.
Pełny tekst źródłaDragan, Paulina, Matthew Merski, Szymon Wiśniewski, Swapnil Ganesh Sanmukh i Dorota Latek. "Chemokine Receptors—Structure-Based Virtual Screening Assisted by Machine Learning". Pharmaceutics 15, nr 2 (3.02.2023): 516. http://dx.doi.org/10.3390/pharmaceutics15020516.
Pełny tekst źródłaRozprawy doktorskie na temat "CCR3"
Duchesnes, Cecile Emmanuelle. "Molecular characterisation of the chemokine receptor CCR3". Thesis, Imperial College London, 2004. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.407171.
Pełny tekst źródłaBrasseit, Jennifer. "Mutagenese und funktionelle Charakterisierung des humanen CCR3-Rezeptors". [S.l. : s.n.], 2008. http://nbn-resolving.de/urn:nbn:de:bsz:352-opus-61848.
Pełny tekst źródłaJoubert, Philippe. "Expression and function of chemokine receptors on airway smooth muscle cells". Thesis, McGill University, 2007. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=103385.
Pełny tekst źródłaFor the first time, this work describes the expression of chemokine receptors by ASMC. We have shown that eotaxin, an important chemokine in asthma, induces migration of ASMC through the activation of CCR3. Although CCR3 expression is not regulated by Th2 cytokines in vitro, ASMC isolated from asthmatic patients expressed intrinsically higher levels of the surface receptor when compared to controls. We also describe the expression of CCR1 by ASMC, a receptor involved in airway remodelling in an animal model of asthma. We reported the expression of CCR1 mRNA in biopsies obtained from mild, moderate and severe asthmatics and showed that mild group express the highest level of CCR1. We also confirmed that ASMC express the receptor in vivo and showed that stimulation of this receptor with its ligands induces intra-cellular calcium mobilization, which confirms its functionality. Regulation of CCR1 on ASMC was also assessed using proinflammatory, Th1 and Th2 cytokines. We found that TNF-alpha and to a lesser extent, IFN-gamma, upregulated CCR1 mRNA and protein expression, while Th2 cytokines had no effect. The effect of these two cytokines was totally suppressed by either dexamethasone or mithramycin.
Collectively, our results demonstrate the expression of functional C-C chemokine receptors by ASMC. Interestingly, we have shown that CCR3 activation mediates ASMC migration and provides a new possible mechanism for the increased smooth muscle mass observed in asthmatic patients. Although the exact function of the CCR1 expressed by ASMC is unknown, our results suggest an involvement in asthma pathogenesis, possibly through airway remodelling.
Fulkerson, Patricia C. "A Critical Role for Eosinophils and CCR3 Signal Transduction in Allergic Airway Disease". University of Cincinnati / OhioLINK, 2005. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1120337075.
Pełny tekst źródłaHablot, Julie. "Liens entre inflammations articulaire et digestive : étude expérimentale chez la souris et contribution de l’immunité mucosale". Thesis, Université de Lorraine, 2018. http://www.theses.fr/2018LORR0095/document.
Pełny tekst źródłaNumerous type 3 immune cells (Th17 and ILC3) are physiologically located in lamina propria of the intestine. Microbial agents within the gut shape the immune system to make it efficient against threats but peaceful with commensals. Recent studies demonstrated changes in gut microbiota composition (dysbiosis) in chronic inflammatory rheumatism. These results suggest a role for mucosal immunity alteration in articular inflammation occurrence. Indeed, some type 3 immune cells once activated by microbiota, are thought to migrate to joints, involving notably chemokines receptors. Transcription factor RORγt, the master regulator of type 3 immune cells, could be negatively regulated by nuclear receptor PPARγ. Using experimental murine models, we studied the consequence of PPARγ deficiency and consequence of the chemokine receptor CCR3 inhibition on the joint-gut axis. Firstly, we demonstrated that experimental colitis induces microbiota changes, delays and reduces collagen-induced arthritis severity. Secondly, we showed that PPARγ deficient mice display spontaneous joint inflammation associated with abnormal type 3 distribution within the gut. Dysbiosis with enrichment in facultative anaerobic Enterobacteriaceae was found in these mice. Fecal microbiota transfer demonstrated this microbiota is non-arthritogenic. Finally, we demonstrated that CCR3 inhibition has profound anti-arthritic potencies associated with changes in leukocytes distribution within the joint-gut axis
Kirchem, 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 źródłaAraújo, Jéssica Maria Dantas. "Participação do receptor CCR3 na migração de eosinófilos induzida por estrogênio para o útero de camundongos C57/BL6 ovariectomizados". Pós-Graduação em Ciências Fisiológicas, 2017. https://ri.ufs.br/handle/riufs/6889.
Pełny tekst źródłaEosinophils are commonly described as cells from innate immunity that act on parasitic infections and lung diseases. However, in recent years, new functions are being added to these cells, among them, the maintenance of reproductive homeostasis. In addition, since the 1960s, studies have shown the estrogen relationship and the selective eosinophils migration to the uterus of castrated rats. The elucidation of the mechanism for the migration of these cells appears to be based on findings showing that the CCR3 receptor and its CCL11 chemokine are expressed in the human endometrium. Objective: The objective of this study was to evaluate the CCR3 participation in the eosinophils migration to the uterus of castrated mice, induced by 17-β-estradiol (E2). Methods: C57/BL6 mice, which received subcutaneous E2 injection, were used to determine the time and dose response of E2 (times 6, 12, 24 and 48 hours and doses of 0.1, 1, 3, 10, 30, 100 and 300 μg/kg) that promotes uterine weight gain and eosinophil migration. Subsequently, using the air bubble model, we sought to standardize CCL11- induced eosinophil recruitment, and the dose of the CCR3 antagonist (SB 328437 at doses of 1, 3 and 10 mg/kg) which promotes reduction in eosinophils migration. In addition, in the same model, the effect of the uterine extract with and without the administration of E2 (at the times of 6, 12 and 24 h) on the leukocyte migration was evaluated. Finally, an investigation was carried out on the effect of SB 328437 on uterine weight and eosinophil recruitment. The eosinophil peroxidase (EPO) absorbance and histology were used to evaluate the eosinophil migration, in which the uterus was stained with orcein specific for eosinophils. Results: The results demonstrated that the dose of 100 μg/kg E2 in the 24 hour period promoted a 40% increase in uterine weight, accompanied by eosinophil migration. In the air bubble model, it was observed that CCL11 recruited eosinophils, and SB 328437 promoted a 55% reduction in migration of these cells. The extract of the uterus caused the migration of total and eosinophilic leukocytes, but there was no difference between the groups with and without the administration of E2. Corroborating the results of SB 328437 in the air bubble experiment, the evaluation of its effect on uterine weight and eosinophils recruitment demonstrated that dose of 3 mg/kg reduced both parameters (approximately 45% and 56%, respectively) when stimulated with E2. The results were analyzed using ANOVA with Tukey post-test (more than two groups), and t test (two groups). Conclusion: Based on the results, it was possible to confirm the hypothesis that the CCR3 receptor participates in the eosinophils migration to the uterus of C57/BL6 mice after E2 induction. Furthermore, it represents an important pathway to be considered in studies aimed at elucidating mechanisms in in physiological and pathological processes involving the eosinophils recruitment.
Os eosinófilos são comumente descritos como células pertencentes à imunidade inata que agem em infecções parasitárias e nas doenças pulmonares. Porém, nos últimos anos, novas funções estão sendo acrescidas a essas células, dentre as quais, de manutenção da homeostase reprodutiva. Além disso, desde a década de 60, estudos demonstraram a relação do estrogênio com a migração seletiva de eosinófilos para o útero de ratas castradas. A elucidação do mecanismo para a migração dessas células baseia-se em achados evidenciando que o receptor CCR3 e sua quimiocina CCL11 estão expressos no endométrio humano. Objetivo: Diante do exposto, o estudo objetivou avaliar a participação do CCR3 na migração de eosinófilos para o útero de camundongos castrados, induzida por 17-β-estradiol (E2). Metodologia: Camundongos C57/BL6 receberam a injeção de E2 subcutânea, objetivando determinar o tempo e a dose resposta do E2 (tempos de 6, 12, 24 e 48 horas e doses de 0,1, 1, 3, 10, 30, 100 e 300 μg/kg) que promove aumento do peso do útero e migração de eosinófilos. Posteriormente, utilizando o modelo de bolha de ar, buscou-se padronizar o recrutamento de eosinófilos induzido por CCL11, e a dose do antagonista do CCR3 (SB 328437, nas doses de 1, 3 e 10 mg/kg) que promove redução da migração de eosinófilos. Ademais, no mesmo modelo, avaliou-se o efeito do extrato do útero com e sem a administração de E2 (nos tempos de 6, 12 e 24 h), na migração de leucócitos. Por último, foi realizada uma investigação sobre o efeito do SB 328437 no peso do útero e no recrutamento de eosinófilos. Para avaliação da migração de eosinófilos foi utilizada a absorbância da Peroxidase de Eosinófilos (EPO) e a histologia, no qual, os úteros foram corados com orceína, específico para eosinófilos. Resultados: Os resultados demonstraram que a dose de 100 μg/kg de E2 no tempo de 24 horas promoveu aumento de 40% no peso do útero, acompanhado da migração de eosinófilos. No modelo de bolha de ar, observou-se que a CCL11 recrutou os eosinófilos, e o SB 328437 promoveu redução de 55% na migração dessas células. O extrato do útero provocou a migração de leucócitos totais e de eosinófilos, porém não houve diferença entre os grupos com ou sem a administração de E2. Corroborando os resultados do SB 328437 no experimento da bolha de ar, a avaliação do efeito do antagonista no peso do útero e no recrutamento de eosinófilos, demonstrou que a dose de 3 mg/kg reduziu ambos os parâmetros (aproximadamente em 45% e 56%, respectivamente) quando estimulados com E2. Os resultados foram analisados utilizando o ANOVA com pós- teste de Tukey (mais de dois grupos), e o teste t (em dois grupos). Conclusão: Perante os resultados encontrados, foi possível confirmar a hipótese de que o receptor CCR3 participa da migração de eosinófilos para o útero de camundongos C57/BL6, após indução com E2. Outrossim, representa uma importante via a ser considerada em estudos que visam a elucidação de mecanismos em processos fisiológicos e patológicos envolvendo o recrutamento de eosinófilos.
São Cristóvão, SE
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 źródłaSANTUCCI, MARILINA BENEDETTA. "Ruolo della sfingosina 1-fosfato nella risposta immunitaria all’ infezione da mycobacterium tuberculosis". Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2004. http://hdl.handle.net/2108/208530.
Pełny tekst źródłaApel, Anna-Katharina [Verfasser]. "Biophysical and structural analysis of the chemokine receptors CCR2A and CCR3, leading to a 2.7 Å resolution structure of CCR2A / Anna-Katharina Apel". Ulm : Universität Ulm, 2019. http://d-nb.info/1188320963/34.
Pełny tekst źródłaKsiążki na temat "CCR3"
Pass CCRN! Wyd. 4. St. Louis, Mo: Elsevier, 2013.
Znajdź pełny tekst źródłaPass CCRN! St.Louis, Mo: Mosby, 1996.
Znajdź pełny tekst źródłaR, Rogelet Keri, red. Pediatric CCRN certification review. Sudbury, MA: Jones & Bartlett Learning, 2012.
Znajdź pełny tekst źródłaR, Rogelet Keri, red. Adult CCRN certification review. Sudbury, MA: Jones and Bartlett Publishers, 2009.
Znajdź pełny tekst źródłaBrorsen, Ann J. Adult CCRN certification review. Wyd. 2. Burlington, MA: Jones & Bartlett Learning, 2014.
Znajdź pełny tekst źródłaBhat, B. V. Rajarama. Cocycles of CCR flows. Providence, R.I: American Mathematical Society, 2001.
Znajdź pełny tekst źródłaHorgan, Carmel Mary Teresa. Studies on Mitozolomide (CCRG 81010), a new antineoplastic agent. Birmingham: University of Aston.Department of Pharmacy, 1985.
Znajdź pełny tekst źródłaGallagher, A. M. Attitudes to higher education: Report to CCRU and DENI. Belfast: Centre for Research on Higher Education, 1996.
Znajdź pełny tekst źródłaCentro Cultural Recoleta (Buenos Aires, Argentina), red. Testa + Bedel + Benedit: 30 años del CCR. Buenos Aires: Centro Cultural Recoleta, 2010.
Znajdź pełny tekst źródłaLeNeveu, D. M. Analysis specifications for the CC3 vault model. Pinawa, Man: AECL Research, 1994.
Znajdź pełny tekst źródłaCzęści książek na temat "CCR3"
Pease, James Edward. "Targeting CCR3". W Methods and Principles in Medicinal Chemistry, 339–57. Weinheim, Germany: Wiley-VCH Verlag GmbH & Co. KGaA, 2011. http://dx.doi.org/10.1002/9783527631995.ch15.
Pełny tekst źródłaBahl, Ash, Brian Springthorpe i Rob Riley. "Chemokine CCR3 antagonists". W New Drugs and Targets for Asthma and COPD, 153–59. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320814.
Pełny tekst źródłaLi, Yiwen, Deqiang Huang, Xin Xia, Zhengying Wang, Lingyu Luo i Rong Wen. "What Is the Role of CCR3 in Choroidal Neovascularization?" W Retinal Degenerative Diseases, 279–84. Boston, MA: Springer US, 2011. http://dx.doi.org/10.1007/978-1-4614-0631-0_36.
Pełny tekst źródłaPaquet, Luc, Paolo Renzi, Nicolay Ferrari i Mark Parry-Billings. "A multitargeted antisense therapy directed at CCR3 and the common β-chain of IL-3/IL-5/GM-CSF". W New Drugs and Targets for Asthma and COPD, 297–302. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320834.
Pełny tekst źródłaHütter, Gero. "CCR5". W Encyclopedia of Signaling Molecules, 828–32. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101567.
Pełny tekst źródłaRepeke, Carlos Eduardo, Thiago Pompermaier Garlet, Carolina Favaro Francisconi, Daiana Broll, Ana Paula Favaro Trombone i Gustavo Pompermaier Garlet. "CCL3". W Encyclopedia of Signaling Molecules, 799–804. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_579.
Pełny tekst źródłaHoruk, Richard. "CCR1". W Compendium of Inflammatory Diseases, 260–68. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_153.
Pełny tekst źródłaHütter, Gero. "CCR5". 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_101567-1.
Pełny tekst źródłaRepeke, Carlos Eduardo, Thiago Pompermaier Garlet, Carolina Favaro Francisconi, Daiana Broll, Ana Paula Favaro Trombone i Gustavo Pompermaier Garlet. "CCL3". W Encyclopedia of Signaling Molecules, 1–7. New York, NY: Springer New York, 2016. http://dx.doi.org/10.1007/978-1-4614-6438-9_579-1.
Pełny tekst źródłavan Roy, Frans, Volker Nimmrich, Anton Bespalov, Achim Möller, Hiromitsu Hara, Jacob P. Turowec, Nicole A. St. Denis i in. "CCL3". W Encyclopedia of Signaling Molecules, 261–65. New York, NY: Springer New York, 2012. http://dx.doi.org/10.1007/978-1-4419-0461-4_579.
Pełny tekst źródłaStreszczenia konferencji na temat "CCR3"
Bacon, Kevin, Emma Moss, Karen Bingham, Louis-Philippe Boulet, Mark Fitzgerald, Gail Gauvreau, Paul O'Byrne i in. "LATE-BREAKING ABSTRACT: A novel role for CCR3 in promoting airways hyperreactivity; Role for CCR3-muscarinic M3 receptor heterodimers". W Annual Congress 2015. European Respiratory Society, 2015. http://dx.doi.org/10.1183/13993003.congress-2015.oa288.
Pełny tekst źródłaUhm, Tae-Ki, Byung Soo Kim, Seol Kyoung Lee, Jin Hyun Kang, Do Jin Kim i Il Yup Chung. "CCR3 Transcriptional Control By Multiple, But Not A Single, Gata Elements". W 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.a5717.
Pełny tekst źródłaProboszcz, Małgorzata, Patrycja Nejman-Gryz, Magdalena Paplińska-Goryca, Katarzyna Górska, Paulina Misiukiewicz-Stępień i Rafał Krenke. "Expression of CCR3 on sputum macrophages in asthma, COPD and healthy subjects". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4085.
Pełny tekst źródłaUeki, S., G. Mahemuti, H. Kato, M. Takeda, J. Kihara, M. Tanabe, W. Ito, H. Kayaba i J. Chihara. "Retinoic Acids Induce Survival, Cytokine Production, and Expression of CCR3 on Human Eosinophils." 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.a1359.
Pełny tekst źródłaValdameri, Joana Scapinello, Anna Carolina Flumignan Bucharles, Caroline Baldasso Vieira, Thainá Mirella Macedo i Maria Luiza Lyczacovski Riesemberg. "CLASSIFICAÇÃO E CARACTERÍSTICAS HISTOLÓGICA DOS CARCINOMAS DE CÉLULAS RENAIS MAIS FREQUENTES". W I Congresso On-line Nacional de Histologia e Embriologia Humana. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/rems/3214.
Pełny tekst źródłaYao, Xin, Xiaoyi Yan, Xinyu Jiang, Jie Jiang, Man Jia i Mao Huang. "IL-4/13-induced up-regulation of METEORIN-LIKE (ML) in alveolar macrophages promotes epithelial CCR3 expression". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3552.
Pełny tekst źródłaKrammer, Susanne, Nina Li, Zuqin Yang, Julia Koelle, Carol Immanuel Geppert, Ralf J. Rieker, Gerard Graham i Susetta Finotto. "Late Breaking Abstract - The Role of the chemokine receptor CCR3 in House Dust Mite (HDM) induced experimental asthma". W ERS International Congress 2020 abstracts. European Respiratory Society, 2020. http://dx.doi.org/10.1183/13993003.congress-2020.306.
Pełny tekst źródłaDosanjh, Amrita, i Sunil M. Kurian. "Activation Of Eosinophil CCR3 Signaling And Eotaxin Using A Bioinformatics Approach To Study A Mouse Model Of Obliterative Airway Disease". W American Thoracic Society 2012 International Conference, May 18-23, 2012 • San Francisco, California. American Thoracic Society, 2012. http://dx.doi.org/10.1164/ajrccm-conference.2012.185.1_meetingabstracts.a5133.
Pełny tekst źródłaMoura, Maria Eduarda Gobara de, Letícia Ganem Rillo Paz Barateiro, Jacqueline Zanone i Jaqueline de Carvalho Rinaldi. "AVALIAÇÃO DA POPULAÇÃO DE MASTÓCITOS DA PRÓSTATA DORSOLATERAL DE RATOS WISTAR". W I Congresso Brasileiro de Estudos Patológicos On-line. Revista Multidisciplinar em Saúde, 2022. http://dx.doi.org/10.51161/conbesp/19.
Pełny tekst źródłaNanni, Bernardino P., Justin L. Bolender i Spencer D. Whittier. "Wastewater Treatment in Support of Ash Pond Closures". W ASME 2013 Power Conference. American Society of Mechanical Engineers, 2013. http://dx.doi.org/10.1115/power2013-98091.
Pełny tekst źródłaRaporty organizacyjne na temat "CCR3"
Adair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219632.
Pełny tekst źródłaAdair, M. The CCRS Quicklook Swath Browser. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2000. http://dx.doi.org/10.4095/219646.
Pełny tekst źródłaCyr, I., i Th Toutin. RADARSAT-1 Stereo Advisor on CCRS Web. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2001. http://dx.doi.org/10.4095/219705.
Pełny tekst źródłaGraham, D. F., A. N. Rencz i V. H. Singhroy. GSC - CCRS Storefront Project, conclusions from selected projects. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1994. http://dx.doi.org/10.4095/193706.
Pełny tekst źródłaVachon, P. W., A. L. Gray i K. E. Mattar. RADARSAT and ERS Repeat-Pass SAR Interferometry at CCRS. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1998. http://dx.doi.org/10.4095/219176.
Pełny tekst źródłaBoyle, J. S. Comparison of CCM3 simulations using two climatological ozone data sets. Office of Scientific and Technical Information (OSTI), luty 1997. http://dx.doi.org/10.2172/632787.
Pełny tekst źródłaBentz, Dale P., Xiuping Feng, Claus-Jochen Haecker i Paul E. Stutzman. Analysis of CCRL proficiency cements 135 and 136 using CEMHYD3D. Gaithersburg, MD: National Institute of Standards and Technology, 2000. http://dx.doi.org/10.6028/nist.ir.6545.
Pełny tekst źródłaWolfe, S. A. Permafrost science at ESS: a workshop on GSC/CCRS scientific opportunities. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 2010. http://dx.doi.org/10.4095/263373.
Pełny tekst źródłaMcGurrin, B. Remote Sensing Information: How and Why CCRS Developed an Online Database. Natural Resources Canada/CMSS/Information Management, 1990. http://dx.doi.org/10.4095/217657.
Pełny tekst źródłaBanks, G. N., J. K. Wong i H. Whaley. Combustion evaluation of eureka residue in the CCRL pilot-scale flame tunnel furnace. Natural Resources Canada/ESS/Scientific and Technical Publishing Services, 1989. http://dx.doi.org/10.4095/304418.
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