Relevant bibliographies by topics / Interleukin-4

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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 'Interleukin-4'

Author: Grafiati
Published: 4 June 2021
Last updated: 21 February 2023

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Journal articles on the topic "Interleukin-4"

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Wu, Albert Y., Sanjiv Sur, J. Andrew Grant, and Julia W. Tripple. "Interleukin-4/interleukin-13 versus interleukin-5." Current Opinion in Allergy and Clinical Immunology 19, no. 1 (February 2019): 30–37. http://dx.doi.org/10.1097/aci.0000000000000490.

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&NA;. "Interleukin-4." Reactions Weekly &NA;, no. 606 (June 1996): 9. http://dx.doi.org/10.2165/00128415-199606060-00029.

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&NA;. "Interleukin-4." Reactions Weekly &NA;, no. 468 (September 1993): 8. http://dx.doi.org/10.2165/00128415-199304680-00038.

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&NA;. "Interleukin 4." Reactions Weekly &NA;, no. 399 (May 1992): 8. http://dx.doi.org/10.2165/00128415-199203990-00030.

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&NA;. "Interleukin 4." Reactions Weekly &NA;, no. 492 (March 1994): 8. http://dx.doi.org/10.2165/00128415-199404920-00033.

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Isakson, Peter. "Interleukin 4." Advances in Neuroimmunology 2, no. 1 (January 1992): 55–65. http://dx.doi.org/10.1016/s0960-5428(06)80005-7.

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Arreaza, Guillermo A., Mark J. Cameron, and Terry L. Delovitch. "Interleukin-4." Clinical Immunotherapeutics 6, no. 4 (October 1996): 251–60. http://dx.doi.org/10.1007/bf03259087.

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Jansen, J. H., W. E. Fibbe, R. Willemze, and J. C. Kluin-Nelemans. "Interleukin-4." Blut 60, no. 5 (May 1990): 269–74. http://dx.doi.org/10.1007/bf01736226.

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Banchereau, Jacques. "Interleukin 4." International Journal of Radiation Applications and Instrumentation. Part B. Nuclear Medicine and Biology 17, no. 7 (January 1990): 619–23. http://dx.doi.org/10.1016/0883-2897(90)90074-b.

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Van Epps, Heather L. "Indecisive interleukin-4?" Journal of Experimental Medicine 201, no. 12 (June 20, 2005): 1867. http://dx.doi.org/10.1084/jem20112iti3.

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Dissertations / Theses on the topic "Interleukin-4"

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Silfverswärd, Carl-Johan. "Effects of Interleukin-4 and Interleukin-13 on Bone." Doctoral thesis, Uppsala University, Department of Surgical Sciences, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8414.

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Cytokines play important roles in bone metabolism, participating in the complex interplay necessary for normal bone formation and turnover. The aim of the present thesis was to investigate the effects of two anti-inflammatory cytokines, interleukin-4 (IL-4) and interleukin-13 (IL-13) on bone.

Influence of pro- and anti-inflammatory cytokines on interleukin-6 (IL-6) formation in cultured human osteoblasts (hOBs) was investigated. IL-4 and IL-13 as well as interleukin-1 (IL-1) and tumour necrosis factor alpha and beta (TNF-α/β) stimulated IL-6 secretion in hOBs. Also, IL-4 and IL-13 synergistically potentiated the effect of IL-1 and TNFs on IL-6 secretion.

Effects of IL-4 and IL-13 on markers of osteoblastic activity in hOBs were investigated. IL-4 and IL-13 induced a dose-dependent increase in the formation of alkaline phosphatase (ALP) and pro-collagen type I carboxy-peptide (PICP) together with enhanced mineralization rate in hOBs. Formation of osteocalcin (OC) was unaffected.

The mechanism behind inhibited proliferation by IL-4 and IL-13 in hOBs was investigated. IL-4 and IL-13 caused a dose-dependent increase in DNA-fragmentation together with escalating Caspase-3 activity in hOBs, reflecting induced apoptosis. Osteoblast apoptosis was also confirmed by TNF-α, dexamethasone and by serum starvation.

The skeletal phenotype of IL-13-/-, IL-4-/-IL-13-/- and WT mice was compared. An altered cortical bone mass was detected in adult male IL-4-/-IL-13-/- mice. They displayed a reduction in cortical bone mineral content (BMC) secondary to reduced cortical thickness. Mechanical strength of the cortical bone was reduced in level with the reduction detected in BMC. Trabecular bone mineral density (tvBMD) was unaffected.

Callus formation in IL-4-/-IL-13-/- and WT male mice was compared. No differences were found concerning radiological healing, biomechanical properties, callus parameters or histology. Heterotopic bone formation in IL-4-/-IL-13-/- and WT mice was compared using DXBM implants. No differences were found concerning mineralization of implants. Immuno-histology showed inhibition of autonomic nerves and lack of implant vascularization in IL-4-/-IL-13-/- mice.

In summery, the two anti-inflammatory cytokines IL-4 and IL-13 influence osteoblast activity and apoptosis in vitro. They also selectively influence cortical bone formation in vivo. These findings suggest a role for IL-4 and IL-13 in osteoblast differentiation, in bone metabolism and in bone formation.

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Silfverswärd, Carl-Johan. "Effects of Interleukin-4 and Interleukin-13 on Bone /." Uppsala : Acta Universitatis Upsaliensis, 2008. http://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-8414.

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Parker, Ruth E. "The rat interleukin-4 receptor." Thesis, University of Oxford, 1995. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.318893.

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Traub, Benno [Verfasser]. "Einfluss der Interleukin-4-Interleukin-4-Rezeptor-Kaskade auf den malignen Phänotyp kultivierter Pankreaskarzinomzellen / Benno Traub." Ulm : Universität Ulm, 2017. http://d-nb.info/1140118161/34.

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Piehler, Daniel. "The inflammatory response against Cryptococcus neoformans is regulated by eosinophilic granulocytes and the interleukin-4/interleukin-4 receptor axis." Doctoral thesis, Universitätsbibliothek Leipzig, 2011. http://nbn-resolving.de/urn:nbn:de:bsz:15-qucosa-78248.

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Cytokines play an important regulatory role during immune responses against pathogens. The outcome of an induced cytokine pattern is determined by many factors. It strongly depends on the nature of the pathogen and the host’s ability to control the quality and strength of cytokine signals. In pulmonary infection with Cryptococcus neoformans T helper (Th) 1 and Th17 cell subsets and their associated cytokines confer protection, whereas a Th2-biased response with production of interleukin (IL) -4 confers susceptibility. Since inappropriate Th responses often lead to death in immunosuppressed human patients, especially HIV-1 infected patients, this work aimed to elucidate mechanisms of Th2 induction and regulation by assessing the Th2 hallmark cytokine IL-4 in an experimental model of cryptococcosis. Therefore, a kinetic study of IL-4 expression during 70 days after intranasal infection was performed in susceptible mice. The analyses included characterization of pulmonary leukocytes and Th cell cytokine profiling. IL-4 profiling revealed Cryptococcus-specific IL-4 production not before six weeks after infection. This unexpected finding was further validated by equal results observed in a kinetic study done in IL-4 reporter mice. These mice express a green fluorescent protein simultaneously to IL-4 expression in the same cell and this protein can be detected by flow cytometry. Two cellular sources of IL-4 were identified: Th2 cells were found as expected, but also, as shown for the first time, eosinophilic granulocytes could be demonstrated to secrete IL-4. Next, the influence of eosinophils on pulmonary inflammation and disease development was investigated using ΔdblGATA-1 mice constitutively devoid of eosinophilic granulocytes. Experiments with infected ΔdblGATA-1 mice revealed novel regulatory functions of eosinophils in cryptococcosis. In the absence of eosinophils pulmonary Th cell recruitment was significantly diminished. In addition, Th2 polarization was reduced in ΔdblGATA-1 mice as shown by reduced numbers of Th2 cells expressing the Th2-related surface marker T1/ST2 and reduced albeit not absent IL-4 production by Th cells. In addition to reduced IL-4 production, in the absence of eosinophils Th cells with enhanced interferon-γ and IL-17 production were observed. However, control of pulmonary fungal growth was only slightly enhanced in the absence of eosinophils and dissemination of cryptococci to the brain was unaltered. This may be related to the shared IL-4 production by not only eosinophils but also Th2 cells. Blocking more than one cellular source of IL-4 could be required to prevent immunopathology. To test the hypothesis of gradual IL-4-dependent immunopathology, experiments were conducted using mice expressing only one allele of the IL-4receptor (R) alpha (α) chain (+/-) instead of two (+/+). Indeed, mono-allelic expression of the IL-4Rα resulted in an intermediate expression of the IL-4R on the surface of myeloid and lymphoid cells indicating a gene-dosage effect for IL-4R expression. Infected IL-4Rα+/- mice displayed reduced susceptibility as compared with IL-4Rα+/+ mice, and IL-4Rα-/- mice completely lacking IL-4R expression were found to be protected with survival for the complete time period of the experiment (i.e. up to 275 days). Reduced susceptibility found in infected IL-4Rα+/- mice was associated with decreased serum levels of immunoglobulin E, reduced mucus production by airway epithelia, attenuation of airway hyper-reactivity, and reduced formation of alternatively activated macrophages in lung parenchyma – pathophysiological features, which are typically found in experimental models of asthma but also in asthma of humans and animals. Since no up-regulation of IL-4R by the infection with Cryptococcus neoformans was found, the experimental pulmonary infection model used appears to be a very sensitive low-level IL-4 system. This work highlights the outstanding role of IL-4 and its different cellular sources as well as its receptor in cryptococcosis and provides novel insights into pathogenesis. Moreover, a cellular (i.e. eosinophils) and a molecular (i.e. IL-4R) target for treatment of this mycosis and possibly of asthma is provided.
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McKenzie, Grahame James. "Analysis of interleukin-13 and interleukin-4 function using gene targeting." Thesis, University of Cambridge, 1998. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.624953.

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Moga, Simona. "Bestimmung der Zytokine Interleukin-1α, Interleukin-1β, Interleukin-2, Interleukin-3 und Interleukin-4 im Vaginalsekret bei Frauen mit Bakterieller Dysbiose." Diss., lmu, 2007. http://nbn-resolving.de/urn:nbn:de:bvb:19-75888.

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Clarke, Christopher Jeremy Paul. "Molecular mechanisms of the anti-inflammatory cytokines interleukin-4 and interleukin-10." Thesis, Imperial College London, 1997. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.285172.

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Alvi, Azra Johanna. "Heterogeneity of lymphokine-activated killer cells: Role of interleukin-2 and interleukin-4." Thesis, University of Ottawa (Canada), 1990. http://hdl.handle.net/10393/5579.

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Our main objective was to determine if the Lymphokine Activated Killer cells (LAK) activity is restricted to Natural Killer (NK) cells or if it is also detectable in T cell subsets, especially in CD3+ T cells that are also negative for CD4 and CD8 cell surface markers. We were able to obtain highly purified subsets of NK cells, helper/inducer (CD3+4+8$-$), suppressor/cytotoxic (CD3+4$-$8+) and double negative (CD3+4$-$8$-$) T cells. The double negative T cells are now known to be a subset of $\gamma\delta$-T cells. Highly purified subsets were obtained using antibody (sheep anti-mouse IgG) coated magnetic particles and monoclonal antibodies. The purified subsets were tested for LAK activity against a standard target cell (K562), a NK resistant/LAK sensitive target cell (HTB 38), and a NK/LAK resistant target cell. We found NK cells develop LAK activity after IL-2 stimulation and that two T cell subsets (cytotoxic/suppressor and double negative) consistently showed LAK activity (3 experiments). The helper/inducer subset showed LAK activity in 2 of 3 experiments. Interleukin 4 had an inhibitory effect on the proliferative activity of IL-2 stimulated T cells and was not used in the LAK experiments. In conclusion we have found that the LAK function is a property of an heterogeneous group of lymphocyte subsets that includes NK cells and T cell subsets. (Abstract shortened by UMI.)
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Schardt, Victor. "Vergleichende Untersuchungen zur Hefepilzbesiedelung von Mundhöhle und Vagina und Bestimmung von Interleukin-4, Interleukin-10 und Interleukin-12." Diss., lmu, 2013. http://nbn-resolving.de/urn:nbn:de:bvb:19-155152.

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Books on the topic "Interleukin-4"

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1948-, Spits Hergen, ed. IL-4: Structure and function. Boca Raton, FL: CRC Press, 1992.

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1946-, Kluger Matthew J., Oppenheim Joost J. 1934-, and Powanda M. C, eds. The Physiologic, metabolic, and immunologic actions of interleukin-1: Proceedings of a symposium held in Ann Arbor, Michigan, June 4-6, 1985. New York: Liss, 1985.

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Cuffe, Leonie M. Effect of moderate exercise induced stress on the Th1 (Interferon-gamma) and Th2 (Interleukin-4) cytokine subset response. London: University of Surrey Roehampton, 2001.

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Jankowski, Marek, and Tomasz Wandtke. Interleukin-27: Biological Properties and Clinical Application. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-39664-4.

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Baggiolini, M. Interleukin-8 (Cytokines, Vol 4). S. Karger Publishers (USA), 1991.

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Geha, Raif, and FRED Rosen. Case Studies in Immunology: Interleukin 1 Receptor-associated Kinase 4 Deficiency. W.W. Norton & Company, 2010. http://dx.doi.org/10.4324/9780203853498.

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Geha, Raif, and Fred Rosen. Case Studies in Immunology : Interleukin 1 Receptor-Associated Kinase 4 Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.

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Geha, Raif, and Fred Rosen. Case Studies in Immunology : Interleukin 1 Receptor-Associated Kinase 4 Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.

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Geha, Raif, and Fred Rosen. Case Studies in Immunology : Interleukin 1 Receptor-Associated Kinase 4 Deficiency: A Clinical Companion. Taylor & Francis Group, 2010.

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Geha, Raif, and Fred Rosen. Case Studies in Immunology : Interleukin 1 Receptor-Associated Kinase 4 Deficiency: A Clinical Companion. Norton & Company, Incorporated, W. W., 2010.

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Book chapters on the topic "Interleukin-4"

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Yokota, T., N. Arai, K. I. Arai, and A. Zlotnik. "Interleukin-4." In Peptide Growth Factors and Their Receptors I, 577–607. Berlin, Heidelberg: Springer Berlin Heidelberg, 1990. http://dx.doi.org/10.1007/978-3-642-49295-2_12.

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Farrar, William L. "Interleukin-4." In Encyclopedia of Cancer, 1–3. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-27841-9_3098-2.

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Yokota, T., N. Arai, K. I. Arai, and A. Zlotnik. "Interleukin-4." In Peptide Growth Factors and Their Receptors I, 577–607. New York, NY: Springer New York, 1991. http://dx.doi.org/10.1007/978-1-4612-3210-0_12.

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Farrar, William L. "Interleukin-4." In Encyclopedia of Cancer, 2315–17. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_3098.

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Farrar, William L. "Interleukin-4." In Encyclopedia of Cancer, 1892–94. Berlin, Heidelberg: Springer Berlin Heidelberg, 2011. http://dx.doi.org/10.1007/978-3-642-16483-5_3098.

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Izuhara, Kenji, Shoichiro Ohta, Hiroshi Shiraishi, and Shoichi Suzuki. "Interleukin 4, Interleukin 13, and Interleukin 9." In Inflammation and Allergy Drug Design, 173–85. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch13.

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Borish, Larry, and Jan M. Agosti. "Interleukin-4 Antagonism." In New Drugs for Asthma, Allergy and COPD, 256–59. Basel: KARGER, 2001. http://dx.doi.org/10.1159/000062183.

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Sears, Alison, and Andrew Pink. "Interleukin-4/13 Inhibitors." In Handbook of Systemic Drug Treatment in Dermatology, 131–36. 3rd ed. London: CRC Press, 2022. http://dx.doi.org/10.1201/9781003016786-19.

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Skevaki, Chrysanthi, Christoph Hudemann, and Harald Renz. "Interleukin 4 and the Related Cytokines (Interleukin 5 and Interleukin 13)." In Compendium of Inflammatory Diseases, 678–86. Basel: Springer Basel, 2016. http://dx.doi.org/10.1007/978-3-7643-8550-7_158.

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Skevaki, Chrysanthi, Christoph Hudemann, and Harald Renz. "Interleukin 4 and the Related Cytokines (Interleukin 5 and Interleukin 13)." In Encyclopedia of Inflammatory Diseases, 1–9. Basel: Springer Basel, 2014. http://dx.doi.org/10.1007/978-3-0348-0620-6_158-1.

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Conference papers on the topic "Interleukin-4"

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Tadjibayeva, K., and T. R. Romanovskaya. "REGULATORY ROLE OF INTERLEUKINS-4, 5 AND 6 IN THE DEVELOPMENT OF GLOMERULONEPHRITIS OF VARIOUS ETIOLOGIES." In SAKHAROV READINGS 2022: ENVIRONMENTAL PROBLEMS OF THE XXI CENTURY. International Sakharov Environmental Institute of Belarusian State University, 2022. http://dx.doi.org/10.46646/sakh-2022-2-24-27.

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The relationship between the concentration of interleukin-4, 5, and 6 with the content of eosinophils and the level of C-reactive protein in patients with chronic glomerulonephritis was established. An increase in eosinophils was found in patients with chronic glomerulonephritis with a predominance of interleukin-4 compared with patients with a predominance of interleukin-5 and 6, which may be an important diagnostic marker of glomerulonephritis.
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Keenan, Christine R., Trudi Harris, and Alastair G. Stewart. "Tumour Necrosis Factor-±, Interleukin-4 And Interleukin-13 Impair Glucocorticoid Transactivation In Human Bronchial Epithelial Cells." In 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.a6678.

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Basyar, Masrul, and Sabrina Ermayanti. "Analysis on the Relationship Between Chronic Asthma Based on Spirometry, and Interleukin 4 and Interleukin 13." In Proceedings of the 1st EAI International Conference on Medical And Health Research, ICoMHER November 13-14th 2018, Padang, West Sumatera, Indonesia. EAI, 2019. http://dx.doi.org/10.4108/eai.13-11-2018.2283644.

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Atamas, Sergei P., Virginia Lockatell, Sachin Lavania, Edward M. Pickering, Phillip H. Kang, Yulia N. Bashkatova, Sergey M. Andreev, and Irina G. Luzina. "Expression And Functional Effects Of Alternatively Spliced Interleukin-4 In Asthma." In 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.a3934.

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DiTullio, A. E., S. Park, P. A. Torzilli, and C. T. Chen. "Cyclic Compression of Chondrocytes Counteracts Pro-Inflammatory Tissue Remodeling Induced by Interleukin-1." In ASME 2008 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2008. http://dx.doi.org/10.1115/sbc2008-193027.

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Chondrocytes in tissue engineered constructs face challenging environments when first transplanted into a synovial joint, including high levels of compression/shear and pro-inflammatory cytokines. The joint level of interleukin 1 (IL-1) after trauma injury and in a repaired joint is acutely elevated. Matrix remodeling in tissue engineered constructs can be easily affected by the elevation and activation of aggrecanases (ADAMTS-4 and ADAMTS-5) and matrix metalloproteinases (MMPs) [2–4, 7–9, 11]. Several recent studies suggest that tensile loading and unconfined compression of chondrocytes has some anti-inflammatory effects against interleukin 1 (IL-1) by the downregulation of COX-2 and iNOS genes [1, 5, 6]. However, the role of loading in tissue repair at physiological levels is not clear. The objective of this study was to determine the effect of cyclic confined compression on the gene expression of MMPs and tissue inhibitors of metalloproteinases (TIMPs) in agarose-embedded chondrocytes in the presence of interleukin 1 (IL-1).
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Venmar, Katherine T., Daniel G. Hwang, Ashley Dozier, Kathy J. Carter, Sareena Gillani, and Barbara Fingleton. "Abstract 5328: Interleukin-4 receptor regulates metastasis of mammary epithelial cancer cells." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-5328.

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Hwang, Daniel G., Ashley Dozier, Kathy J. Carter, and Barbara Fingleton. "Abstract 2422: Epithelial interleukin-4 receptor promotes metastasis of mammary tumor cells." In Proceedings: AACR 102nd Annual Meeting 2011‐‐ Apr 2‐6, 2011; Orlando, FL. American Association for Cancer Research, 2011. http://dx.doi.org/10.1158/1538-7445.am2011-2422.

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Daulay, Milahayati, and Mutiara Indah Sari. "Interleukin-4 Gene Polymorphisms in Type 2 Diabetes Mellitus in Medan, Indonesia." In International Conference of Science, Technology, Engineering, Environmental and Ramification Researches. SCITEPRESS - Science and Technology Publications, 2018. http://dx.doi.org/10.5220/0010078905750577.

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Erb, Holger H., Frédéric R. Santer, and Zoran Culig. "Abstract 3350: Implications of the STAT6 pathway by interleukin-4 in prostate cancer." In Proceedings: AACR 103rd Annual Meeting 2012‐‐ Mar 31‐Apr 4, 2012; Chicago, IL. American Association for Cancer Research, 2012. http://dx.doi.org/10.1158/1538-7445.am2012-3350.

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Contoli, M., G. Caramori, S. Baraldo, M. Edwards, M. Saetta, SL Johnston, and A. Papi. "Interleukin-4 Modulates Rhinovirus Replication and Antiviral Immune Response in Respiratory Epithelial Cells." In 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.a5167.

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Reports on the topic "Interleukin-4"

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Fingleton, Barbara. Inhibition of Interleukin-4, a Survival Factor for Breast Cancer Cells, as an Antimetastatic Approach. Fort Belvoir, VA: Defense Technical Information Center, September 2010. http://dx.doi.org/10.21236/ada542731.

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Fingleton, Barbara. Inhibition of Interleukin-4, a Survival Factor for Breast Cancer Cells, as an Antimetastatic Approach. Fort Belvoir, VA: Defense Technical Information Center, September 2011. http://dx.doi.org/10.21236/ada555225.

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Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang, and Chenming Xu. Association of IL-4 and IL-10 Polymorphisms with Preterm Birth Susceptibility: A Systematic Review and Meta-Analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, April 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.

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Review question / Objective: The aim of our systematic review and meta-analysis was to summarize the effects of IL-4 and IL-10 gene polymorphism and clarify their possible association with PTB. Condition being studied: World Health Organization (WHO) defines preterm birth (PTB) as babies born alive before 37 weeks of pregnancy are completed. The new estimates show that the prevalence of PTB during 2014 ranged from 8.7% to13.4% of all live births, about 15 million preterm babies born each year. Besides, PTB is the leading cause of death worldwide for children below 5 years of age. Babies born preterm are at an increased risk of short-term and long-term complications attributed to immaturity of multiple organ systems, such as cerebral palsy, intellectual disabilities, vision and hearing impairments, and impaired cognitive development. PTB has become a worldwide public health problem, but its etiology remains unclear. Accumulating evidence shows that PTB is a syndrome that can be attributed to a variety of pathological processes(5). Inflammatory diseases and genetic background are known risk factors for PTB, many studies had shown that genetic variations in proinflammatory cytokines such as tumor necrosis factor-α (TNF-α) and interleukin-1 α (IL-1 α) are associated with increased risk of PTB, but the relationship between genetic polymorphism in anti-inflammatory cytokines and risk of PTB remains controversial.
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