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Artykuły w czasopismach na temat "IL-4"
Usha, Prof. "IL-4 and IL-6 in Bronchial Asthma Does IL-6 Plays More Important Role than IL-4? A Preliminary Study". Journal of Medical Science And clinical Research 05, nr 04 (18.04.2017): 20446–50. http://dx.doi.org/10.18535/jmscr/v5i4.115.
Pełny tekst źródłaKelly-Welch, A., E. M. Hanson i A. D. Keegan. "Interleukin-4 (IL-4) Pathway". Science Signaling 2005, nr 293 (12.07.2005): cm9. http://dx.doi.org/10.1126/stke.2932005cm9.
Pełny tekst źródłaBorish, Larry. "IL-4 and IL-13 Dual Antagonism". American Journal of Respiratory and Critical Care Medicine 181, nr 8 (15.04.2010): 769–70. http://dx.doi.org/10.1164/rccm.201002-0147ed.
Pełny tekst źródłaSchindler, C., H. Kashleva, A. Pernis, R. Pine i P. Rothman. "STF-IL-4: a novel IL-4-induced signal transducing factor." EMBO Journal 13, nr 6 (marzec 1994): 1350–56. http://dx.doi.org/10.1002/j.1460-2075.1994.tb06388.x.
Pełny tekst źródłaGause, W. C., T. Takashi, J. D. Mountz, F. D. Finkelman i A. D. Steinberg. "Activation of CD 4-, CD 8- thymocytes with IL 4 vs IL 1 + IL 2." Journal of Immunology 141, nr 7 (1.10.1988): 2240–45. http://dx.doi.org/10.4049/jimmunol.141.7.2240.
Pełny tekst źródłaNAKANISHI, KENJI. "Interleukin cascade of IL-4,IL-5 and IL-2." Japanese Journal of Clinical Immunology 13, nr 5 (1990): 438–40. http://dx.doi.org/10.2177/jsci.13.438.
Pełny tekst źródłaAtamas, S. P., J. Choi, V. V. Yurovsky i B. White. "An alternative splice variant of human IL-4, IL-4 delta 2, inhibits IL-4-stimulated T cell proliferation." Journal of Immunology 156, nr 2 (15.01.1996): 435–41. http://dx.doi.org/10.4049/jimmunol.156.2.435.
Pełny tekst źródłaNoben-Trauth, N., L. D. Shultz, F. Brombacher, J. F. Urban, H. Gu i W. E. Paul. "An interleukin 4 (IL-4)-independent pathway for CD4+ T cell IL-4 production is revealed in IL-4 receptor-deficient mice". Proceedings of the National Academy of Sciences 94, nr 20 (30.09.1997): 10838–43. http://dx.doi.org/10.1073/pnas.94.20.10838.
Pełny tekst źródłaHo, S. N., R. T. Abraham, A. Nilson, B. S. Handwerger i D. J. McKean. "Interleukin 1-mediated activation of interleukin 4 (IL 4)-producing T lymphocytes. Proliferation by IL 4-dependent and IL 4-independent mechanisms." Journal of Immunology 139, nr 5 (1.09.1987): 1532–40. http://dx.doi.org/10.4049/jimmunol.139.5.1532.
Pełny tekst źródłaReich, Adam, Justyna Szczęch i Dominik Samotij. "Biologics for Itch: IL-4/IL-13, IL-31, IL-17, and IL-23 Antagonists". Current Dermatology Reports 6, nr 4 (17.10.2017): 263–72. http://dx.doi.org/10.1007/s13671-017-0204-7.
Pełny tekst źródłaRozprawy doktorskie na temat "IL-4"
Dawson, Charlotte Helen. "STAT 6 and IL-4 signalling". Thesis, University of Sheffield, 1996. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.245716.
Pełny tekst źródłaNieuwenhuizen, Natalie. "Immune and allergic responses to Anisakis pegreffii, with focus on the roles of IL-4, IL-13 and the IL-4 receptor alpha". Doctoral thesis, University of Cape Town, 2007. http://hdl.handle.net/11427/3115.
Pełny tekst źródłaThe fish-parasitizing nematode Anisakis pegreffii induces gastrointestinal disease and allergy when ingested by humans, and can cause occupational allergy in seafood processing workers. The present study examines immune and allergic responses to A. pegreffii in wildtype and gene deficient mice, with special focus on interleukin(IL)-4, IL-13, and the IL-4 receptor alpha (IL-4Rα). Experimental murine models of Anisakis infection, Anisakis-induced anaphylaxis and Anisakis-induced dermatitis were established in order to gain insight into the immune responses generated against Anisakis and unravel mechanisms of allergic disease.
Oksuz, Samet. "Targeting IL-4 locus for epigenetic reprogramming". University of Cincinnati / OhioLINK, 2014. http://rave.ohiolink.edu/etdc/view?acc_num=ucin1423581203.
Pełny tekst źródłaGovender, Melissa. "Investigating the role of IL-4/IL-13 signalling through the IL-4 receptor alpha (IL-4Rα) on keratinocytes in murine models of Leishmania major and Schistosoma mansoni". Doctoral thesis, University of Cape Town, 2017. http://hdl.handle.net/11427/24890.
Pełny tekst źródłaМозгова, Юлія Анатоліївна, Юлия Анатольевна Мозговая i Yuliia Anatoliivna Mozghova. "Динаміка вмісту IL-4 та IL-6 при хронічному тонзиліті в дітей". Thesis, Сумський державний університет, 2013. http://essuir.sumdu.edu.ua/handle/123456789/32359.
Pełny tekst źródłaPizzuti, Lucas. "Síntese de 4-(fur-2-il)- e 4-(tien-2-il)-pirimidinas a partir de β-Alcoxivinil trifluormetil cetonas". Universidade Federal de Santa Maria, 2005. http://repositorio.ufsm.br/handle/1/10401.
Pełny tekst źródłaThe cyclocondensation of the 1,1,1-trifluoro-4-methoxy-4-(2-heteroaryl)-3-buten-2-ones (heteroaryl = furyl and thienyl) with urea and amidines (acetamidine, benzamidine, guanidine, 1H-pyrazole-1-carboxamidine and 2-methyl-2-thiopseudourea) for synthesis of two 4-(2-heteroaryl)-6-trifluoromethylpyrimidinones and a series of ten 4-(2-heteroaryl)-6-trifluoromethylpyrimidines is reported. The reaction of the 1,1,1-trifluoro-4-methoxy-4-(2-heteroaryl)-3-buten-2-ones with urea was carried out in the presence of boron trifluoride etherate as a catalyst, at 50°C for 20 hours. The reactions of the same substracts with amidines were carried out in the presence of a 1 M solution of sodium hydroxide at r.t.-50°C for 1 hour. Under this conditions, only aromatic pyrimidines were obtained in 48-67%.
Este trabalho relata a síntese e isolamento de duas 4-(2-heteroaril)-6-trifluormetilpirimidinonas e uma série de dez 4-(2-heteroaril)-6-trifluormetilpirimidinas (heteroaril = furil e tienil), a partir da ciclocondensação de 1,1,1-trifluor-4-metoxi-4-(2-heteroaril)-3-buten-2-onas com uréia e amidinas (acetamidina, benzamidina, guanidina, 1Hpirazolil-1-carboxamidina e 2-metil-2-tiopseudouréia). A reação de 1,1,1-trifluor-4-metoxi-4-(2-heteroaril)-3-buten-2-onas com uréia ocorreu na presença de BF3.Et2O como catalisador, à 50°C por 20 horas. As reações dos mesmos substratos com amidinas ocorreu na presença de uma solução 1 M de NaOH à t.a.-50°C por 1 hora. Nestas condições, foram obtidas somente pirimidinas aromáticas com rendimentos entre 48-67%.
Cirocco, Robert E. "Cytokine analisys in atlantic bottlenose dolphins: molecular characterization of IL-4, IL-6, and IL-10". FIU Digital Commons, 2001. http://digitalcommons.fiu.edu/etd/2370.
Pełny tekst źródłaVale, Mariana Lima. "Atividade analgesica das interleucinas 4, 10 e 13 (IL-4, IL-10 e il-13) na dor inflamatoria experimental : papel de celulas residentes e citocinas". reponame:Repositório Institucional da UFC, 2000. http://www.repositorio.ufc.br/handle/riufc/2569.
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The release of cyclo-oxigenase products and sympathomimetics amines, the final mediators of inflammatory pain, is preceded by the generation of cytokines by resident cells. In recent years a number of cytokines such as IL-4, IL-10, IL-13, IL-6, TGF-β e IFN-α have been described to inhibit the production of TNF-α, IL-1β, IL-6 and IL-8 (cytokines regarded as pró-inflammatory) and possibly to exert their modulatory effect on macrophages and mast cells. Since it is known the capacity of those cytokines to inhibit the production of pro-inflammatory cytokines and the pivotal role of resident cells in the development of inflammatory pain we have decided to test the possibility of IL-4, IL-13 and IL-10 to modulate inflammatory pain. In short, IL-4 (1 – 5ng/animal), IL-13 (0.4 - 2.5ng/animal) or IL-10 (0.4 - 10ng/animal) was given 30 min before acetic acid (AAc) or zymosan (Zym) administration in the writhing model. IL-4 (2.5 e 5 ng/animal), IL-13 (1 e 2.5 ng/animal) or IL-10 (2 e 10 ng/animal) were injected, ip, 30 min before Zym (1 mg/animal; intra-articular) in the rat knee joint incapacitation test up to the 4th hour (the number of leukocytes was determined in the articular exsudate 6 hours later). Doses of those cytokines that exerted maximum effect in the writhing test were also injected 30 min before the hot plate test. These same doses were injected ip before naloxone administration in the AAc-induced writhing model in mice. TNF-α and IL-1β were determined in the supernatant of a macrophage culture which were collected from peritoneal fluid of mice treated with Zym and pre-treated with the cytokines under test. Our results show that interleukins 4, 13 and 10 inhibit writhing response in mice induced by AAc or Zym up to 58.7, 89.2 and 52%, and up to 62.6, 61.7 and 74.4%, respectively (p<0.05). Similar results were observed in the rat knee joint incapacitation test induced by Zym: 49.2, 56.6, 69,9% of inhibition (p<0.05). The same interleukins were able to inhibit Zym-induced leukocyte influx into articular cavity (53.8, 92.1 e 62% of inhibition, respectively - p<0,05). The analgesic activity of IL-4, IL-13 and IL-10 seems to be peripheral, since these cytokines presented no effect in the reaction time of the animals on hot plate test. This antinociceptive effect seems to have no relation with endogen opioid release since naloxone (opioid receptor antagonist) had no effect in reverting the antinociceptive effect of cytokines in the AAc-induced writhing in mice. However, IL-4 and IL-10 inhibit the release of TNF-α (42 e 41.2%, respectively - p<0.05) and of IL-1β (61.9 e 80.9%, respectively - p<0,05) by macrophages stimulated in vivo by Zym, indicating that their antinociceptive activities may be due to the inhibition of those cytokines release by resident cells.
Já está estabelecido que a liberação de produtos da cicloxigenase e aminas simpatomiméticas, mediadores finais da dor inflamatória é precedido pela geração, por células residentes, de uma cascata de citocinas. Recentemente dados do nosso laboratório demonstraram que no modelo de contorções abdominais (CA) a ativação dessa cascata é dependente também da presença de células residentes como macrófagos e mastócitos. Dados da literatura apontam algumas citocinas capazes de modular negativamente a função dessas células: IL-4,. IL-10, IL-13, IL-6, TGF-β e IFN-α . Com base nesses dados, o objetivo do presente trabalho foi estudar uma possível atividade analgésica de três citocinas: IL-4, IL-13 e IL-10. Para tanto injetou-se, via ip, IL-4 (1–5ng/animal), IL-13 (0.4-2.5ng/animal) ou IL-10 (0.4-10ng/animal) 30 min antes da administração de zymosan (Zym) ou ácido acético (AAc) para o teste de CA. IL-4 (2.5 e 5ng/animal), IL-13 (1 e 2.5ng/animal) ou IL-10 (2 e 10ng/animal) foi injetada, ip, 30 min antes do Zym (1 mg/animal; intra-articular) e logo após foi medida a incapacitação articular (IA) até a 4ª hora e na 6ª hora foi feita a contagem de leucócitos no fluido articular. As interleucinas estudadas também foram administradas (30 min antes) na dose que melhor inibiu as CA no teste da placa quente (PQ) e em camundongos que haviam recebido ou não a naloxona previamente ao estímulo (AAc) no teste de CA. IL-4 (5 ng/animal) ou IL-10 (10 ng/animal) foi injetada ip 30 min antes do Zym (ip) e após 15 min os animais foram sacrificados e o exsudato peritoneal foi colhido e posto em cultura para a dosagem de IL-1β e TNF-α no sobrenadante. No presente trabalho ficou demonstrado que as interleucinas-4, 13 e 10 são analgésicas tanto no modelo de CA induzidas por AAc (58.7, 89.2, 52% de inibição, efeito máximo, respectivamente, p<0.05) ou Zym (62.6, 61.7, 74.4% de inibição, efeito máximo, respectivamente, p<0.05) como também no modelo de IA induzido por Zym (49.2, 56.6, 69,9% de inibição, efeito máximo, respectivamente, p<0.05). As citocinas estudadas foram capazes de inibir o influxo de leucócitos para a cavidade articular (53.8, 92.1 e 62%, respectivamente - p<0,05). Foi demonstrado que o efeito analgésico parece ser de domínio periférico visto que nenhuma das citocinas modificou o tempo de reação na PQ, teste algesimétrico sensível apenas para drogas que exercem efeito central. Também foi demonstrado que a atividade analgésica das interleucinas testadas não depende da liberação de opióides endógenos, visto que o pré-tratamento com naloxona não foi capaz de reverter a atividade analgésica de nenhuma das interleucinas no modelo de CA. Contudo essa atividade analgésica parece depender da inibição da liberação de citocinas por células residentes visto que IL-4 e IL-10 foram capazes de diminuir a liberação de TNF-α (42 e 41.2% de inibição respectivamente - p<0.05) e IL-1β (61.9 e 80.9% de inibição respectivamente - p<0,05) por macrófagos peritoneais residentes.
Toor, Iqbal Singh. "Investigating the role of eosinophils in cardiac remodelling following myocardial infarction". Thesis, University of Edinburgh, 2018. http://hdl.handle.net/1842/31187.
Pełny tekst źródłaDheda, Keertan Unkha Jairam. "The expression and role of IL-4 and IL-4(delta)2 in tuberculosis with and without HIV co-infection". Thesis, University College London (University of London), 2006. http://discovery.ucl.ac.uk/1445411/.
Pełny tekst źródłaKsiążki na temat "IL-4"
Samolot bombowy DB-3/Ił-4. Warszawa: Dom Wydawniczy Bellona, 2006.
Znajdź pełny tekst źródłaMutin, U. G. Lichnai︠a︡ voĭna mekhanika Il-4. Staryĭ Oskol: Rosa, 2012.
Znajdź pełny tekst źródła1948-, Spits Hergen, red. IL-4: Structure and function. Boca Raton, FL: CRC Press, 1992.
Znajdź pełny tekst źródłaKotelnikov, Vladimir. Il-4: "vozdushnye kreĭsera" Stalina. Moskva: I︠A︡uza, 2009.
Znajdź pełny tekst źródłaLazara, Silvia Ferri de, Giulia D'Amaro Valle i Enoch Battagin. Cos'è il contemporaneo? 4: What is the contemporary? 4. Padova: CLEUP, 2012.
Znajdź pełny tekst źródłaTrevisi, Giuseppe. Il delitto Fanin: 4 novembre 1948. Bologna: Il Mulino, 1998.
Znajdź pełny tekst źródłaIl gastigamatti: Commedia in 4 atti. Firenze: FirenzeLibri, 2010.
Znajdź pełny tekst źródłaGiuseppe, Verdi. Il trovatore: Dramma in 4 parti. Roma: Gremese Editore, 1988.
Znajdź pełny tekst źródłaGiuseppe, Verdi. Il Trovatore: Dramma in 4 parti. Roma: Gremese Editore, 1988.
Znajdź pełny tekst źródłaNatacha, Godeau, red. Shrek 4: Il était une fin. [Paris]: Hachette jeunesse, 2010.
Znajdź pełny tekst źródłaCzęści książek na temat "IL-4"
Ranasinghe, Charani, Sreeja Roy, Zheyi Li, Mayank Khanna i Ronald J. Jackson. "IL-4 and IL-13 Receptors". W Encyclopedia of Signaling Molecules, 2549–57. Cham: Springer International Publishing, 2018. http://dx.doi.org/10.1007/978-3-319-67199-4_101978.
Pełny tekst źródłaRanasinghe, Charani, Sreeja Roy, Zheyi Li, Mayank Khanna i Ronald J. Jackson. "IL-4 and IL-13 Receptors". W Encyclopedia of Signaling Molecules, 1–8. New York, NY: Springer New York, 2017. http://dx.doi.org/10.1007/978-1-4614-6438-9_101978-1.
Pełny tekst źródłaPelaia, Girolamo, Alessandro Vatrella i Rosario Maselli. "Anti-IL-4/IL-13 Biologics". W Asthma: Targeted Biological Therapies, 67–81. Cham: Springer International Publishing, 2016. http://dx.doi.org/10.1007/978-3-319-46007-9_6.
Pełny tekst źródłaBorish, Larry, John W. Steinke, Marion Kasaian i Samuel J. Goldman. "IL-4- and IL-13-directed approaches". W New Drugs and Targets for Asthma and COPD, 115–21. Basel: KARGER, 2010. http://dx.doi.org/10.1159/000320808.
Pełny tekst źródłaSchroeder, John T. "Diagnostic Components: T Helper Cell Cytokines (IL-4, IL-5, IL-9, IL-10, IL-13, IL-17)". W Encyclopedia of Medical Immunology, 221–26. New York, NY: Springer New York, 2014. http://dx.doi.org/10.1007/978-1-4614-9194-1_298.
Pełny tekst źródłaKeegan, Achsah, Keats Nelms i William E. Paul. "The IL-4 Receptor — Signaling Mechanisms". W Advances in Experimental Medicine and Biology, 211–15. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4899-0987-9_21.
Pełny tekst źródłaClair, R. P. "Saturday, September 4, 2010—Chicago, IL". W Zombie Seed and the Butterfly Blues, 323–25. Rotterdam: SensePublishers, 2013. http://dx.doi.org/10.1007/978-94-6209-308-9_60.
Pełny tekst źródłaClair, R. P. "Saturday, September 4, 2010—Chicago, IL". W Zombie Seed and the Butterfly Blues, 327. Rotterdam: SensePublishers, 2013. http://dx.doi.org/10.1007/978-94-6209-308-9_61.
Pełny tekst źródłaShirokaze, J., K. Yanagida, K. Shudo, K. Konomoto, K. Kamiya i K. Sagara. "IL-4 Production Using Macroporous Microcarrier". W Animal Cell Technology: Developments Towards the 21st Century, 877–81. Dordrecht: Springer Netherlands, 1995. http://dx.doi.org/10.1007/978-94-011-0437-1_141.
Pełny tekst źródłaKhan, Manzoor M. "Regulation of IL-4 and IL-5 Secretion by Histamine and PGE2". W Advances in Experimental Medicine and Biology, 35–42. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1891-4_5.
Pełny tekst źródłaStreszczenia konferencji na temat "IL-4"
Kalinauskaitė-Žukauskė, Virginija, Andrius Januškevičius, Ieva Janulaitytė i Kęstutis Malakauskas. "IL-4, IL-8, IL-13, IL-17, IL-33 serum levels changes in acute allergic asthma model". W Abstracts from the 17th ERS Lung Science Conference: ‘Mechanisms of Acute Exacerbation of Respiratory Disease’. European Respiratory Society, 2019. http://dx.doi.org/10.1183/23120541.lungscienceconference-2019.pp237.
Pełny tekst źródłaMuchtar, R. Masri. "294 Polymorphism promotor gene of il-4 and il-4 level at graves disease patients". W LUPUS 2017 & ACA 2017, (12th International Congress on SLE &, 7th Asian Congress on Autoimmunity). Lupus Foundation of America, 2017. http://dx.doi.org/10.1136/lupus-2017-000215.294.
Pełny tekst źródłaHaque, S. Jaharul, Rikhia Chakraborty, Pankaj Sharma, Suzy Comhair, Sudakshina Ghosh, Weiling Xu, Manoj M. Veleeparambil i in. "Antioxidant-Mediated Negative Regulation Of IL-4/IL-13 Signaling". 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.a2794.
Pełny tekst źródłaKalinauskaitė-Žukauskė, Virginija, Andrius Januškevičius, Ieva Janulaitytė i Kęstutis Malakauskas. "LSC - 2019 - IL-4, IL-8, IL-13, IL-17, IL-33 serum levels changes in acute allergic asthma model". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa4083.
Pełny tekst źródłaButova, Tatiana, Mykhailo Kuzhko, Dmytro Butov i Nataliya Piriatinskaa. "Association between IL-2,IL-4 gene polymorphisms and pulmonary MDRTB". W ERS International Congress 2017 abstracts. European Respiratory Society, 2017. http://dx.doi.org/10.1183/1393003.congress-2017.pa3035.
Pełny tekst źródłaYadav, Aravind, Rakesh Naidu i Gopala Krishnan Govindasamy. "IL-4, IL-13 And IL-4RA Gene Polymorphisms And The Risk For Developing Idiopathic Nonallergic Rhinitis". 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.a4191.
Pełny tekst źródłaPunia, Navneet, Jennifer Thomson, Irene Babirad i Roma Sehmi. "IL-4 And IL-13 Prime The Transmigrational Responses Of Hemopoietic Progenitor Cells". 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.a4034.
Pełny tekst źródłaWirth, F., A. Lubosch, C. Zöller, K. Huck i I. Nakchbandi. "Osteoblasten stimulieren die Hämatopoese durch IL-4 Produktion". W Jahreskongress DVO OSTEOLOGIE 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0040-1722115.
Pełny tekst źródłaLe Floc’H, Audrey, Jeanne Allinne, Kirsten Nagashima, George Scott, Dylan Birchard, Seblewongel Asrat, Matthew Sleeman, Andrew Murphy i Jamie Orengo. "Il-4 and IL-13 act independently and synergistically to drive type 2 inflammation". W ERS International Congress 2019 abstracts. European Respiratory Society, 2019. http://dx.doi.org/10.1183/13993003.congress-2019.pa5206.
Pełny tekst źródłaBlauvelt, Andrew, i Susanne Kammerer. "Novel IL-4/IL-13 blocker shows high efficacy with only modest conjunctivitis signal". W 2022 American Academy of Dermatology Annual Meeting, redaktor Peter van de Kerkhof. Baarn, the Netherlands: Medicom Medical Publishers, 2022. http://dx.doi.org/10.55788/8aee17f2.
Pełny tekst źródłaRaporty organizacyjne na temat "IL-4"
Cao, Xianling, Xuanyou Zhou, Naixin Xu, Songchang Chang i 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, kwiecień 2022. http://dx.doi.org/10.37766/inplasy2022.4.0044.
Pełny tekst źródłaGilroy, Jill M. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, październik 2001. http://dx.doi.org/10.21236/ada403390.
Pełny tekst źródłaGooch, Jennifer L. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, lipiec 1999. http://dx.doi.org/10.21236/ada390684.
Pełny tekst źródłaGooch, Jennifer. Overexpression of IL-4 Signaling Pathway to Inhibit Breast Tumor Growth. Fort Belvoir, VA: Defense Technical Information Center, lipiec 2000. http://dx.doi.org/10.21236/ada384372.
Pełny tekst źródłaSachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2001. http://dx.doi.org/10.21236/ada396609.
Pełny tekst źródłaSachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2002. http://dx.doi.org/10.21236/ada407504.
Pełny tekst źródłaSachdev, Deepali. Role of IRS-1 Phosphorylation in IGF-1 and IL-4 Signaling in Breast Cancer. Fort Belvoir, VA: Defense Technical Information Center, czerwiec 2003. http://dx.doi.org/10.21236/ada418308.
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