Gotowe bibliografie tematyczne / Tumor necrosis factor

Gotowa bibliografia na temat „Tumor necrosis factor”

Autor: Grafiati
Data publikacji: 4 czerwca 2021
Data aktualizacji: 21 lutego 2023

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Artykuły w czasopismach na temat "Tumor necrosis factor"

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Chung, Phil-Sang, i Pil-Seob Jeong. "Antitumor effect of Tumor Necrosis Factor-α". Journal of Clinical Otolaryngology Head and Neck Surgery 7, nr 1 (maj 1996): 45–55. http://dx.doi.org/10.35420/jcohns.1996.7.1.45.

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KEYSTONE, E. C., i C. F. WARE. "Tumor Necrosis Factor and Anti-Tumor Necrosis Factor Therapies". Journal of Rheumatology Supplement 85 (1.05.2010): 27–39. http://dx.doi.org/10.3899/jrheum.091463.

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Inoue, Mamoru, Hidetoshi Inoko i Kimiyoshi Tsuji. "Tumor necrosis factor." Ensho 12, nr 1 (1992): 21–32. http://dx.doi.org/10.2492/jsir1981.12.21.

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Old, Lloyd J. "Tumor Necrosis Factor". Scientific American 258, nr 5 (maj 1988): 59–75. http://dx.doi.org/10.1038/scientificamerican0588-59.

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Wenzel, Richard P., Roger C. Bone i Michel P. Glauser. "Tumor necrosis factor". Critical Care Medicine 21, Supplement (październik 1993): S414–422. http://dx.doi.org/10.1097/00003246-199310001-00001.

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TRACEY, KEVIN J., i ANTHONY CERAMI. "Tumor necrosis factor". Critical Care Medicine 21, Supplement (październik 1993): S423–435. http://dx.doi.org/10.1097/00003246-199310001-00002.

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Vilcek, J., i T. H. Lee. "Tumor necrosis factor." Journal of Biological Chemistry 266, nr 12 (kwiecień 1991): 7313–16. http://dx.doi.org/10.1016/s0021-9258(20)89445-9.

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Chu, Wen-Ming. "Tumor necrosis factor". Cancer Letters 328, nr 2 (styczeń 2013): 222–25. http://dx.doi.org/10.1016/j.canlet.2012.10.014.

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Duerrschmid, Clemens, JoAnn Trial, Yanlin Wang, Mark L. Entman i Sandra B. Haudek. "Tumor Necrosis Factor". Circulation: Heart Failure 8, nr 2 (marzec 2015): 352–61. http://dx.doi.org/10.1161/circheartfailure.114.001893.

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Varfolomeev, Eugene E., i Avi Ashkenazi. "Tumor Necrosis Factor". Cell 116, nr 4 (luty 2004): 491–97. http://dx.doi.org/10.1016/s0092-8674(04)00166-7.

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Rozprawy doktorskie na temat "Tumor necrosis factor"

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Björnberg, Flemming. "Processing of TNF-receptors to soluble receptor forms in myeloid cells". Lund : Dept. of Hematology, Lund University, 1998. http://catalog.hathitrust.org/api/volumes/oclc/39176479.html.

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Engelberts, Ingeborg. "Tumor necrosis factor during sepsis king of cytokines? /". Maastricht : Maastricht : Universitaire Pers Maastricht ; University Library, Maastricht University [Host], 1994. http://arno.unimaas.nl/show.cgi?fid=6955.

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Krugten, Michiel Volkert van. "Tumor necrosis factor gene polymorphisms and rheumatic diseases /". Leiden, 2003. http://catalogue.bnf.fr/ark:/12148/cb40223074h.

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Watts, Alan D. "The biological role of transmembrane tumour necrosis factor [alpha]". Thesis, The University of Sydney, 1998. https://hdl.handle.net/2123/27668.

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Tumour necrosis factor (TNF) exists in two physiological forms. One is a soluble polypeptide of 17 kDa, and the other a type II integral membrane protein of 26 kDa designated transmembrane TNF. Soluble TNF is derived from the transmembrane form by proteolytic processing. The soluble TNF molecule exerts potent cytotoxic activity against certain types of cancer cells, and plays a critical role in the functioning of the immune and inflammatory system. The transmembrane TNF molecule shares many of the properties of the soluble form in vitro, but its function in the immune system is not as clearly defined as for the sTNF form. In this thesis the biological role of transmembrane TNF was investigated. The synthesis and expression of both soluble TNF and transmembrane TNF forms was examined in macrophage cells stimulated with LPS. Basic parameters for the production of transmembrane TNF were established to enable further analysis of its function. Using a hydroxamic acid-based inhibitor of TNF processing it was possible to obtain macrophage cells that expressed transmembrane TNF, but not soluble TNF; This enabled the investigation of transmembrane TNF free from the complicating effects of soluble TNF. It was found that inhibition of TNF processing in this way caused an accumulation of transmembrane TNF on the macrophage cells surface 5.1-7.5-fold greater than in cells not treated with the hydroxamic acid-based inhibitor. This corresponded to a 6.4-fold increase in TNF-mediated cytotoxicity of macrophage cells towards cells sensitive to transmembrane TNF. By radiolabelling macrophages, and using a specialised immunoprecipitation method, it was demonstrated that a soluble form of one of the TNF receptors (sTNFFi) binds transmembrane TNF. The consequence of this binding was neutralisation of transmembrane TNF-mediated cytotoxicity, but not inhibition of proteolytic processing of transmembrane TNF to release soluble TNF. The possibility that transmembrane TNF is capable of transducing a signal upon ligation with sTNFR was investigated. A broad range of cellular parameters were measured to see whether sTNFFi treatment of macrophages expressing transmembrane TNF induced a biochemical/physiochemical change. It was found that sTNFR caused a large increase (~200%) in ix intracellular calcium levels after 15 min treatment. This is the first direct evidence that transmembrane TNF is capable of acting like a receptor. The composition of the predicted amino acid sequence of transmembrane TNF was closely examined to determine the presence of features important for both structure and intracellular signalling. A model is presented in Chapter 6 which outlines in diagrammatic form likely structural features of transmembrane TNF. The molecule is predicted to possess a region of cytoplasmic alpha-helices corresponding to a highly conserved domain of the sequence. The structure of transmembrane TNF is consistent with that of a transmembrane receptor, capable of transducing signals initiated by ligation with an extracellular ligand. The comparison of predicted amino acid sequences of transmembrane TNF from different mammalian species revealed the presence of a conserved casein kinase | site. This site was also found to be present in most members of the TNF ligand family. Using orthophosphate labelling, it was shown that mouse transmembrane TNF is phosphorylated in macrophages. Ligation of sTNFR with transmembrane TNF induced de-phosphorylation of mTNF. This de-phosphorylation could be prevented by pre-incubation of the cells with serine phosphatase inhibitors. A selective inhibitor of casein kinase | dramatically reduced the phosphorylation of transmembrane TNF produced by macrophages. In addition, a recombinant form of casein kinase l phosphorylated transmembrane TNF in vitro on the site naturally phosphorylated by the endogenous kinase in vivo. The evidence presented in this study supports an entirely new role for transmembrane TNF, one in which the molecule is capable of acting like a transmembrane receptor, with the ligand being sTNFR. This phenomenon is known as "reverse signalling", and has been shown by other researchers to occur in the majority of members of the TNF ligand family. Implications of mTNF "reverse signalling" are relevant to the treatment of human diseases in which sTNFRs are currently being assessed in clinical trials.
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Langton, Amy Jean. "The role of TRUSS in TNFα-TNFRI signalling : implications for inflammatory lung diseases". Thesis, University of Cambridge, 2013. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.608019.

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Atkinson, Yvelle Hope. "Regulation of neutrophil functions by tumor necrosis factor-alpha /". Title page, contents and summary only, 1989. http://web4.library.adelaide.edu.au/theses/09PH/09pha878.pdf.

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Bond, Arden Lenore. "The production and characterization of a putative anti-idiotypic antibody to tumor necrosis factor-[alpha] /". This resource online, 1992. http://scholar.lib.vt.edu/theses/available/etd-05042010-020132/.

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Tan, Ern Yu. "Loss of protein folding gene expression in human tumors". Thesis, University of Oxford, 2007. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.670106.

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Han, Jiahuai. "Study of the regulation of cachectin/tumor necrosis factor expression". Doctoral thesis, Universite Libre de Bruxelles, 1990. http://hdl.handle.net/2013/ULB-DIPOT:oai:dipot.ulb.ac.be:2013/213139.

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Hel, Zden™ek. "Posttranscriptional regulation of tumor necrosis factor-à production in macrophages". Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1997. http://www.collectionscanada.ca/obj/s4/f2/dsk2/tape16/PQDD_0010/NQ36980.pdf.

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Książki na temat "Tumor necrosis factor"

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Corti, Angelo, i Pietro Ghezzi. Tumor Necrosis Factor. New Jersey: Humana Press, 2004. http://dx.doi.org/10.1385/1592597718.

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Tumor necrosis factor. New York: Nova Biomedical Books, 2009.

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Gregory, Bock, Marsh Joan i Symposium on Tumour Necrosis Factor and Related Cytotoxins (1987 : London, England), red. Tumour necrosis factor and related cytotoxins. Chichester: Wiley, 1987.

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Benjamin, Bonavida, red. Tumor necrosis factor/cachectin and related cytokines. Basel: Karger, 1988.

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T, Osawa, i Bonavida Benjamin, red. Tumor necrosis factor: Structure-function relationship and clinical application. Basel: Karger, 1992.

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D, Wu Hao Ph, red. TNF receptor associated factors (TRAFs). New York: Springer Science+Business Media, 2007.

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Kollias, G. TNF pathophysiology: Molecular and cellular mechanisms. Basel, Switzerland: Karger, 2010.

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Anti-tumor necrosis factor therapy in inflammatory bowel disease. Basel: Karger, 2015.

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S, Grewal Iqbal, red. Therapeutic targets of the TNF superfamily. New York: Springer Science+Business Media, 2009.

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International TNF Congress (8th 2000 Trondheim, Norway). 8th International TNF Congress: Conference on tumor necrosis factor and related molecules, scientific advances and medical applications : May 14-18, 2000, Trondheim, Norway : program and abstracts. Redaktor Capra J. Donald 1937-. Edinburgh: Blackwell Science, 2000.

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Części książek na temat "Tumor necrosis factor"

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Chu, Wen-Ming. "Tumor Necrosis Factor". W Encyclopedia of Cancer, 1–4. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27841-9_6040-8.

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Barger, Steven W. "Tumor Necrosis Factor". W Neuroprotective Signal Transduction, 163–83. Totowa, NJ: Humana Press, 1998. http://dx.doi.org/10.1007/978-1-59259-475-7_9.

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Chu, Wen-Ming. "Tumor Necrosis Factor". W Encyclopedia of Cancer, 4679–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 2017. http://dx.doi.org/10.1007/978-3-662-46875-3_6040.

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Ulich, Thomas R. "Tumor Necrosis Factor". W Cytokines of the Lung, 307–32. Boca Raton: CRC Press, 2022. http://dx.doi.org/10.1201/9781003066927-11.

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Manogue, Kirk R., i Anthony Cerami. "Cachectin (Tumor Necrosis Factor)". W Cellular and Molecular Aspects of Inflammation, 123–50. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4684-5487-1_8.

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Brightling, Christopher, Latifa Chachi, Dhan Desai i Yassine Amrani. "Tumor Necrosis Factor Alpha". W Inflammation and Allergy Drug Design, 225–35. Oxford, UK: Wiley-Blackwell, 2011. http://dx.doi.org/10.1002/9781444346688.ch18.

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Johnson, Victor J. "Tumor Necrosis Factor-α". W Encyclopedia of Immunotoxicology, 927–31. Berlin, Heidelberg: Springer Berlin Heidelberg, 2015. http://dx.doi.org/10.1007/978-3-642-54596-2_1522.

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Arampatzis, Adamantios, Lida Mademli, Thomas Reilly, Mike I. Lambert, Laurent Bosquet, Jean-Paul Richalet, Thierry Busso i in. "Tumor Necrosis Factor Alpha". W Encyclopedia of Exercise Medicine in Health and Disease, 883. Berlin, Heidelberg: Springer Berlin Heidelberg, 2012. http://dx.doi.org/10.1007/978-3-540-29807-6_3152.

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Papp, K. A., i Mathew N. Nicholas. "Tumor Necrosis Factor Inhibition". W Biologic and Systemic Agents in Dermatology, 111–21. Cham: Springer International Publishing, 2017. http://dx.doi.org/10.1007/978-3-319-66884-0_13.

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Johnson, Victor J. "Tumor Necrosis Factor-α". W Encyclopedia of Immunotoxicology, 1–5. Berlin, Heidelberg: Springer Berlin Heidelberg, 2014. http://dx.doi.org/10.1007/978-3-642-27786-3_1522-2.

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Streszczenia konferencji na temat "Tumor necrosis factor"

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Goel, Raghav, Guilio F. Paciotti i John C. Bischof. "Tumor necrosis factor-alpha induced enhancement of cryosurgery". W Biomedical Optics (BiOS) 2008, redaktorzy Nikiforos Kollias, Bernard Choi, Haishan Zeng, Reza S. Malek, Brian J. Wong, Justus F. R. Ilgner, Kenton W. Gregory, Guillermo J. Tearney, Henry Hirschberg i Steen J. Madsen. SPIE, 2008. http://dx.doi.org/10.1117/12.764020.

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Blanco, A., R. Bonfil, O. Bustoabad i M. Lazzari. "FACTOR II ACTIVATING ACTIVITY IN EXTRACTS OF TUMORAL NECROSIS FROM TWO MURINE BREAST ADENOCARCINOMAS". W XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1643206.

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Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC.The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table:C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p>0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.
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Rivas, MA, M. Tkach, CJ Proietti, C. Rosemblit, W. Beguelin, V. Sundblad, MC Díaz Flaqué, EH Charreau, PV Elizalde i R. Schillaci. "Tumor necrosis factor transactivates ErbB2 in breast cancer cells." W CTRC-AACR San Antonio Breast Cancer Symposium: 2008 Abstracts. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-4056.

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abla, hedia ben, Sonia Rekik, Soumaya Boussaid, Samia Jammali, Hela Sahli, Elhem Cheour i Mohamed Elleuch. "AB0699 EFFECT OF SWITCHING BETWEEN TUMOR NECROSIS FACTOR INHIBITOR IN SPONDYLOARTHRITIS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3834.

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Pass, Harvey I., Steven Evans, Roger Perry i Wilbert Matthews. "Kinetics of tumor necrosis factor production by photodynamic-therapy-activated macrophages". W OE/LASE '90, 14-19 Jan., Los Angeles, CA, redaktor Thomas J. Dougherty. SPIE, 1990. http://dx.doi.org/10.1117/12.17660.

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Laabidi, S., S. Bizid, A. Ben Mahmoud, G. Mohamed, H. Ben Abdallah, MR Bouali, MN Abdelli i E. Ghazouani. "Anti-Tumor Necrosis Factor Drug Response in Chronic Inflammatory Bowel Disease and Influencing Factors". W ESGE Days 2021. Georg Thieme Verlag KG, 2021. http://dx.doi.org/10.1055/s-0041-1724752.

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Huang, Yun-Ju, Yao-Fan Fang, Shue-Fen Luo, Kuang-Hui Yu, Chang-Fu Kuo, Ping-Ha Tsai i Yen-Fu Chen. "AB0383 LATENT TUBERCULOSIS INFECTION SHOULD BE MONITORED IN BOTH TUMOR NECROSIS FACTOR INHIBITORS AND NON-TUMOR NECROSIS FACTOR INHIBITORS IN BIOLOGICAL-NAïVE PATIENTS WITH RHEUMATOID ARTHRITIS". W Annual European Congress of Rheumatology, EULAR 2019, Madrid, 12–15 June 2019. BMJ Publishing Group Ltd and European League Against Rheumatism, 2019. http://dx.doi.org/10.1136/annrheumdis-2019-eular.3054.

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Rego, Stephen, Krista Ricci, Muthulekha Swamydas i Didier Dreau. "Abstract 397: Soluble Tumor Necrosis Factor Receptor shed by breast tumor cells modulates macrophage migration". W 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.am2012-397.

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Iwona, Grądzka, Sikorska Katarzyna i Brzóska Kamil. "Interference of Silver Nanoparticles with Tumor Necrosis Factor Action in Epithelial Cells". W The 2nd World Congress on Recent Advances in Nanotechnology. Avestia Publishing, 2017. http://dx.doi.org/10.11159/icnb17.116.

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Membriani, Evangelina, Erika Cuenca, Leticia Limongi, Ana Putruele i Carlos Luna. "Latent tuberculosis screening and entering antibody therapy monoclonares against tumor necrosis factor". W ERS International Congress 2016 abstracts. European Respiratory Society, 2016. http://dx.doi.org/10.1183/13993003.congress-2016.pa2701.

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Raporty organizacyjne na temat "Tumor necrosis factor"

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Larrick, James W., Vera Morhenn, Yawen L. Chiang i Tim Shi. Activated Langerhans Cells Release Tumor Necrosis Factor. Fort Belvoir, VA: Defense Technical Information Center, styczeń 1988. http://dx.doi.org/10.21236/ada206646.

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Gao, Li-nan, Lian-gang Ge, Ming-zhe Zhu i Xin-xin Yao. Association between tumor necrosis factor α and uterine fibroids: a protocol of systematic review. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, lipiec 2020. http://dx.doi.org/10.37766/inplasy2020.7.0010.

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Li, Peng, i Junjun Liu. Effect of tumor necrosis factor inhibitors on the risk of adverse cardiovascular events in patients with psoriasis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, sierpień 2022. http://dx.doi.org/10.37766/inplasy2022.8.0090.

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Review question / Objective: Previous studies have indicated a cardioprotective effect of tumor necrosis factor inhibitor (TNFi) therapy in adult patients with psoriasis (Pso). However, most were retrospective studies, and the association between cardiometabolic comorbidities and major adverse cardiovascular events (MACE) has not been validated in randomized controlled trials (RCTs). Condition being studied: Because the available evidence has recently increased, we performed the present updated meta-analysis and meta-regression of cohort studies and RCTs to evaluate whether TNFi therapy can decrease the risk of MACE among patients with Pso and to assess the associations between cardiometabolic comorbidities and MACE.
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Behbakht, Kian. Modulators of Response to Tumor Necrosis-Factor-Related Apoptosis Inducing Ligand (TRAIL) Therapy in Ovarian Cancer. Fort Belvoir, VA: Defense Technical Information Center, kwiecień 2010. http://dx.doi.org/10.21236/ada532993.

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Borra, Himabindu, Daniel F. Battafarano, Ramon Arroyo, Michael J. Morris, Michelle Sit i Gerald Merrill. Reliability of Tuberculosis Screening Test in Patients Receiving Tumor Necrosis Factor Antagonist Therapy in a United States Rheumatology Clinic. Fort Belvoir, VA: Defense Technical Information Center, maj 2013. http://dx.doi.org/10.21236/ada577631.

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Dotsenko, S. S., L. N. Shilova, A. S. Trofimenko, S. A. Bedina, E. A. Tikhomirova i M. A. Mamus. The role of cytokines in predicting the effectiveness of combined treatment with tumor necrosis factor α inhibitors in rheumatoid arthritis. ООО "ИМА-Пресс", 2018. http://dx.doi.org/10.18411/1995-4484-2018-56-33-17.

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Meidan, Rina, i Joy Pate. Roles of Endothelin 1 and Tumor Necrosis Factor-A in Determining Responsiveness of the Bovine Corpus Luteum to Prostaglandin F2a. United States Department of Agriculture, styczeń 2004. http://dx.doi.org/10.32747/2004.7695854.bard.

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The corpus luteum (CL) is a transient endocrine gland that has a vital role in the regulation of the estrous cycle, fertility and the maintenance of pregnancy. In the absence of appropriate support, such as occurs during maternal recognition of pregnancy, the CL will regress. Prostaglandin F2a (PGF) was first suggested as the physiological luteolysin in ruminants several decades ago. Yet, the cellular mechanisms by which PGF causes luteal regression remain poorly defined. In recent years it became evident that the process of luteal regression requires a close cooperation between steroidogenic, endothelial and immune cells, all resident cells of this gland. Changes in the population of these cells within the CL closely consort with the functional changes occurring during various stages of CL life span. The proposal aimed to gain a better understanding of the intra-ovarian regulation of luteolysis and focuses especially on the possible reasons causing the early CL (before day 5) to be refractory to the luteolytic actions of PGF. The specific aims of this proposal were to: determine if the refractoriness of the early CL to PGF is due to its inability to synthesize or respond to endothelin–1 (ET-1), determine the cellular localization of ET, PGF and tumor necrosis factor a (TNF a) receptors in early and mid luteal phases, determine the functional relationships among ET-1 and cytokines, and characterize the effects of PGF and ET-1 on prostaglandin production by luteal cell types. We found that in contrast to the mature CL, administration of PGF2a before day 5 of the bovine cycle failed to elevate ET-1, ETA receptors or to induce luteolysis. In fact, PGF₂ₐ prevented the upregulation of the ET-1 gene by ET-1 or TNFa in cultured luteal cells from day 4 CL. In addition, we reported that ECE-1 expression was elevated during the transitionof the CL from early to mid luteal phase and was accompanied by a significant rise in ET-1 peptide. This coincides with the time point at which the CL gains its responsiveness to PGF2a, suggesting that ability to synthesize ET-1 may be a prerequisite for luteolysis. We have shown that while ET-1 mRNA was exclusively localized to endothelial cells both in young and mature CL, ECE-1 was present in the endothelial cells and steroidogenic cells alike. We also found that the gene for TNF receptor I is only moderately affected by the cytokines tested, but that the gene for TNF receptor II is upregulated by ET-1 and PGF₂ₐ. However, these cytokines both increase expression of MCP-1, although TNFa is even more effective in this regard. In addition, we found that proteins involved in the transport and metabolism of PGF (PGT, PGDH, COX-2) change as the estrous cycle progresses, and could contribute to the refractoriness of young CL. The data obtained in this work illustrate ET-1 synthesis throughout the bovine cycle and provide a better understanding of the mechanisms regulating luteal regression and unravel reasons causing the CL to be refractory to PGF2a.
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Blanken, Annelies, Bafrin Abdulmajid, Eva van Geel, Joost Daams, Martin van der Esch i Michael Nurmohamed. Effect of tumor necrosis factor inhibiting treatment on arterial stiffness and arterial wall thickness in rheumatoid arthritis patients: protocol for a systematic review and planned meta-analysis. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, styczeń 2022. http://dx.doi.org/10.37766/inplasy2022.1.0131.

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Review question / Objective: The aim of this systematic review is to evaluate the effect of TNF inhibiting treatment on arterial stiffness (as measured with pulse wave velocity and augmentation index) and arterial wall thickness (as measured with carotid intima media thickness) in rheumatoid arthritis patients. Condition being studied: Rheumatoid arthritis is a chronic autoimmune disorder, which affects approximately 1% of the population worldwide. Information sources: The following electronic databases will be searched for potentially eligible studies: EMBASE, MEDLINE, ClinicalTrials.gov and WHO International Clinical Trials Registry Platform. For the studies identified as eligible for inclusion, similarity tracking will be used to identify more potentially relevant articles with the ‘related article’ feature in PubMed. In addition, a citation search will be performed for included studies to identify articles that have cited them. Reference lists of the included studies and previous reviews on the subject will be searched for potentially relevant studies. ResearchGate profiles of top authors on the subject will be investigated to identify potentially relevant data points. For ongoing or finished studies that are potentially eligible, but without a publication, study authors will be contacted for information. When additional information is needed, study authors will be contacted as well.
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Tian, Cong, Jianlong Shu, Wenhui Shao, Zhengxin Zhou, Huayang Guo i Jingang Wang. The efficacy and safety of IL Inhibitors, TNF-α Inhibitors, and JAK Inhibitor on ankylosing spondylitis: A Bayesian network meta-analysis of a “randomized, double-blind, placebo-controlled” trials. INPLASY - International Platform of Registered Systematic Review and Meta-analysis Protocols, wrzesień 2022. http://dx.doi.org/10.37766/inplasy2022.9.0117.

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Review question / Objective: In this study, we conducted a Bayesian network meta-analysis to evaluate the efficacy and safety of interleukin (IL) inhibitors, tumor necrosis factor-alpha (TNF-α) inhibitors, and Janus kinase (JAK) inhibitors on ankylosing spondylitis (AS).The purpose of this study is to compare the effectiveness and safety of different interventions for treating AS to provide insights into the decision-making in clinicalpractice. Condition being studied: Ankylosing spondylitis. Based on the Bayesian hierarchical model, we conducted a network meta-analysis using the gemtc package in R software (version 4.1.3) and Stata software (version 15.1). Cong Tian and Jianlong Shu contributed to the conception and design of the study and supervised the tweet classification. All authors drafted the manuscript. Wenhui Shao, Zhengxin Zhou, Huayang Guo and Jingang Wang contributed to data management and tweet classification. Cong Tian, Jianlong Shu and Zhengxin Zhou performed the statistical analysis. Cong Tian, Jianlong Shu, Wenhui Shao and Zhengxin Zhou reviewed the manuscript.
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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.

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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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