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Dissertations / Theses on the topic 'Tumor Necrosis Factor/metabolism'

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1

Miller, Katherine. "Genetic susceptibility in Alzheimer's Disease and the role of lipid metabolism." Connect to text online, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=case1164830757.

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Thesis (Ph. D.)--Case Western Reserve University, 2006.<br>[School of Medicine] Department of Epidemiology and Biostatistics. Includes bibliographical references. Available online via OhioLINK's ETD Center.
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2

Kerzic, Patrick James. "Inhibition of NF-[kappa]B by the benzene metabolite hydroquinone /." Connect to full text via ProQuest. Limited to UCD Anschutz Medical Campus, 2006.

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Thesis (Ph.D. in Toxicology) -- University of Colorado at Denver and Health Sciences Center, 2006.<br>Typescript. Includes bibliographical references (leaves 121-141). Free to UCDHSC affiliates. Online version available via ProQuest Digital Dissertations;
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3

Puliti, Elisa. "Role of sphingosine 1-phosphate metabolism and signalling in skeletal muscle atrophy and fibrosis." Doctoral thesis, Università di Siena, 2022. http://hdl.handle.net/11365/1195603.

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In the last 30 years, multiple roles of S1P have been demonstrated in the regulation of skeletal muscle biology. The presented study is focused on the role of S1P metabolism in myogenic differentiation, where SPL was found playing a crucial role in regulating S1P cellular levels and responsible for onset of myogenic program. The role of S1P axis was also confirmed in skeletal muscle atrophy induced by TNF-alpha. S1P signalling pathwayplays a crucial role in the development and maintenance of the fibrotic process. New S1P3 antagonists were tested to antagonise the receptor involved in fibrosis,
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4

Molgat, André. "The Effect of Macrophage-secreted Factors on Preadipocyte Survival." Thèse, Université d'Ottawa / University of Ottawa, 2013. http://hdl.handle.net/10393/23628.

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Adipose tissue (AT) expansion and remodeling that maintains healthy function relies on stromal preadipocytes capable of differentiating into new adipocytes (adipogenesis). During chronic positive energy balance, a relative deficit in adipogenesis, from either a decrease in preadipocyte number or their capacity to differentiate, leads to excessive adipocyte hypertrophy and AT dysfunction. AT contains macrophages whose number and activation state is dynamically regulated with changes in AT mass. This study aims to investigate the effect of macrophage-secreted factors on preadipocyte survival. To
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5

Ferreira, João Marcos Bemfica Barbosa. "Avaliação do metabolismo e atividade inflamatória nas diversas formas evolutivas da doença de Chagas: correlação com disfunção autonômica." Universidade de São Paulo, 2013. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-07022014-144651/.

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INTRODUÇÃO: A cardiopatia chagásica crônica (CCC) apresenta características específicas, tais como: disfunção autonômica e atividade inflamatória exacerbada. Esta fisiopatologia sugere que alguns parâmetros metabólicos podem estar alterados em pacientes chagásicos. O objetivo deste estudo foi avaliar os parâmetros metabólicos e inflamatórios nas diversas formas evolutivas de doença de Chagas e sua correlação com medidas de avaliação do Sistema Nervoso Autônomo (SNA). MÉTODOS: Foram avaliados 60 indivíduos divididos em 4 grupos (n=15): Grupo controle (GC), Grupo FI - forma indeterminada, Grupo
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6

Boussouar, Fayçal. "Production et transport de lactate au cours de la spermatogenèse : rôle des facteurs de croissance et des hormones sur la lactate déshydrogénase A et les transporteurs de monocarboxylates I et II." Lyon 1, 1999. http://www.theses.fr/1999LYO1T198.

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7

Andersson, Jonas. "Inflammation and lifestyle in cardiovascular medicine." Doctoral thesis, Umeå universitet, Medicin, 2010. http://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-36221.

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Despite major advances in the treatment and prevention of atherosclerosis the last several decades, cardiovascular disease still accounts for the majority of deaths in Sweden. With the population getting older, more obese and with rising numbers of diabetics, the cardiovascular disease burden may increase further in the future. The focus in cardiovascular disease has shifted with time from calcification and narrowing of arteries to the biological processes within the atherosclerotic plaque. C-reactive protein (CRP) has emerged as one of many proteins that reflect a low grade systemic inflammat
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8

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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9

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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10

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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11

Oukacha, Khadija. "Perturbation chimique du transport de Tumor Necrosis Factor." Electronic Thesis or Diss., Université Paris sciences et lettres, 2023. http://www.theses.fr/2023UPSLS067.

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Alors qu'il est essentiel pour lutter contre les agents pathogènes, TNF (Tumor Necrosis factor) secrété́ en excès devient nocif pour l'organisme comme dans le cas de maladies inflammatoires chroniques (polyarthrite rhumatoïde ou maladie de Crohn). Les thérapies actuelles sont basées sur des injections récurrentes d'anti-TNF contre lesquelles 30% des patients développent une résistance. Il existe donc un fort besoin de composés chimiques réduisant la sécrétion de TNF. Nous avons exploité la diversité́ des voies de sécrétion dépendantes de l’appareil de Golgi pour identifier des molécules inhiba
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12

Dabarian, André Luiz. "Mediadores inflamatórios e metabólicos em pacientes com miocardiopatia dilatada idiopática e chagásica: correlação com disfunção autonômica." Universidade de São Paulo, 2017. http://www.teses.usp.br/teses/disponiveis/5/5131/tde-28032018-090855/.

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Alterações metabólicas, inflamatórias e do sistema nervoso autônomo estão presentes em pacientes com insuficiência cardíaca. No entanto, não há até o momento, consenso de que tais alterações são decorrentes da disfunção ventricular ou da síndrome de insuficiência cardíaca. Objetivo: Avaliacão do metabolismo e atividade inflamatória em pacientes com miocardiopatia dilatada chagásica e idiopática e sua correlação com medidas de funcão do sistema nervoso autônomo. Casuística: Foram avaliados 46 pacientes divididos em três grupos: pacientes com miocardiopatia dilatada idiopática, chagásica e contr
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13

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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14

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 c
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15

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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16

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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17

Mustapha, Shareef. "Signaling pathways of tumor necrosis factor à in ventricular myocytes." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk2/ftp01/MQ41751.pdf.

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18

Hel, Zdenĕk. "Posttranscriptional regulation of tumor necrosis factor-a production in macrophages." Thesis, McGill University, 1997. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=34642.

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The production of tumor necrosis factor-alpha (TNF-alpha), a key cytokine regulator of an early immune response and a central mediator of the deleterious effects of systemic inflammatory response syndrome, is regulated at both the transcriptional and posttranscriptional level. The 3' -untranslated region (3'-UTR) of TNF-alpha mRNA contains sequences that confer its translational repression in quiescent cells and are responsible for the induction of TNF-alpha production following macrophage contact with bacterial lipopolysaccharide, live bacteria, or viruses.<br>We demonstrate that two distinct
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19

Koelen, Jorien Anne. "Arming ColoAd1 with tumor necrosis factor α and lymphotoxin α". Thesis, University of Oxford, 2015. https://ora.ox.ac.uk/objects/uuid:bfc9d84f-2677-45db-8705-791219446348.

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Colon and rectum cancers (CRCs) are the third most prevalent cause of cancer-related mortality. Advanced metastatic CRC has a very poor prognosis; indicating the need for improved therapy. Tumour necrosis factor (TNF) can induce an immune response against tumours and cause cell death of the tumour-associated vasculature. However, dose-limiting toxicity occurs with systemic TNF treatment. In order to assess the effects of expressing TNF and lymphotoxin a (LTA) locally in the tumour microenvironment, a syngeneic CT26 CRC model expressing soluble (sm), full length (fm) or membranebound (mbm) muri
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20

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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21

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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22

Babu, Kesavan Suresh. "The role of tumor necrosis factor alpha (TNF-α) in asthma." Thesis, University of Southampton, 2006. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.439378.

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23

Debets, Jacobus Maria Hubert. "Studies on tumor necrosis factor endogenous mediators of sepsis and cachexia /." Maastricht : Maastricht : Datawyse ; University Library, Maastricht University [Host], 1989. http://arno.unimaas.nl/show.cgi?fid=5468.

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24

Di, Marco Sergio. "Posttranscrip[t]ional regulation of tumor necrosis factor production in macrophages." Thesis, McGill University, 2001. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=37648.

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Tumor necrosis factor alpha (TNFalpha) is a key proinflammatory cytokine which is produced primarily by macrophages. Although this cytokine is very beneficial to the host when released in small amounts or in localized fashion, abnormally high levels of TNFalpha can however be very detrimental. The biological effects of this cyokine is thus dependent on its timing, location and extent of release. In recent years major interest has been placed on the AU rich elements (ARE) present in the 3' untranslated region of the TNFalpha mRNA as it plays a pivitol role in the posttranscriptional control of
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25

Cantwell, Mark J. "The Tumor necrosis factor family : roles in disease pathology and therapy /." Diss., Connect to a 24 p. preview or request complete full text in PDF format. Access restricted to UC campuses, 1998. http://wwwlib.umi.com/cr/ucsd/fullcit?p9824693.

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26

Yang, Junbao. "Genetic engineering of a fusion protein possessing anti-tumor Fv and tumor necrosis factor alpha." Thesis, National Library of Canada = Bibliothèque nationale du Canada, 1999. http://www.collectionscanada.ca/obj/s4/f2/dsk1/tape8/PQDD_0030/NQ63940.pdf.

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27

SERINO, MATTEO. "Aploinsufficienza di TACE e omeostasi del glucosio: effetti protettivi su insulino-resistenza e obesità durante un regime di dieta grassa." Doctoral thesis, Università degli Studi di Roma "Tor Vergata", 2008. http://hdl.handle.net/2108/434.

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E’ noto che il TNF (Tumor Necrosis Factor)-α altera la sensibilità insulinica e i metabolismi glucidico e lipidico attraverso meccanismi diversi e ridondanti, sia a livello traduzionale che post-traduzionale. Il TNF-α esercita i suoi effetti paracrini in seguito al taglio proteolitico della forma ancorata alla membrana plasmatica e al rilascio della forma solubile ad opera dell’enzima TACE (TNF-α Converting Enzyme), che regola la funzione di altre proteine di membrana come il recettore dell’interleuchina-6 e i ligandi del recettore EGFR (Epidermal Growth Factor Receptor). Per comprendere il
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28

Yadav, Ajay Kumar. "Relationship between human hemoglobin and tumor necrosis factor a : immunochemistry and bioactivity studies." Thesis, JAMIA HAMDARD (IIAMDARD UNIVERSITY), 2002. http://hdl.handle.net/123456789/1468.

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29

Youseff, Brian. "The Role of Tumor Necrosis Factor Receptor-Associated Factor 6 in Tick-Borne Flavivirus Infection." University of Toledo Health Science Campus / OhioLINK, 2019. http://rave.ohiolink.edu/etdc/view?acc_num=mco155691388498993.

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30

Zwaveling, Jan Harm. "Systemic side effects of isolated limb perfusion with tumor necrosis factor alpha." [S.l. : [Groningen] : s.n.] ; [University Library Groningen] [Host], 1997. http://irs.ub.rug.nl/ppn/15723665X.

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31

Hakim, Akhlaq Waheed. "Tumor necrosis factor alpha and non-inflammatory sensitization of masseter muscle nociceptors." Thesis, University of British Columbia, 2011. http://hdl.handle.net/2429/34182.

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Behavioral evidence in rats indicates that injection of tumor necrosis factor alpha (TNFalpha into skeletal muscle results in a prolonged mechanical sensitization without gross inflammation. The present series of studies were conducted to test the idea that injection of TNFalpha causes mechanical sensitization of skeletal muscle through a peripheral mechanism that involves lowering of the mechanical threshold (MT) of muscle nociceptors without inflammation. In- vivo extracellular electrophysiological recording was used to assess the effect of TNFalpha (1 or 0.1microgram) and other drugs on th
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32

Hurst, Liam Andrew. "The role of tumour necrosis factor alpha in pulmonary arterial hypertension." Thesis, University of Cambridge, 2014. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.648471.

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33

劉耀南 and Yiu-nam Lau. "Interferons and tumour necrosis factor in chronic hepatitis B virus infection." Thesis, The University of Hong Kong (Pokfulam, Hong Kong), 1990. http://hub.hku.hk/bib/B31981446.

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34

Lau, Yiu-nam. "Interferons and tumour necrosis factor in chronic hepatitis B virus infection." Hong Kong : University of Hong Kong, 1990. http://sunzi.lib.hku.hk/hkuto/record.jsp?B2158879X.

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35

Mallet, Dominique. "Interet du tumor necrosis factor alpha dans le suivi precoce des transplantations renales." Aix-Marseille 2, 1994. http://www.theses.fr/1994AIX20913.

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36

Atzeni, Fabiola. "Antibody profiles in patients treated with tumor necrosis factor-alpha antagonists: new findings." Doctoral thesis, Universitat Autònoma de Barcelona, 2005. http://hdl.handle.net/10803/3771.

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It has been reported that patients with rheumatoid arthritis (RA), Crohn's disease (CD) and spondyloarthritis (SpA) treated with selective tumor necrosis factor-alpha (TNF-?) inhibitors develop autoantibodies such as antinuclear antibodies (ANA) and anti-double stranded DNA (anti-dsDNA) antibodies. TNF-? is a pro-inflammatory cytokine that is produced by multiple cell types, including blood monocytes, macrophages, mast cells and endothelial cells, and plays multiple complex functional roles within the immune system, including the stimulation of inflammation, cytotoxicity, the regulation cell a
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37

Rogers, Gabrielle Marie. "Tumor necrosis factor- alpha production induced by peptidoglycan-polysaccharide in early pregnant ewes." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4712.

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Thesis (M.S.)--West Virginia University, 2006.<br>Title from document title page. Document formatted into pages; contains vi, 45 p. : ill. (some col.). Includes abstract. Includes bibliographical references (p. 40-45).
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38

Chang, Wei-Chuan. "The role of caspases in lytic mechanisms of tumor necrosis factor-mediated cytolysis." Thesis, University of Hawaii at Manoa, 2002. http://hdl.handle.net/10125/3008.

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TNF activates several signaling pathways, some lead to cell death by apoptosis or necrosis. For our cell lines (B/C-N, 10ME, and L88.3), which represent a tumor progression model, it has not been determined whether TNF induces apoptosis or necrosis. B/C-N is not tumorigenic and represents normal cells; it is TNF-resistant. 10ME forms tumors only in immunodeficient animals and thus is intermediate on the pathway to cancer; it is TNF-sensitive. L88.3 forms tumors in normal mice and thus is cancerous; it is TNF resistant. TNF resistant cells can be rendered TNF-sensitive by addition of transcript
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39

Fisher, Anat. "Comparative persistence of tumor necrosis factor alpha antagonists in patients with rheumatoid arthritis." Thesis, University of British Columbia, 2012. http://hdl.handle.net/2429/43055.

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Introduction: This thesis comprises three studies examining treatment persistence with tumour necrosis factor alpha (TNFα) antagonists in rheumatoid arthritis (RA) patients. Persistence, also commonly known as duration of treatment, has been suggested as an indirect measure that balances benefit and harm, and it is important for cost-effectiveness analysis and budget planning. Previous research has examined the effect of drug and patient characteristics on persistence with TNFα antagonists. Objectives: 1) To estimate pairwise comparative persistence with TNFα antagonists infliximab, adalimuma
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40

Anto, Michel Nathaly [Verfasser], Andreas [Akademischer Betreuer] Zirlik, and Rudolf [Akademischer Betreuer] Grosschedl. "The role of tumor necrosis associated factor (TRAF)-1 in cardio-metabolic disease." Freiburg : Universität, 2017. http://d-nb.info/1173086897/34.

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41

Barsacchi, Rico. "Role of nitric oxide in the regulation of tumor necrosis factor alpha signalling." Thesis, Open University, 2003. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.252359.

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42

Nguyen, Thanh Minh. "Tumor necrosis factor alpha (TNF-[alpha]) signal transduction pathways in cyclooxygenase-2 expression /." The Ohio State University, 2002. http://rave.ohiolink.edu/etdc/view?acc_num=osu1486459267519688.

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43

Kumari, Vandana. "Mechanisms underlying the regulatory function of tumor necrosis factor-alpha in skin inflammation." Doctoral thesis, Humboldt-Universität zu Berlin, Lebenswissenschaftliche Fakultät, 2015. http://dx.doi.org/10.18452/17389.

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Die Haut ist das größte Organ des Menschen und bildet die Barriere gegenüber Einwirkungen aus der Umwelt. Die Störung der Hautbarriere durch exogene und endogene Reize führt zu einer Entzündungsreaktion in der Haut. In der Folge können Hauterkrankungen wie die irritative oder Atopische Dermatitis entstehen. Der Tumor Nekrose Faktor-α (TNF-α) ist ein pleiotrop wirksames Zytokin, das eine zentrale Rolle bei entzündlichen Prozessen spielt. Ziel der vorgelegten Promotionsarbeit war zu untersuchen, ob und wie TNF-α zu Entzündungsgeschehen, ausgelöst durch exogene und endogene Faktoren, beiträgt.
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44

Sutherland, Andrew Peter Robert St Vincents Clinical School UNSW. "BAFF regulation of peripheral T cell responses." Awarded by:University of New South Wales. St Vincents Clinical School, 2005. http://handle.unsw.edu.au/1959.4/22788.

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The activation and effector function of CD4+ T cells are critical points of regulation during an antigen specific T cell response. Dysregulation of these processes can lead to the development of human diseases, encompassing both immunodeficiency and autoimmunity. Members of the TNF superfamily have recently emerged as important regulators of T cell responses, with their overexpression causing autoimmune inflammation in animal models. As overproduction of the novel TNF superfamily ligand BAFF is associated with several autoimmune conditions, we sought to examine the potential role of BAFF as a
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45

Ano, Monfils Nadhia. "Etude de la production et des caracteristiques biologiques du tnf alpha humain produit a partir d'une lignee cellulaire humaine." Lillle 2, 1993. http://www.theses.fr/1993LIL2P256.

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46

Li, Rui Xin. "Scutellarin inhibits TNF-induced proliferative expansion of Tregs by blocking TNF-TNFR2 interactions." Thesis, University of Macau, 2018. http://umaclib3.umac.mo/record=b3952140.

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47

Laureau, Serge. "Le tumor necrosis factor (tnf) en dermatologie : etude de la production de tnf par les monocytes circulants au cours du psoriasis : revue de la litterature." Aix-Marseille 2, 1990. http://www.theses.fr/1990AIX20817.

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48

Pistilli, Emidio E. "The extrinsic apoptotic pathway in aged skeletal muscle roles of tumor necrosis factor-[alpha] and interleukin-15 /." Morgantown, W. Va. : [West Virginia University Libraries], 2006. https://eidr.wvu.edu/etd/documentdata.eTD?documentid=4912.

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Thesis (Ph. D.)--West Virginia University, 2006.<br>Title from document title page. Document formatted into pages; contains x, 189 p. : ill. (some col.). Includes abstract. Includes bibliographical references.
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49

Lampa, Jon. "Studies of pharmacological interventions and pathogenesis of rheumatoid arthritis /." Stockholm, 2002. http://diss.kib.ki.se/2002/91-7349-372-4/.

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50

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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