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Littérature scientifique sur le sujet « Tumor necrosis factor Physiological effect »

Auteur : Grafiati

Publié le 4 juin 2021

Mis à jour le 28 janvier 2023

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Articles de revues sur le sujet "Tumor necrosis factor Physiological effect"

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Todorov, Vladimir, Markus Müller, Frank Schweda та Armin Kurtz. "Tumor necrosis factor-α inhibits renin gene expression". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, № 5 (1 листопада 2002): R1046—R1051. http://dx.doi.org/10.1152/ajpregu.00142.2002.

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Renin, produced in renal juxtaglomerular (JG) cells, is a fundamental regulator of blood pressure. Accumulating evidence suggests that cytokines may directly influence renin production in the JG cells. TNF-α, which is one of the key mediators in immunity and inflammation, is known to participate in the control of vascular proliferation and contraction and hence in the pathogenesis of cardiovascular diseases. Thus TNF-α may exert its effects on the cardiovascular system through modulation of renal renin synthesis. Therefore we have tested the effect of TNF-α on renin transcription in As4.1 cell

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Greenberg, S., J. Xie, Y. Wang, B. Cai, J. Kolls, S. Nelson, A. Hyman, W. R. Summer, and H. Lippton. "Tumor necrosis factor-alpha inhibits endothelium-dependent relaxation." Journal of Applied Physiology 74, no. 5 (May 1, 1993): 2394–403. http://dx.doi.org/10.1152/jappl.1993.74.5.2394.

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Tumor necrosis factor-alpha (TNF-alpha) stimulates nitric oxide (NO) in vascular endothelium by induction of the enzyme NO synthase II (NOS II). We examined the effects of TNF-alpha on 1) endothelium-dependent (EDR) and endothelium-independent (EIR) relaxation and 2) contraction of bovine intralobar pulmonary arteries (BPA) and veins (BPV) in vitro. Acetylcholine (ACh), bradykinin (BK), histamine, and A23187 produced EDR of BPA contracted with a 50% effective concentration of U-46619 (15 nM), because relaxation was abolished by endothelium-rubbing and attenuated by L-NG-mono-methylarginine (L-

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Moller, A. D., and P. O. Grande. "Low-dose prostacyclin has potent capillary permeability-reducing effect in cat skeletal muscle in vivo." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 1 (July 1, 1997): H200—H207. http://dx.doi.org/10.1152/ajpheart.1997.273.1.h200.

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The dose-response effects of intravenous infusion of prostacyclin on capillary permeability (the capillary filtration coefficient technique), hydrostatic capillary pressure, transcapillary filtration, and vascular tone were analyzed in vivo on cat skeletal muscle from a normal and an increased permeability level. Increased permeability was accomplished by intra-arterial infusion of tumor necrosis factor-alpha or histamine. Permeability effects of bradykinin were also analyzed. Prostacyclin decreased capillary permeability by 8% at a dose of 0.1 ng.kg-1.min-1 and at most by 30% below control at

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Alexander, H. R., G. G. Wong, G. M. Doherty, D. J. Venzon, D. L. Fraker, and J. A. Norton. "Differentiation factor/leukemia inhibitory factor protection against lethal endotoxemia in mice: synergistic effect with interleukin 1 and tumor necrosis factor." Journal of Experimental Medicine 175, no. 4 (April 1, 1992): 1139–42. http://dx.doi.org/10.1084/jem.175.4.1139.

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Differentiation factor (D factor), also called leukemia inhibitory factor (LIF), is a glycoprotein that has been increasingly recognized to possess a wide range of physiological activities. We examined the possibility that the administration of D factor may confer beneficial effects and enhance host resistance against lethal endotoxemia. A single intravenous dose of recombinant human D factor completely protected C57/Bl6 mice from the lethal effect of Escherichia coli endotoxin (lipopolysaccharide [LPS]). The protective effects were dose dependent and observed when administered 2-24 h before L

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Takahashi, Satoshi, Levente Kapás, Jidong Fang, and James M. Krueger. "Somnogenic relationships between tumor necrosis factor and interleukin-1." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 4 (April 1, 1999): R1132—R1140. http://dx.doi.org/10.1152/ajpregu.1999.276.4.r1132.

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Both tumor necrosis factor (TNF) and interleukin (IL)-1 are somnogenic cytokines. They also induce each other’s production and both induce nuclear factor kappa B activation, which in turn enhances IL-1 and TNF transcription. We hypothesized that TNF and IL-1 could influence each other’s somnogenic actions. To test this hypothesis, we determined the effects of blocking both endogenous TNF and IL-1 on spontaneous sleep and on sleep rebound after sleep deprivation in rabbits. Furthermore, the effects of inhibition of TNF on IL-1-induced sleep and the effects of blocking IL-1 on TNF-induced sleep

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Tseng, Wei-Cheng, Hou-Chuan Lai, Yi-Hsuan Huang, Shun-Ming Chan, and Zhi-Fu Wu. "Tumor Necrosis Factor Alpha: Implications of Anesthesia on Cancers." Cancers 15, no. 3 (January 25, 2023): 739. http://dx.doi.org/10.3390/cancers15030739.

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Cancer remains a major public health issue and a leading cause of death worldwide. Despite advancements in chemotherapy, radiation therapy, and immunotherapy, surgery is the mainstay of cancer treatment for solid tumors. However, tumor cells are known to disseminate into the vascular and lymphatic systems during surgical manipulation. Additionally, surgery-induced stress responses can produce an immunosuppressive environment that is favorable for cancer relapse. Up to 90% of cancer-related deaths are the result of metastatic disease after surgical resection. Emerging evidence shows that the in

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Ramseyer, Vanesa D., та Jeffrey L. Garvin. "Tumor necrosis factor-α: regulation of renal function and blood pressure". American Journal of Physiology-Renal Physiology 304, № 10 (15 травня 2013): F1231—F1242. http://dx.doi.org/10.1152/ajprenal.00557.2012.

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Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that becomes elevated in chronic inflammatory states such as hypertension and diabetes and has been found to mediate both increases and decreases in blood pressure. High levels of TNF-α decrease blood pressure, whereas moderate increases in TNF-α have been associated with increased NaCl retention and hypertension. The explanation for these disparate effects is not clear but could simply be due to different concentrations of TNF-α within the kidney, the physiological status of the subject, or the type of stimulus initiating the inflammat

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Salama, Salama A., Marwa W. Kamel, Concepcion R. Diaz-Arrastia, Xia Xu, Timothy D. Veenstra, Sana Salih, Shaleen K. Botting та Raj Kumar. "Effect of Tumor Necrosis Factor-α on Estrogen Metabolism and Endometrial Cells: Potential Physiological and Pathological Relevance". Journal of Clinical Endocrinology & Metabolism 94, № 1 (1 січня 2009): 285–93. http://dx.doi.org/10.1210/jc.2008-1389.

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Wang, Chen, Yuchen Wang, Na Liu, Chuan Cai та Lulu Xu. "Effect of tumor necrosis factor α on ability of SHED to promote osteoclastogenesis during physiological root resorption". Biomedicine & Pharmacotherapy 114 (червень 2019): 108803. http://dx.doi.org/10.1016/j.biopha.2019.108803.

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Matsumoto, Yutaka, Yohko Kawai, Kiyoaki Watanabe, Kazuo Sakai, Mitsuru Murata, Makoto Handa, Shin Nakamura та Yasuo Ikeda. "Fluid Shear Stress Attenuates Tumor Necrosis Factor-α–Induced Tissue Factor Expression in Cultured Human Endothelial Cells". Blood 91, № 11 (1 червня 1998): 4164–72. http://dx.doi.org/10.1182/blood.v91.11.4164.

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Abstract Hemodynamic forces modulate various endothelial cell functions under gene regulation. Previously, we have shown that fibrinolytic activity of endothelial cells is enhanced by the synergistic effects of shear stress and cytokines. In this study, we investigated the effect of shear stress on tumor necrosis factor (TNF)-α–induced tissue factor (TF) expression in cultured human umbilical vein endothelial cells (HUVECs), using a modified cone-plate viscometer. Shear stresses at physiological levels reduced TNF-α (100 U/mL)–induced TF expression at both mRNA and antigen levels, in a shear-i

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Thèses sur le sujet "Tumor necrosis factor Physiological effect"

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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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Caughey, Gillian Elizabeth. "Regulation of interleukin-1[Beta] and tumor necrosis factor[alpha] synthesis by fatty acids and eicosanoids /." Title page, table of contents and summary only, 1998. http://web4.library.adelaide.edu.au/theses/09PH/09phc371.pdf.

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Penglis, Peter Savas. "The relationships between eicosanoid production and pro-inflammatory cytokines." Title page, contents and summary only, 2001. http://web4.library.adelaide.edu.au/theses/09PH/09php3985.pdf.

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Includes bibliographical references (leaves 182-240). Explores alternate strategies that may alter inflammatory cytokine production, particularly tumour necrosis factor đ [tumor necrosis factor-alpha], and therefore provide a possible treatment for rheumatoid arthritis.

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Berry, Mark P. McMurray Robert G. "The effect of exercise in the heat on circulating tumor necrosis factor-[alpha] concentration." Chapel Hill, N.C. : University of North Carolina at Chapel Hill, 2008. http://dc.lib.unc.edu/u?/etd,1878.

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Thesis (M.A.)--University of North Carolina at Chapel Hill, 2008.<br>Title from electronic title page (viewed Dec. 11, 2008). "... in partial fulfillment of the requirements for the degree of Master of Arts in the Department of Exercise and Sport Science Exercise Physiology." Discipline: Exercise and Sports Science; Department/School: Exercise and Sport Science. On t.p. and in abstract, [alpha] is Greek letter.

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Lo, Susan Z. Y. "NF-kB- and mitochondria-linked signaling events that contribute to TNFa action in deferring physiological and chemotherapeutic drug-induced apoptosis in macrophages." University of Western Australia. School of Medicine and Pharmacology, 2008. http://theses.library.uwa.edu.au/adt-WU2008.0095.

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TNF defers apoptosis in macrophages undergoing spontaneous or pharmacologically (thapsigargin, ceramide, CCCP, etoposide or cisplatin)-induced apoptosis, as determined by measurements of caspase-3 activity and annexin-V staining (Chapter 2). The action requires TNF interaction with TNF-R1, not TNF-R2. Survival is uniquely reliant on the activity of the NF-B signaling pathway, and does not require activities arising from the PI3K/Akt, JNK, ERK, p38 MAP kinase or iNOS pathways (Chapter 3). Further, the general anti-apoptotic property of TNF and its specific antagonism of CCCP-induced apoptosis l

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Salimi-Ghezelbash, Afsar. "In vitro effect of recombinant interferon gamma and tumor necrosis factor alpha on killing of entamoeba histolytica trophozoites by murine macrophages." Thesis, McGill University, 1992. http://digitool.Library.McGill.CA:80/R/?func=dbin-jump-full&object_id=61236.

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The present study examines the role of liver macrophages (Kupffer cells), of C57BL/6 mice, as effector cells responsible for the killing of Entamoeba histolytica trophozoites in vitro. Interferon gamma (IFN-$ gamma$) and tumor necrosis factor alpha (TNF) were each shown to endow murine Kupffer cells with significant amoebicidal activity. Interferon gamma alone was not able to activate Kupffer cells to amoebicidal state. However, IFN-$ gamma$ and lipopolysaccharide (LPS) acted synergistically in this phenomenon. It seems that the acquisition of amoebicidal activity is associated with the involv

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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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Farrow, Michael John. "The effect of androstenediol on gene expression and NF-kappaB activation in vitro." Columbus, Ohio : Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc%5Fnum=osu1187109346.

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Albuquerque, Assis Filipe Medeiros. "Effect of preemptive analgesia on tissue levels of interleukin-1 beta and tumor necrosis factor alpha in third molar surgery: a triple-blinded randomized placebo-controlled study." Universidade Federal do CearÃ, 2016. http://www.teses.ufc.br/tde_busca/arquivo.php?codArquivo=16231.

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Conselho Nacional de Desenvolvimento CientÃfico e TecnolÃgico<br>A cirurgia para remoÃÃo de terceiros molares constitui-se um procedimento frequentemente realizado em odontologia, estando associado a variados graus de dor pÃs-operatÃria, podendo afetar a qualidade de vida dos pacientes. Considerando o benefÃcio mÃximo ao paciente submetido a uma cirurgia, insere-se a analgesia preemptiva como estratÃgia farmacolÃgica amplamente pesquisada nas Ãltimas dÃcadas. O objetivo do presente estudo foi avaliar o efeito da analgesia preemptiva sob os efeitos inflamatÃrios e sob os nÃveis de citocinas prÃ

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Farrow, Michael John. "The effect of androstenediol on gene expression and NF-κB activation in vitro". The Ohio State University, 2007. http://rave.ohiolink.edu/etdc/view?acc_num=osu1187109346.

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Livres sur le sujet "Tumor necrosis factor Physiological effect"

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

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service), SpringerLink (Online, ed. Death receptors and cognate ligands in cancer. Heidelberg: Springer, 2009.

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Marialuisa, Melli, and Parente Luca, eds. Cytokines and lipocortins in inflammation and differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of IL-1, TNF, and Lipocortins in Inflammation and Differentiation, held in Siena, Italy, October 22-25, 1989. New York, NY: Wiley-Liss, 1990.

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Kalthoff, Holger. Death Receptors and Cognate Ligands in Cancer. Springer, 2012.

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(Editor), Marialuisa Melli, and Luca Parente (Editor), eds. Cytokines and Lipocortins in Inflammation and Differentiation: Proceedings of the International Conference on Molecular and Cellular Biology of Il-1, (Progress in Clinical & Biological Research). Wiley-Liss, 1990.

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Chapitres de livres sur le sujet "Tumor necrosis factor Physiological effect"

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Jacob, Chaim O., and Hugh O. McDevitt. "The Effect of Tumor Necrosis Factor (TNF) on (NZB × NZW)F1 Lupus Nephritis." In Immunobiology of HLA, 539–41. Berlin, Heidelberg: Springer Berlin Heidelberg, 1989. http://dx.doi.org/10.1007/978-3-662-39946-0_234.

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Kongshavn, Patricia A. L., and Esfandiar Ghadirian. "Effect of Tumor Necrosis Factor on Growth of Trypanosoma Musculi in Vivo and in Vitro." In Host Defenses and Immunomodulation to Intracellular Pathogens, 257–62. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4757-5421-6_26.

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Uchida, Y., K. Irie, F. Tsukahara, K. Ohba, T. Nomoto, and T. Muraki. "Effect of Tumor Necrosis Factor on the Lipoprotein Lipase Gene Expression in Brown Adipocytes Differentiated in Culture." In Thermal Balance in Health and Disease, 121–27. Basel: Birkhäuser Basel, 1994. http://dx.doi.org/10.1007/978-3-0348-7429-8_16.

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Perez-Verdia, Alex, Sonny J. Stetson, Susan McRee, Wojciech Mazur, Michael M. Koerner, and Guillermo Torre-Amione. "The Effect of Cytokines on Cardiac Allograft Function: Tumor Necrosis Factor-α: A Mediator of Chronic Injury." In Developments in Cardiovascular Medicine, 77–81. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1449-7_9.

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Longhi, L., F. Ortolano, E. R. Zanier, C. Perego, N. Stocchetti, and M. G. De Simoni. "Effect of traumatic brain injury on cognitive function in mice lacking p55 and p75 tumor necrosis factor receptors." In Acta Neurochirurgica Supplements, 409–13. Vienna: Springer Vienna, 2008. http://dx.doi.org/10.1007/978-3-211-85578-2_80.

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Rainard, Pascal, and Bernard Poutrel. "Effect of C5a and Tumor Necrosis Factor-α on Phagocytosis of Streptococcus agalactiae NT/X and IV/X by Bovine Neutrophils." In Streptococci and the Host, 953–55. Boston, MA: Springer US, 1997. http://dx.doi.org/10.1007/978-1-4899-1825-3_224.

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Quentmeier, H., D. Fleckenstein, W. G. Dirks, C. C. Uphoff, M. Zaborski, and H. G. Drexler. "GM-CSF is the Mediator of the Proliferative Effect of Tumor Necrosis Factor Alpha in Acute Myeloid Leukemia-Derived Cell Lines." In Haematology and Blood Transfusion Hämatologie und Bluttransfusion, 267–72. Berlin, Heidelberg: Springer Berlin Heidelberg, 2003. http://dx.doi.org/10.1007/978-3-642-59358-1_42.

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Hadem, Khetbadei Lysinia Hynniewta, Lakhon Kma, Rajeshwar N. Sharan, and Arnab Sen. "Anticancer Effect of Aristolochia tagala and Curcuma caesia Acting Through Tumor Necrosis Factor-a." In Handbook of Research on Advanced Phytochemicals and Plant-Based Drug Discovery, 366–94. IGI Global, 2022. http://dx.doi.org/10.4018/978-1-6684-5129-8.ch019.

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This chapter begins with a brief description of the events associated with carcinogenesis such as what led a normal cell to transform into a pre-neoplastic one, their multiplication, and development into cancer. The authors also described how reactive oxygen species (ROS) are generated endogenously and from carcinogens, their role in carcinogenesis, and the link between inflammation and cancer. Elucidation of how cancer arises contributes to understanding the molecular mechanisms of action of some natural products. Herbal natural products contain metabolites that exert a physiological action on human body. These metabolites are used therapeutically in modern medical practices to prevent and cure various diseases including cancer. This chapter discusses the anticancer property of two herbal plants Aristolochia tagala Cham. and Curcuma caesia Roxb. in diethylnitrosamine-induced mouse liver cancer and describes the most probable molecular mechanisms of action of the metabolites present in these plants contributing to their anticancer effect.

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SHAW, M. W., C. F. McKIEL, M. RUBENSTEIN, and P. D. GUINAN. "EFFECT OF TUMOR NECROSIS FACTOR ON A PROSTATE TUMOR MODEL." In Protides of the Biological Fluids, 351–54. Elsevier, 1987. http://dx.doi.org/10.1016/b978-0-08-035588-7.50080-7.

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Tamulevicius, P., F. Steinberg, and C. Streffer. "Effect of Tumor Necrosis Factor on Tumor Energy Metabolism and Vascularization in Two Different Xenotransplanted Tumor Cell Lines." In Immunodeficient Mice in Oncology, 272–76. S. Karger AG, 1992. http://dx.doi.org/10.1159/000421288.

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Actes de conférences sur le sujet "Tumor necrosis factor Physiological effect"

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abla, hedia ben, Sonia Rekik, Soumaya Boussaid, Samia Jammali, Hela Sahli, Elhem Cheour, and Mohamed Elleuch. "AB0699 EFFECT OF SWITCHING BETWEEN TUMOR NECROSIS FACTOR INHIBITOR IN SPONDYLOARTHRITIS." In 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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Loskutoff, D. J., J. Mimuro, and C. Hekman. "PLASMINOGEN ACTIVATOR INHIBITOR." In XIth International Congress on Thrombosis and Haemostasis. Schattauer GmbH, 1987. http://dx.doi.org/10.1055/s-0038-1644763.

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Plasminogen activation provides an important source of localized proteolytic activity not only during fibrinolysis, but also during ovulation, cell migration, epithelial cell differentiation, tumor invasion and a variety of other physiological processes. Precise regulation of plasminogen activator (PA) activity thus constitutes a critical feature of many biological processes. This control is achieved in large part through the action of specific PA inhibitors (PAIs). Although 4 distinct PAIs have been detected,1the endothelial cellTderived inhibitor (PAI-1) is the only one that efficiently inhi

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Gioia, Chiara, Francesca Spinelli, Roberta Priori, Cristina Iannuccelli, Bruno Lucchino, Annarita Vestri, Guido Valesini, and Manuela DI Franco. "AB0379 GENDER DIFFERENCES IN RHEUMATOID ARTHRITIS: EFFECT OF ANTI-TUMOR NECROSIS FACTOR THERAPY." In 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.6056.

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Qiu, Ping, Xizhong Cui, Junfeng Sun, Judith A. Welsh, Charles Natanson, and Peter Q. Eichacker. "Selective Tumor Necrosis Factor Inhibitors' Effect On Survival In Septic Shock: A Meta-Analysis." 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.a6002.

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Yu, H., R. Tamfu, S. Mohan та M. Natarajan. "Low LET Radiation-Induced Abscopal Effect and Tumor Recurrence: Nuclear Factor Kappa B (NF-κB) and Tumor Necrosis Factor alpha (TNF-α) Mediated Positive Feedback Mechanism." У Abstracts: Thirty-Second Annual CTRC‐AACR San Antonio Breast Cancer Symposium‐‐ Dec 10‐13, 2009; San Antonio, TX. American Association for Cancer Research, 2009. http://dx.doi.org/10.1158/0008-5472.sabcs-09-2149.

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Gorikov, Igor, and Irina Andrievskaya. "RELATIONSHIP OF IMMUNO-HISTOMETRIC INDICATORS OF THE PLACEENTA IN EXACERBATION OF CYTOMEGALOVIRAL INFECTION IN THE SECOND TRIMESTER OF PREGNANCY." In XIV International Scientific Conference "System Analysis in Medicine". Far Eastern Scientific Center of Physiology and Pathology of Respiration, 2020. http://dx.doi.org/10.12737/conferencearticle_5fe01d9c510d54.83584889.

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The relationship between the concentration of tumor necrosis factor-alpha (TNF-α) in the placenta homogenate and its histometric parameters in women during physiological pregnancy and during pregnancy complicated by an exacerbation of cytomegalovirus infection in the second trimester of gestation, leading to the development of chronic compensated placental insufficiency, was studied.

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Jiang, Jing, and John Bischof. "Effect of Dose, Timing and Delivery of Tumor Necrosis Factor Alpha as a Cryoadjuvant in Cryosurgery of ELT-3 Uterine Leiomyoma (Fibroid) Tumor." In ASME 2009 Summer Bioengineering Conference. American Society of Mechanical Engineers, 2009. http://dx.doi.org/10.1115/sbc2009-203929.

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Uterine leiomyoma (fibroid) is the most common indication for hysterectomy in premenopausal women. Cryomyolysis is a uterus sparing procedure in which a myoma is frozen by a cryoprobe, and that causes tissue necrosis upon thawing of the frozen tissue and eventual reduction in myoma size. Cryomyolysis allows both the placement of the minimally invasive cryoprobe and the ensuing iceball growth to be controlled under image guidance (ultrasound - US or magnetic resonance - MR) [1, 2]. Unfortunately, although the iceball is readily visualized, the tissue at the periphery of the iceball is not compl

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Huang, Yupeng, Yuehong Chen, Tao Liu, Sang Lin, Geng Yin, and Qibing Xie. "AB0702 TREATMENT EFFECT OF TUMOR NECROSIS FACTOR A INHIBITORS ON MAGNETIC RESONANCE IMAGING PROGRESSION IN PATIENTS WITH SPONDYLOARTHRITIS: A META-ANALYSIS." In 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.2541.

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Dhamayanti, Maysita, Hening Laswati, Dewi Poerwandari, Widodo, and Hiroaki Kimura. "Effect of Intradialytic Isometric Exercise with or without Neuromuscular Electrical Stimulation on Tumor Necrosis Factor Alpha in Chronic Kidney Disease Patients." In International Meeting on Regenerative Medicine. SCITEPRESS - Science and Technology Publications, 2017. http://dx.doi.org/10.5220/0007320002670270.

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Yarkan Tuğsal, H., G. Can, S. Çapar, B. Zengin, G. Kenar, S. Akar, E. Dalkiliç, et al. "SAT0184 The effect of smoking on response to tumor necrosis factor-alpha inhibitor treatment in ankylosing spondylitis patients: results from the turkbio registry." In Annual European Congress of Rheumatology, EULAR 2018, Amsterdam, 13–16 June 2018. BMJ Publishing Group Ltd and European League Against Rheumatism, 2018. http://dx.doi.org/10.1136/annrheumdis-2018-eular.6586.

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Rapports d'organisations sur le sujet "Tumor necrosis factor Physiological effect"

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Meidan, Rina, and 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, January 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,

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Li, Peng, and 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, August 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 de

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Blanken, Annelies, Bafrin Abdulmajid, Eva van Geel, Joost Daams, Martin van der Esch, and 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, January 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

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