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Bibliografias temáticas / Tumor necrosis factor Physiological effect

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Literatura científica selecionada sobre o tema "Tumor necrosis factor Physiological effect"

Autor: Grafiati

Publicado: 4 de junho de 2021

Última modificação: 28 de janeiro de 2023

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Artigos de revistas sobre o assunto "Tumor necrosis factor Physiological effect"

1

Todorov, Vladimir, Markus Müller, Frank Schweda e Armin Kurtz. "Tumor necrosis factor-α inhibits renin gene expression". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 283, n.º 5 (1 de novembro de 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 cells, which represent transformed mouse JG cells, and in native mouse JG cells in culture. Renin gene expression was also determined in mice lacking the gene for TNF-α (TNF-α knockout mice). TNF-α inhibited renin gene expression via an inhibition of the transcriptional activity, targeting the proximal 4.1 kb of the renin promoter in As4.1 cells. TNF-α also attenuated forskolin-stimulated renin gene expression in primary cultures of mouse JG cells. Mice lacking the TNF-α gene had almost threefold higher basal renal renin mRNA abundance relative to the control strain. The general physiological regulation of renin expression by salt was not disturbed in TNF-α knockout mice. Our data suggest that TNF-α inhibits renin gene transcription at the cellular level and thus may act as a modulator of renin synthesis in (physio)pathological situations.

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Greenberg, S., J. Xie, Y. Wang, B. Cai, J. Kolls, S. Nelson, A. Hyman, W. R. Summer e H. Lippton. "Tumor necrosis factor-alpha inhibits endothelium-dependent relaxation". Journal of Applied Physiology 74, n.º 5 (1 de maio de 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-NMMA; 300 microM). TNF-alpha (0.00417, 0.0417, 0.417, and 1.25 micrograms/ml) incubated with BPA for 60 min inhibited EDR of the BPA to ACh, BK, and histamine. The effects of TNF required 30 min for onset. Recovery of EDR occurred 3–4 h after washout of TNF-alpha. Pentoxifylline (1 microM) did not affect ACh-induced EDR but selectively reversed TNF-alpha-mediated inhibition of ACh-induced EDR. TNF-alpha-mediated inhibition of EDR was not reversible by L-NMMA, an inhibitor of NOS I and NOS II, the cyclooxygenase inhibitor ibuprofen, or CV-3908 (1 microM), a platelet-activating factor antagonist. The inhibitory effect of TNF-alpha on EDR was not mediated by nonspecific sensitization of the endothelium to human protein because recombinant human granulocyte colony-stimulating factor (10, 50, and 500 x 10(3) U/ml) did not affect EDR of BPA. The effect of TNF-alpha was specific for release of NO from the endothelium of BPA because TNF-alpha did not affect 1) EDR of BPV to ACh, BK, or ATP; 2) EIR of BPA or BPV to nitroprusside; and 3) contraction of either BPA or BPV to KCl, U-46619, histamine, norepinephrine, or serotonin. Thus TNF-alpha appears to selectively inhibit receptor-mediated EDR and NO release in BPA. TNF-alpha-mediated inhibition of EDR differs from that of L-arginine-based inhibitors and may represent an endogenous physiological mechanism of regulation of NO in the endothelium.

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3

Moller, A. D., e 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, n.º 1 (1 de julho de 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 attained at 2 ng.kg-1.min-1, also with no effect on vascular tone and hydrostatic capillary pressure. The permeability increase by tumor necrosis factor-alpha and histamine (by 54 and 73%) was more than counteracted by the simultaneous infusion of prostacyclin at 2 ng.kg-1.min-1. The vasodilator effect of tumor necrosis factor-alpha was also restituted. Indomethacin (prostacyclin inhibitor)-induced increase in capillary permeability (25%) was more than restituted by prostacyclin at 2 ng.kg-1.min-1. Surprisingly, bradykinin decreased capillary permeability. We conclude that endogenous prostacyclin may be a physiological regulator of capillary permeability and that low-dose prostacyclin infusion may have clinical relevance in states of increased permeability.

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4

Alexander, H. R., G. G. Wong, G. M. Doherty, D. J. Venzon, D. L. Fraker e 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, n.º 4 (1 de abril de 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 LPS. Previous work has shown that interleukin 1 (IL-1) and tumor necrosis factor (TNF) also protect against a subsequent LPS challenge in a dose-dependent manner. When human D factor was combined with sub-protective doses of IL-1 beta or TNF-alpha, there was dramatic synergistic protection against a subsequent lethal LPS challenge.

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5

Takahashi, Satoshi, Levente Kapás, Jidong Fang e James M. Krueger. "Somnogenic relationships between tumor necrosis factor and interleukin-1". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, n.º 4 (1 de abril de 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 were determined. A TNF receptor fragment (TNFRF), as a TNF inhibitor, and an IL-1 receptor fragment (IL-1RF), as an IL-1 inhibitor, were used. Intracerebroventricular injection of a combination of the TNFRF plus the IL-1RF significantly reduced spontaneous non-rapid eye movement sleep by 87 min over a 22-h recording period. Pretreatment of rabbits with the combination of TNFRF and IL-1RF also significantly attenuated sleep rebound after sleep deprivation. Furthermore, the TNFRF significantly attenuated IL-1-induced sleep but not fever. Finally, the IL-1RF blocked TNF-induced sleep responses but not fever. Results indicate that TNF and IL-1 cooperate to regulate physiological sleep.

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6

Tseng, Wei-Cheng, Hou-Chuan Lai, Yi-Hsuan Huang, Shun-Ming Chan e Zhi-Fu Wu. "Tumor Necrosis Factor Alpha: Implications of Anesthesia on Cancers". Cancers 15, n.º 3 (25 de janeiro de 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 interactions between tumor cells and the tumor microenvironment (TME) not only play decisive roles in tumor initiation, progression, and metastasis but also have profound effects on therapeutic efficacy. Tumor necrosis factor alpha (TNF-α), a pleiotropic cytokine contributing to both physiological and pathological processes, is one of the main mediators of inflammation-associated carcinogenesis in the TME. Because TNF-α signaling may modulate the course of cancer, it can be therapeutically targeted to ameliorate clinical outcomes. As the incidence of cancer continues to grow, approximately 80% of cancer patients require anesthesia during cancer care for diagnostic, therapeutic, or palliative procedures, and over 60% of cancer patients receive anesthesia for primary surgical resection. Numerous studies have demonstrated that perioperative management, including surgical manipulation, anesthetics/analgesics, and other supportive care, may alter the TME and cancer progression by affecting inflammatory or immune responses during cancer surgery, but the literature about the impact of anesthesia on the TNF-α production and cancer progression is limited. Therefore, this review summarizes the current knowledge of the implications of anesthesia on cancers from the insights of TNF-α release and provides future anesthetic strategies for improving oncological survival.

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7

Ramseyer, Vanesa D., e Jeffrey L. Garvin. "Tumor necrosis factor-α: regulation of renal function and blood pressure". American Journal of Physiology-Renal Physiology 304, n.º 10 (15 de maio de 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 inflammatory response. TNF-α alters renal hemodynamics and nephron transport, affecting both activity and expression of transporters. It also mediates organ damage by stimulating immune cell infiltration and cell death. Here we will summarize the available findings and attempt to provide plausible explanations for such discrepancies.

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8

Salama, Salama A., Marwa W. Kamel, Concepcion R. Diaz-Arrastia, Xia Xu, Timothy D. Veenstra, Sana Salih, Shaleen K. Botting e 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, n.º 1 (1 de janeiro de 2009): 285–93. http://dx.doi.org/10.1210/jc.2008-1389.

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9

Wang, Chen, Yuchen Wang, Na Liu, Chuan Cai e Lulu Xu. "Effect of tumor necrosis factor α on ability of SHED to promote osteoclastogenesis during physiological root resorption". Biomedicine & Pharmacotherapy 114 (junho de 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 e Yasuo Ikeda. "Fluid Shear Stress Attenuates Tumor Necrosis Factor-α–Induced Tissue Factor Expression in Cultured Human Endothelial Cells". Blood 91, n.º 11 (1 de junho de 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-intensity and exposure-time dependent manner, whereas shear stress itself did not induce TF expression in HUVECs. TF expressed on the cell surfaces measured by flow cytometry using an anti-TF monoclonal antibody (HTF-K180) was also decreased to one third by shear force applied at 18 dynes/cm2 for 15 hours before and 6 hours after TNF-α stimulation. Furthermore, functional activity of TF, as assessed by the activation of factor X in the presence of FVIIa and Ca2+, was also decreased by shear application. However, the stability of TF mRNA was not decreased in the presence of shear stress. These results suggest that shear force acts as an important regulator of TF expression in endothelium at the transcriptional level.

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Teses / dissertações sobre o assunto "Tumor necrosis factor Physiological effect"

1

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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3

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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4

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.
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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5

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 led to the finding that TNF action prevents cytochrome c release. This protection is likely mediated through effects on components of the MPTP itself, as TNF exhibited functional redundancy with the pore inhibitor cyclosporin A, and did not modify upstream events that promote MPTP opening during apoptosis, namely ROS production, cytosolic Ca2+ increase, or a reduction of total ATP (Chapter 4). Subsequent experiments with the mRNA synthesis inhibitor, actinomycin D, and the translation inhibitor, cycloheximide revealed that the protein(s) responsible for TNF-induced survival was transcribed and translated within 1 hr. However, western analyses provided no convincing evidence of the involvement of Mn-SOD, cIAP-1, XIAP, Bcl-2 or A1 in TNF cytoprotection (Chapter 5). Rather, microarray experiments identified the consistent induction of an early response gene, pim-1, within 30 min of TNF exposure (Chapter 6). This result was verified at the protein level with a specific Pim-1 antibody. Evidence was also found for induction of the anti-apoptotic protein A20, but only at mRNA level. Parthenolide, wortmannin, SP600125, PD98059, SB203580 or L-NAME1 acted against TNF-induced Pim-1 expression in a pattern that exactly matched the effects of these inhibitors on TNF-induced survival. That is, only parthenolide-mediated inactivation of NF-B abolished TNF-induced induction of Pim-1. TNF also stimulated the rapid phosphorylation (inactivation) of the pro-apoptotic BH3-only protein, Bad at Ser112 in a manner sensitive to NF-B inhibition, but not PI3K/Akt, JNK, ERK or p38 MAP kinase inhibition (Chapter 7). As Bad is a known substrate of Pim-1 and Bad 1 Parthenolide, wortmannin, SP600125, PD98059 and SB203580 are inhibitors of the NF-B, PI3K/Akt, JNK, ERK and p38 MAP kinase pathways, respectively. L-NAME inhibits iNOS. NF-B- and mitochondria-linked signaling events that contribute to TNF action in deferring physiological and chemotherapeutic drug-induced apoptosis in macrophages ii phosphorylation occurred coincident with Pim-1 upregulation, it is likely that Pim-1 kinase activity mediates the inactivation of Bad. The overall data therefore supports a model in which TNF ligation of TNF-R1 at the cell surface results in intracellular NF- B activation, leading to the induction of Pim-1 mRNA and protein, and the ensuing phosphorylation of Bad. Inactivation of pro-apoptotic Bad increases the resistance threshold of mitochondria to apoptotic insults, thereby reducing the occurrence of mitochondrial permeability transition, cytochrome c release and subsequent caspase-3 activation.

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6

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 involvement of hydrogen peroxide, because the addition of catalase partially decreases the killing of this parasite by Kupffer cells. In addition, it appears that the amoebicidal activity of IFN-$ gamma$-treated Kupffer cells is contact-dependent.
In our study, Kupffer cells were also shown to be activated by TNF in vitro to an amoebicidal state and this cytolytic effect depends upon the ratio of Kupffer cells to amoebae, the concentrations of TNF used, and the time of exposure of the cells and the parasites to TNF.
Our results indicate that the immunologic production of IFN-$ gamma$ and TNF is important in the activation of Kupffer cells for controlling this parasite and that Kupffer cells are strong effector cells against the amoebae.

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7

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 assess the effect of macrophage-secreted factors on preadipocytes, murine 3T3-L1 preadipocytes or human primary preadipocytes were incubated with macrophage-conditioned medium (MacCM), prepared from either murine (J774A.1, RAW264.7, bone marrow-derived) or human (THP-1, monocyte-derived) macrophage models, respectively. MacCM inhibited preadipocyte apoptosis and activated pro-survival signaling in both preadipocyte models. Inhibition of PDGFR, Akt, or ERK1/2 reduced the pro-survival effect of MacCM in 3T3-L1 preadipocytes. Inhibition of reactive oxygen species (ROS) generation, or enhancement of ROS clearance, reduced MacCM-dependent 3T3-L1 preadipocyte survival. Whereas anti-inflammatory activated macrophages retained the ability to prevent preadipocyte apoptosis, pro-inflammatory activated macrophages did not. TNF-α immunoneutralization restored the survival activity of pro-inflammatory MacCM on 3T3-L1 preadipocytes. These studies reveal a novel pro-survival effect of MacCM on preadipocytes, and identify signaling molecules (PDGF, Akt, ERK1/2, and ROS) that underlie this action. Macrophage activation was found to regulate the pro-survival activity of MacCM. These in vitro cell culture studies are consistent with a model in which the extent of preadipocyte apoptosis in vivo may determine preadipocyte number and the ability of AT to expand while maintaining healthy function during chronic positive energy balance.

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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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9

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
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-inflamatÃrias (TNF-α e IL-1β) em cirurgias de terceiros molares inferiores. Foi realizado um estudo unicÃntrico, triplo-cego, randomizado, placebo-controlado, com 36 pacientes submetidos Ã remoÃÃo cirÃrgica de terceiros molares mandibulares (n=72) que foram randomicamente alocados para receber etoricoxibe 120 mg, ibuprofeno 400mg ou placebo 1 hora prÃ-operatoriamente, e os eventos inflamatÃrios (dor, edema e abertura bucal) foram avaliados. Houve diferenÃa significativa entre os grupos com relaÃÃo aos escores de dor (p<0,001). Etoricoxibe e ibuprofeno reduziram os escores de dor em relaÃÃo ao placebo (p<0,05). A dosagem de TNF-α do grupo placebo nÃo mostrou diferenÃa estatisticamente significante (p=0,127) do tempo 0â para o tempo 30â minutos, enquanto que o ibuprofeno e o etoricoxibe mostraram reduÃÃo significativa entre os tempos. A dosagem de IL-1β dos grupos placebo e etoricoxibe nÃo mostraram variaÃÃo significativa, porÃm, no grupo ibuprofeno houve reduÃÃo significante (p=0,038) dos nÃveis do tempo 0` para o tempo 30`. Como conclusÃo do estudo, os nÃveis de TNF-α e IL-1β, bem como os eventos inflamatÃrios em cirurgias para remoÃÃo de terceiros molares inferiores, mostraram-se inversamente proporcionais Ã seletividade COX-2 do AINE utilizado preemptivamente, e estes apresentaram reduÃÃo significativa dos parÃmetros clÃnicos referentes aos eventos inflamatÃrios em comparaÃÃo ao grupo placebo.

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10

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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Mais fontes

Livros sobre o assunto "Tumor necrosis factor Physiological effect"

1

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

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2

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

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3

Marialuisa, Melli, e 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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4

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

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5

(Editor), Marialuisa Melli, e 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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Capítulos de livros sobre o assunto "Tumor necrosis factor Physiological effect"

1

Jacob, Chaim O., e 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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2

Kongshavn, Patricia A. L., e 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 e 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 e 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 e 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, e 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 e 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 e 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 e 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 e 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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Trabalhos de conferências sobre o assunto "Tumor necrosis factor Physiological effect"

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abla, hedia ben, Sonia Rekik, Soumaya Boussaid, Samia Jammali, Hela Sahli, Elhem Cheour e 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 e 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 inhibits both urokinase (Kd=2.3×10−13M; Kassoc =1.6×108 M−1s−1) and single-chaintissue-type PA (tPA; Kd=1.3×lO−15 M Kd=3.9×lO7M−1s−1). It also inhibits trypsin (Kassoc=6.8×106M−1 s−1 ) ancl Plasmin (Kassoc=7.6×l05 M−1 s5 Analysis of the effect of PAI-1 on the rate of plasminogen activation revealed a competitive type of inhibition when urokinase was employed but a linear mixed type of inhibition when single chain tPA was employed. These results suggest that the interaction of PAI-1 with tPA, in contrast to its interaction with urokinase, may involve 2 sites on the tPA molecule.PAI-1 has been purified from medium conditioned by cultured bovine aortic endothelial cells and partially characterized. It is a major biosynthetic product of these cells, accounting for as much as 12% of the total protein released by the cells in 24 h. It has an M of 50,000, an isoelectric point of 4.5-5.0, and is immunologically and biochemically related to the rapidly acting inhibitor present in human platelets and in the plasma of some patients at risk to develop thrombotic problems. Although it is relatively stable to conditions which inactivate most protease inhibitors (acid pH, SDS), it is extremely sensitive to oxidants. The molecular cloning of the PAI-1 gene revealed that the mature human protein is 379 amino acids long, contains an NH2-terminal valine, lacks cysteines and has a methionine at the Pi position of it's reactive center. The conversion of this methionine to methionine sulfoxide may be responsible for the rapid inactivation of PAI-1 by oxidants. Human PAI-1 has extensive (30%) homology with α1-antitrypsin and antithrombin III and is thus a member of the serine proteinase inhibitor (serpin) family; a group of related molecules that control the major protease cascades of the blood. The PAI-1 gene is approximately 12.2 kilobase pairs in length and is organized into nine exons and eight introns.The production of PAI-1 by endothelial cells is stimulated by endotoxin, interleukin-1, tumor necrosis factor, and transforming growth factor β(TGFβ). The cells are extremely sensitive to TGFβwith maximal effects (100-fold stimulation) observed with 1-2 ng/ml. These changes were relatively specific for PAI-1, and could be detected at both the protein and the RNA level. Interestingly, TGFgalso stimulated the amount of PAI-1 present in the extracellular matrix (ECM) of BAEs. PAI-1 was one of the primary ECM components of these cells, constituting 10-20% of the ECM proteins detected after SDS-PAGE.One of the most unusual properties of PAI-1 is that it exists in blood and in various cellular samples in both an active and an inactive (latent) form, the ratio depending on the source. The latent form can be converted into the active one by treatment with denaturants like SDS or guanidine-HCl. Although the majority of the cell-associated PAI-1 is active, it rapidly decays (t1/2=3 h) into the latent form once it is released from the cells. In contrast, the half-life of ECM associated PAI-1 was greater than 24 h. These data suggest that PAI-1 is produced by BAEs in an active form, and is then either released into the medium where it is rapidly inactivated, or released into the subendothelium where it binds to ECM. The specific binding of PAI-1 to ECM protects it from this inactivation.

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Gioia, Chiara, Francesca Spinelli, Roberta Priori, Cristina Iannuccelli, Bruno Lucchino, Annarita Vestri, Guido Valesini e 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 e 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 e 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." In 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, e 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, e 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 completely destroyed. This not only potentiates the later recurrence of the myoma, but also limits the predictability of the procedure by imaging techniques. Clearly, techniques that can improve the correspondence between the imaged iceball and the destroyed tissue will improve cryomyolysis and other cryosurgical procedures.

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Huang, Yupeng, Yuehong Chen, Tao Liu, Sang Lin, Geng Yin e 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 e 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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Relatórios de organizações sobre o assunto "Tumor necrosis factor Physiological effect"

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Meidan, Rina, e 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, janeiro de 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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Li, Peng, e 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, agosto de 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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Blanken, Annelies, Bafrin Abdulmajid, Eva van Geel, Joost Daams, Martin van der Esch e 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, janeiro de 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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