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Journal articles on the topic 'Tumor necrosis factor. Septische shock'

Author: Grafiati

Published: 4 June 2021

Last updated: 8 February 2022

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1

Baud, L., J. Cadranel, G. Offenstadt, L. Luquel, B. Guidet, and P. Amstutz. "Tumor Necrosis Factor and Septic Shock." Critical Care Medicine 18, no. 3 (1990): 349. http://dx.doi.org/10.1097/00003246-199003000-00034.

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2

Murphey, E. D., and D. L. Traber. "TUMOR NECROSIS FACTOR PRETREATMENT ATTENUATES ENDOTOXIN-INDUCED SHOCK." Shock 9, Supplement (1998): 32. http://dx.doi.org/10.1097/00024382-199806001-00107.

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3

MATUSCHAK, GEORGE M., KARI E. LAMPRECH, and ANDREW J. LECHNER. "Pentoxifylline Inhibits Tumor Necrosis Factor Production in Septic Shock." Journal of Interferon Research 14, no. 5 (1994): 293–95. http://dx.doi.org/10.1089/jir.1994.14.293.

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4

Meldrum, Daniel R. "Tumor necrosis factor in the heart." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 3 (1998): R577—R595. http://dx.doi.org/10.1152/ajpregu.1998.274.3.r577.

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The heart is a tumor necrosis factor (TNF)-producing organ. Both myocardial macrophages and cardiac myocytes themselves synthesize TNF. Accumulating evidence indicates that myocardial TNF is an autocrine contributor to myocardial dysfunction and cardiomyocyte death in ischemia-reperfusion injury, sepsis, chronic heart failure, viral myocarditis, and cardiac allograft rejection. Indeed, locally (vs. systemically) produced TNF contributes to postischemic myocardial dysfunction via direct depression of contractility and induction of myocyte apoptosis. Lipopolysaccharide or ischemia-reperfusion ac

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5

Appoloni, O., E. Dupont, M. Vandercruys, M. Andriens, J. Duchateau, and Jean-Louis Vincent. "Association of tumor necrosis factor-2 allele with plasma tumor necrosis factor-alpha levels and mortality from septic shock." American Journal of Medicine 110, no. 6 (2001): 486–88. http://dx.doi.org/10.1016/s0002-9343(01)00656-8.

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6

Huys, Liesbeth, Filip Van Hauwermeiren, Lien Dejager, et al. "Type I interferon drives tumor necrosis factor–induced lethal shock." Journal of Experimental Medicine 206, no. 9 (2009): 1873–82. http://dx.doi.org/10.1084/jem.20090213.

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Tumor necrosis factor (TNF) is reputed to have very powerful antitumor effects, but it is also a strong proinflammatory cytokine. Injection of TNF in humans and mice leads to a systemic inflammatory response syndrome with major effects on liver and bowels. TNF is also a central mediator in several inflammatory diseases. We report that type I interferons (IFNs) are essential mediators of the lethal response to TNF. Mice deficient in the IFN-α receptor 1 (IFNAR-1) or in IFN-β are remarkably resistant to TNF-induced hypothermia and death. After TNF injection, IFNAR-1−/− mice produced less IL-6, h

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7

Dellinger, R. Phillip. "Tumor necrosis factor in septic shock and multiple system trauma." Critical Care Medicine 25, no. 11 (1997): 1771–73. http://dx.doi.org/10.1097/00003246-199711000-00005.

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8

Rhee, Peter, Kenneth Waxman, Lisa Clark, et al. "Tumor necrosis factor and monocytes are released during hemorrhagic shock." Resuscitation 25, no. 3 (1993): 249–55. http://dx.doi.org/10.1016/0300-9572(93)90122-7.

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9

Teppo, A. M., and C. P. Maury. "Radioimmunoassay of tumor necrosis factor in serum." Clinical Chemistry 33, no. 11 (1987): 2024–27. http://dx.doi.org/10.1093/clinchem/33.11.2024.

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Abstract We present a double-antibody radioimmunoassay for determination of the concentration of tumor necrosis factor (TNF) in serum. TNF in serum competes with a fixed amount of 125I-labeled TNF for the binding sites of specific rabbit antibodies. The bound TNF is precipitated with Sepharose-bound anti-rabbit IgG, then centrifuged, and the radioactivity of the pellets is counted. The detection limit of the assay is 7 ng/L (B0-3 SD). Bound radioactivity in the range of 10% to 90% of the B0 counts corresponds to TNF concentrations of 26 to 10,000 ng/L. Of 40 sera from healthy subjects, 21 (53%

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10

Dinata, Khrisanti, Ari L. Runtunuwu, Jose M. Mandei, and Julius H. Lolombulan. "Correlation between tumor necrosis factor-alpha and septic shock in children." Paediatrica Indonesiana 53, no. 1 (2013): 1. http://dx.doi.org/10.14238/pi53.1.2013.1-5.

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Background The crucial role cytokines play in the pathophysiologyof sepsis is widely accepted. Infection stimulates the productionof cytokines in various cell types. Tumor necrosis factor-alpha(TNF-a) is one of the most extensively investigated cytokines inexperimental and clinical sepsis. Tumor necrosis factor-alpha hasbeen shown to mediate lethality in experimental sepsis.Objective To evaluate for a possible correlation between TNF-alevel and septic shock in children.Methods This cross-sectional study was conducted in Manadofrom June to September 2011. A total of 40 patients with arecent dia

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11

Jäättelä, M., D. Wissing, P. A. Bauer, and G. C. Li. "Major heat shock protein hsp70 protects tumor cells from tumor necrosis factor cytotoxicity." EMBO Journal 11, no. 10 (1992): 3507–12. http://dx.doi.org/10.1002/j.1460-2075.1992.tb05433.x.

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12

Arrigo, A. P. "Tumor necrosis factor induces the rapid phosphorylation of the mammalian heat shock protein hsp28." Molecular and Cellular Biology 10, no. 3 (1990): 1276–80. http://dx.doi.org/10.1128/mcb.10.3.1276.

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Tumor necrosis factor alpha was found to rapidly phosphorylate the unique mammalian small heat shock protein hsp28 without impairing its cytoplasmic localization and without inducing the synthesis of the heat shock proteins. In contrast to the C-kinase-dependent phosphorylation of hsp28 in response to the tumor promoter phorbol-12-myristate-13-acetate, the heat- and tumor necrosis factor-mediated phosphorylation of this heat shock protein appears to occur independently of C kinase. These observations suggest that a C-kinase-independent phosphorylation of hsp28 may be an early event in the cell

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13

Arrigo, A. P. "Tumor necrosis factor induces the rapid phosphorylation of the mammalian heat shock protein hsp28." Molecular and Cellular Biology 10, no. 3 (1990): 1276–80. http://dx.doi.org/10.1128/mcb.10.3.1276-1280.1990.

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Tumor necrosis factor alpha was found to rapidly phosphorylate the unique mammalian small heat shock protein hsp28 without impairing its cytoplasmic localization and without inducing the synthesis of the heat shock proteins. In contrast to the C-kinase-dependent phosphorylation of hsp28 in response to the tumor promoter phorbol-12-myristate-13-acetate, the heat- and tumor necrosis factor-mediated phosphorylation of this heat shock protein appears to occur independently of C kinase. These observations suggest that a C-kinase-independent phosphorylation of hsp28 may be an early event in the cell

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14

Cain, W. C., R. W. Stuart, D. L. Lefkowitz, J. D. Starnes, S. Margolin, and S. S. Lefkowitz. "Inhibition of tumor necrosis factor and subsequent endotoxin shock by pirfenidone." International Journal of Immunopharmacology 20, no. 12 (1998): 685–95. http://dx.doi.org/10.1016/s0192-0561(98)00042-3.

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15

Tang, Gau-Jun, Song-Lih Huang, Huey-Wen Yien, et al. "Tumor necrosis factor gene polymorphism and septic shock in surgical infection." Critical Care Medicine 28, no. 8 (2000): 2733–36. http://dx.doi.org/10.1097/00003246-200008000-00008.

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16

Giroir, B. P., J. W. Horton, D. J. White, K. L. McIntyre, and C. Q. Lin. "Inhibition of tumor necrosis factor prevents myocardial dysfunction during burn shock." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 1 (1994): H118—H124. http://dx.doi.org/10.1152/ajpheart.1994.267.1.h118.

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Tumor necrosis factor-alpha (TNF) is a pluripotent cytokine that mediates many of the hemodynamic manifestations of endotoxic shock. To determine whether TNF is responsible for postburn myocardial dysfunction, we compared cardiac function (Langendorff preparation) in 49 guinea pigs 18 h after thermal injury. Group 1 (n = 15) was sham burned; all remaining animals received a 43% surface area burn under anesthesia. Group 2 (n = 15) received lactated Ringer solution (LR, 4 ml.kg-1.%burn-1). Group 3 (n = 9) received LR and drug vehicle. Group 4 (n = 10) received LR plus 1 mg of TNF inhibitor consi

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17

Cerami, Anthony. "Tumor Necrosis Factor as a Mediator of Shock, Cachexia and Inflammation." Blood Purification 11, no. 2 (1993): 108–17. http://dx.doi.org/10.1159/000170104.

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18

Ashkenazi, A., S. A. Marsters, D. J. Capon, et al. "Protection against endotoxic shock by a tumor necrosis factor receptor immunoadhesin." Proceedings of the National Academy of Sciences 88, no. 23 (1991): 10535–39. http://dx.doi.org/10.1073/pnas.88.23.10535.

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19

Babcock, G. F., and C. D. Kane. "Regulation of Neutrophil Apoptosis by Tumor Necrosis Factor Following Heat Shock." Journal of Burn Care & Rehabilitation 21 (January 2000): S199. http://dx.doi.org/10.1097/00004630-200001001-00129.

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20

Tang, Gun-Jun, Song-Lih Hung, and Huey-Wen Yien. "TUMOR NECROSIS FACTOR GENE POLYMORPHISM AND SEPTIC SHOCK IN SURGICAL INFECTION." Critical Care Medicine 27, Supplement (1999): 48A. http://dx.doi.org/10.1097/00003246-199901001-00076.

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21

Beutler, Bruce, and Anthony Cerami. "Cachectin/tumor necrosis factor: An endogenous mediator of shock and inflammation." Immunologic Research 5, no. 4 (1986): 281–93. http://dx.doi.org/10.1007/bf02935501.

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22

Royall, J. A., R. L. Berkow, J. S. Beckman, M. K. Cunningham, S. Matalon, and B. A. Freeman. "Tumor necrosis factor and interleukin 1 alpha increase vascular endothelial permeability." American Journal of Physiology-Lung Cellular and Molecular Physiology 257, no. 6 (1989): L399—L410. http://dx.doi.org/10.1152/ajplung.1989.257.6.l399.

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Endotoxic shock is associated with acute vascular endothelial injury resulting in edema. Tumor necrosis factor (TNF) and interleukin 1 (IL-1) are cytokines produced by endotoxin-stimulated mononuclear phagocytes that are potential mediators of endotoxic shock. In this study, we investigated the effects of TNF and IL-1 alpha on vascular endothelial cell permeability in vitro. The movement of radiolabeled macromolecules of different sizes (57Co-vitamin B12, 125I-cytochrome c, and 131I-albumin; 6.5-35A) across bovine aortic endothelial cell monolayers was measured after exposure to these cytokine

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23

Nakano, Y., M. Shirai, N. Mori, and M. Nakano. "Neutralization of microcystin shock in mice by tumor necrosis factor alpha antiserum." Applied and Environmental Microbiology 57, no. 1 (1991): 327–30. http://dx.doi.org/10.1128/aem.57.1.327-330.1991.

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24

Altavilla, D., F. Squadrito, P. Canale, et al. "Tumor necrosis factor induces E-selectin production in splanchnic artery occlusion shock." American Journal of Physiology-Heart and Circulatory Physiology 268, no. 4 (1995): H1412—H1417. http://dx.doi.org/10.1152/ajpheart.1995.268.4.h1412.

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Splanchnic arteries were clamped for 45 min to induce splanchnic artery occlusion (SAO) shock in anesthetized rats. Sham-operated animals were used as controls. Survival time, serum tumor necrosis factor-alpha (TNF-alpha), white blood cell (WBC) count, mean arterial blood pressure, myeloperoxidase (MPO) activity, and serum levels of soluble E-selectin (sE-selectin) were investigated. SAO-shocked rats exhibited decreased survival time (95 +/- 11 min, whereas sham-shocked rats survived for > 5 h), reduced mean arterial blood pressure, increased serum levels of TNF-alpha (185 +/- 8 U/ml) and M

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25

Fisher, Charles J., Jan M. Agosti, Steven M. Opal, et al. "Treatment of Septic Shock with the Tumor Necrosis Factor Receptor:Fc Fusion Protein." New England Journal of Medicine 334, no. 26 (1996): 1697–702. http://dx.doi.org/10.1056/nejm199606273342603.

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26

Waelput, Wim, Daniël Broekaert, Joël Vandekerckhove, Peter Brouckaert, Jan Tavernier, and Claude Libert. "A Mediator Role For Metallothionein in Tumor Necrosis Factor–induced Lethal Shock." Journal of Experimental Medicine 194, no. 11 (2001): 1617–24. http://dx.doi.org/10.1084/jem.194.11.1617.

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Tumor necrosis factor (TNF) is a proinflammatory cytokine, which is centrally involved in several inflammatory disorders. Administration of TNF leads to a potentially lethal systemic inflammatory response syndrome (SIRS). We observed that (a) mice lacking functional genes for metallothionein 1 and 2 (MT-null) were protected compared with wild-type controls (P = 0.0078), and (b) mice overexpressing MT-1 (MT-TG) were more sensitized for the lethal effect of TNF than control mice (P = 0.0003), indicating a mediating role for MT in TNF induced SIRS. As MT is involved in the body zinc homeostasis,

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27

Clark, Daniel L., Rajash K. Handa, Cynthia D. Johnson, Bret A. Connors, and Andrew P. Evan. "TUMOR NECROSIS FACTOR-ALPHA RESPONSE TO SHOCK WAVE LITHOTRIPSY-INDUCED RENAL INJURY." Journal of Urology 179, no. 4S (2008): 506. http://dx.doi.org/10.1016/s0022-5347(08)61493-7.

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28

Bloom, Ona, Haichao Wang, Svetlana Ivanova, Jaideep M. Vishnubhakat, Michael Ombrellino, and Kevin J. Tracey. "HYPOPHYSECTOMY, HIGH TUMOR NECROSIS FACTOR LEVELS, AND HEMOGLOBINEMIA IN LETHAL ENDOTOXEMIC SHOCK." Shock 10, no. 6 (1998): 395–400. http://dx.doi.org/10.1097/00024382-199812000-00003.

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29

Nwariaku, Fiemu E., Kendra L. Mclntyre, Patricia J. Sikes, and William J. Mileski. "ALTERATIONS IN ALVEOLAR MACROPHAGE TUMOR NECROSIS FACTOR (TNF) RESPONSE FOLLOWING HEMORRHAGIC SHOCK." Shock 4, no. 3 (1995): 200–203. http://dx.doi.org/10.1097/00024382-199509000-00008.

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30

Barroso-Aranda, Jorge, Benjamin W. Zweifach, John C. Mathison, and Geert W. Schmid-Schönbein. "Neutrophil Activation, Tumor Necrosis Factor, and Survival After Endotoxic and Hemorrhagic Shock." Journal of Cardiovascular Pharmacology 25 (1995): S23—S29. http://dx.doi.org/10.1097/00005344-199500252-00006.

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31

Ikejima, T., S. Okusawa, J. W. M. Van Der Meer, and C. A. Dinarello. "Toxic Shock Syndrome is Mediated by Interleukin 1 and Tumor Necrosis Factor." Clinical Infectious Diseases 11, Supplement_1 (1989): S316—S317. http://dx.doi.org/10.1093/clinids/11.supplement_1.s316.

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32

Ishizaki, Keiji, Yasushi Youda, Duck Mi Yoon, Kenichi Arai, and Tatsushi Fujita. "Therapy with antibody to tumor necrosis factor against endotoxin shock in rabbits." Journal of Anesthesia 8, no. 3 (1994): 305–10. http://dx.doi.org/10.1007/bf02514656.

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33

Shimamoto, Y. "Monoclonal antibodies against human recombinant tumor necrosis factor: prevention of endotoxic shock." Immunology Letters 17, no. 4 (1988): 311–17. http://dx.doi.org/10.1016/0165-2478(88)90003-x.

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34

ISHIZAKI, KEIJI, KENICHI ARAI, and TATSUSI FUJITA. "SHOCK INDUCED RECOMBINANT TUMOR NECROSIS FACTOR AND ITS PREVENTION IN THE RAT." KITAKANTO Medical Journal 41, no. 6 (1991): 845–51. http://dx.doi.org/10.2974/kmj1951.41.845.

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35

Porat, Reuven, Heather N. Paddock, Stephen D. Schwaitzberg, et al. "Glycosylated recombinant human tumor necrosis factor binding protein-1 reduces mortality, shock, and production of tumor necrosis factor in rabbit Escherichia coli sepsis." Critical Care Medicine 23, no. 6 (1995): 1080–89. http://dx.doi.org/10.1097/00003246-199506000-00014.

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36

Wang, J. H., H. P. Redmond, R. W. Watson, and D. Bouchier-Hayes. "Role of lipopolysaccharide and tumor necrosis factor-alpha in induction of hepatocyte necrosis." American Journal of Physiology-Gastrointestinal and Liver Physiology 269, no. 2 (1995): G297—G304. http://dx.doi.org/10.1152/ajpgi.1995.269.2.g297.

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The occurrence of acute hepatic failure during systemic inflammatory response syndrome (SIRS) is related to the extent of hepatocyte (HC) damage and cell death resulting from necrosis or apoptosis. We hypothesized that proinflammatory mediators such as lipopolysaccharide (LPS) and tumor necrosis factor-alpha (TNF-alpha) can, either directly or indirectly through neutrophil (PMN) and Kupffer cell (KC) activation, induce HC damage and cell death, and that the mechanism is cellular necrosis rather than apoptosis. The results in this study demonstrated that LPS and TNF-alpha alone and in combinati

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37

Zingarelli, B., F. Squadrito, D. Altavilla, G. Calapai, M. Di Rosa, and A. P. Caputi. "Role of tumor necrosis factor-alpha in acute hypovolemic hemorrhagic shock in rats." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 4 (1994): H1512—H1515. http://dx.doi.org/10.1152/ajpheart.1994.266.4.h1512.

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Hemorrhagic shock was induced in male anesthetized rats by intermittently withdrawing blood from an iliac catheter until mean arterial blood pressure (MAP) fell and stabilized within the range of 20-30 mmHg. Survival rate, MAP, and serum and macrophage levels of tumor necrosis factor-alpha (TNF-alpha) were then evaluated. Furthermore, in ex vivo studies, the responsiveness to phenylephrine (PE; 1 nM to 10 microM) was investigated in aortic rings from hemorrhagic shocked rats. Antibodies raised against TNF-alpha (anti-TNF-alpha; 2 mg/kg) or vehicle (phosphate-buffered saline, 1 ml/kg) were inje

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38

Zingarelli, Basilia, Francesco Squadrito, Mariapatrizia Ioculano, et al. "Platelet activating factor interaction with tumor necrosis factor and myocardial depressant factor in splanchnic artery occlusion shock." European Journal of Pharmacology 222, no. 1 (1992): 13–19. http://dx.doi.org/10.1016/0014-2999(92)90456-e.

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39

Sturniolo, R., F. Squadrito, D. Altavilla, A. Arena, M. Ioculano, and A. P. Caputi. "Splanchnic artery occlusion (SAO) shock in the rat and tumor necrosis factor (TNF)." Pharmacological Research 22 (September 1990): 472. http://dx.doi.org/10.1016/s1043-6618(09)80476-3.

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40

Maskin, Bernardo C. "CORRELATION BETWEEN TROPONIN I AND TUMOR NECROSIS FACTOR-ALPHA CONCENTRATIONS IN SEPTIC SHOCK." Critical Care Medicine 30, Supplement (2002): A113. http://dx.doi.org/10.1097/00003246-200212001-00384.

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41

Tani, Tohru, Mitsuhiro Fujino, Kazuyoshi Hanasawa, Tomoharu Shimizu, Yoshihiro Endo та Masashi Kodama. "Bacterial translocation and tumor necrosis factor-α gene expression in experimental hemorrhagic shock". Critical Care Medicine 28, № 11 (2000): 3705–9. http://dx.doi.org/10.1097/00003246-200011000-00028.

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42

Lin, Wen-Jye, and Wen-Chen Yeh. "IMPLICATION OF TOLL-LIKE RECEPTOR AND TUMOR NECROSIS FACTOR ?? SIGNALING IN SEPTIC SHOCK." Shock 24, no. 3 (2005): 206–9. http://dx.doi.org/10.1097/01.shk.0000180074.69143.77.

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43

Squadrito, F., D. Altavilla, G. Squadrito, G. M. Campo, M. Ferlito, and A. P. Caputi. "Tacrolimus (FK506) reduces Tumor Necrosis Factor and protects against splanchnic artery occlusion shock." Shock 9, Supplement (1998): 16. http://dx.doi.org/10.1097/00024382-199806001-00053.

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44

LIVINGSTON, DAVID H., MARK A. MALANGONI, and GERALD SONNENFELD. "Immune Enhancement by Tumor Necrosis Factor-alpha Improves Antibiotic Efficacy after Hemorrhagic Shock." Journal of Trauma: Injury, Infection, and Critical Care 29, no. 7 (1989): 967–71. http://dx.doi.org/10.1097/00005373-198907000-00010.

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45

Busund, Rolf. "Tumor Necrosis Factor and Interleukin 1 Appearance in Experimental Gram-negative Septic Shock." Archives of Surgery 126, no. 5 (1991): 591. http://dx.doi.org/10.1001/archsurg.1991.01410290067014.

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46

Zwaveling, Jan H., Jan K. Maring, Han Moshage, et al. "Role of nitric oxide in recombinant tumor necrosis factor-alpha-induced circulatory shock." Critical Care Medicine 24, no. 11 (1996): 1806–10. http://dx.doi.org/10.1097/00003246-199611000-00008.

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47

Lloyd, Sarah S., Albert K. Chang, Fletcher B. Taylor, Edward G. Janzen, and Paul B. McCay. "Free radicals and septic shock in primates: The role of tumor necrosis factor." Free Radical Biology and Medicine 14, no. 3 (1993): 233–42. http://dx.doi.org/10.1016/0891-5849(93)90020-u.

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48

Rothstein, J. L., and H. Schreiber. "Synergy between tumor necrosis factor and bacterial products causes hemorrhagic necrosis and lethal shock in normal mice." Proceedings of the National Academy of Sciences 85, no. 2 (1988): 607–11. http://dx.doi.org/10.1073/pnas.85.2.607.

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49

Rong, He, and Xiao Suhong. "EFFECTS OF PENTOXIFYLLINE ON PLASMA TUMOR NECROSIS FACTOR, TISSUE FACTOR AND TISSUE FACTOR PATHWAY INHIBITOR IN ENDOTOXIN SHOCK." Shock 4, Supplement (1995): 48. http://dx.doi.org/10.1097/00024382-199512001-00191.

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50

Libert, C., P. Brouckaert, and W. Fiers. "Protection by alpha 1-acid glycoprotein against tumor necrosis factor-induced lethality." Journal of Experimental Medicine 180, no. 4 (1994): 1571–75. http://dx.doi.org/10.1084/jem.180.4.1571.

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We here report that alpha 1-acid glycoprotein, a typical acute phase protein, protects mice from lethal shock induced by tumor necrosis factor (TNF) or endotoxin. The protection is observed both in normal and in galactosamine-sensitized mice. Optimal desensitization requires at least 3 mg alpha 1-acid glycoprotein administered 2 h before the lethal challenge. Under these conditions, complete inhibition of all TNF-induced metabolic changes was observed: fall in body temperature, release of liver transaminases, enhanced clotting time, and mortality. The known platelet aggregation-inhibitory acti

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