The Experts below are selected from a list of 291 Experts worldwide ranked by ideXlab platform
Henk C S Wallenburg - One of the best experts on this subject based on the ideXlab platform.
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Soluble Tumor Necrosis factor receptor II and soluble cell adhesion molecule 1 as markers of Tumor Necrosis factor-α release in preeclampsia
Acta obstetricia et gynecologica Scandinavica, 2002Co-Authors: W. Visser, Ilse Beckmann, Marco A. H. Knook, Henk C S WallenburgAbstract:Acta Obstet Gynecol Scand 2002; 81: 713-719. © Acta Obstet Gynecol Scand 2002 Background. The purpose of this case-controlled study was to investigate whether plasma concentrations of TNF-receptors I and II and Tumor Necrosis factor-α-induced cell adhesion molecule 1 VCAM-1 could serve as more sensitive markers of Tumor Necrosis factor-α release in preeclamptic women than a direct measurement of circulating Tumor Necrosis factor-α. Methods. Plasma concentrations of soluble Tumor Necrosis factor receptor I and II, immunoreactive Tumor Necrosis factor-a and soluble cell adhesion molecule VCAM-1 were determined in 21 patients with severe proteinuric preeclampsia (23-35 weeks' gestation) and 21 gestational age-matched normotensive controls by enzyme-linked immunoassays. Concentrations of bioactive Tumor Necrosis factor-α were assessed by the WEHI 164 bioassay. Data were statistically evaluated by Wilcoxon's rank sum and sign tests, and Spearman's test was used to evaluate clinical and biochemical correlations...
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circulating bioactive Tumor Necrosis factor α Tumor Necrosis factor α receptors fibronectin and Tumor Necrosis factor α inducible cell adhesion molecule vcam 1 in uncomplicated pregnancy
American Journal of Obstetrics and Gynecology, 1997Co-Authors: Ilse Beckmann, Willy Visser, P C Struijk, Marieke Van Dooren, Joan Glavimans, Henk C S WallenburgAbstract:Abstract Objectives: Our goal was to assess in a longitudinal study of uncomplicated pregnancy the course of maternal plasma concentrations of the bioactive cytokine Tumor Necrosis factor-α, the soluble Tumor Necrosis factor-α receptors sTNFRI and sTNFRII, the soluble cell adhesion molecule sVCAM-1, and circulating fibronectin. Study Design: Blood was collected from 22 healthy pregnant women at 7 to 17, 18 to 22, 23 to 28, and 30 to 36 weeks' gestation and post partum. Plasma samples were measured by bioassay for bioactive Tumor Necrosis factor-α, by immunoassay for sTNFRI, sTNFRII, and VCAM-1, and by radial immunodiffusion for circulating fibronectin, and data were statistically analyzed. Results: Plasma concentrations of all variables were significantly linked with gestational age. Levels of bioactive Tumor Necrosis factor-α and sTNFRII showed a parallel rise in the second trimester and a decrease thereafter. Values for sTNFRI and sTNFRII and for these receptors and VCAM-1 were correlated, a weak correlation between bioactive Tumor Necrosis factor-α and sTNFRII was observed, and no correlation between circulating fibronectin and other variables was apparent. Conclusions: All variables studied exhibited a characteristic pattern depending on gestational age, which supports the concept of a physiologic role of Tumor Necrosis factor-α in pregnancy.
Alberto Martini - One of the best experts on this subject based on the ideXlab platform.
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Treatment of Takayasu's arteritis with Tumor Necrosis factor antagonists.
The Journal of pediatrics, 2008Co-Authors: Giovanni Filocamo, Antonella Buoncompagni, Stefania Viola, Anna Loy, Clara Malattia, Angelo Ravelli, Alberto MartiniAbstract:Four children with Takayasu's arteritis were treated with Tumor Necrosis factor antagonists because of disease relapse during conventional therapy or as a first-line agent. Two patients went into remission; in the other 2, the response was partial. Anti-Tumor Necrosis factor agents can have a role in the treatment of Takayasu's arteritis; further controlled studies are required.
D G Mutch - One of the best experts on this subject based on the ideXlab platform.
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The role of Tumor Necrosis factor receptors in Tumor Necrosis factor-alpha-mediated cytolysis of ovarian cancer cell lines.
American journal of obstetrics and gynecology, 1996Co-Authors: E R Kost, T J Herzog, L M Adler, S Williams, D G MutchAbstract:Our purpose was to define the expression of Tumor Necrosis factor receptors on ovarian cancer cells and determine what role these receptors play in Tumor Necrosis factor-alpha-mediated cytolysis. Cell surface expression of Tumor Necrosis factor-alpha receptors was determined on ovarian cancer cell lines Caov-3, SK-OV-3, NIH:OVCAR-3, and A2780 by a Tumor Necrosis factor-alpha-binding assay that used iodine 125-labeled Tumor Necrosis factor-alpha. Monoclonal antibodies specific for the 55 to 60 kd (TR60) and 75 to 80 kd (TR80) Tumor Necrosis factor receptors were used to determine the relative density of each receptor type. To elucidate which receptor(s) was responsible for mediating the signal for cytolysis, 24-hour MTT cytolytic assays that used Tumor Necrosis factor-alpha and emetine were performed in the presence or absence of receptor-specific monoclonal antibodies. The four ovarian cell lines expressed a similar number of surface receptors, 4500 to 7000 per cell, had similar dissociation constants, 0.3 to 0.6 nmol/L, and expressed predominately the TR60 receptor subtype. Receptor function studies showed that the presence of the monoclonal antibody to the TR60 receptor completely inhibited Tumor Necrosis factor-alpha-mediated cytolysis, whereas the monoclonal antibody to the TR80 receptor only partially blocked cytolysis. Ovarian cancer cell lines express both Tumor Necrosis factor receptors, with the TR60 receptor being the dominant subtype. Tumor Necrosis factor-alpha-mediated cytolysis appears to be dependent on the presence of a functional TR60 receptor. The TR80 receptor does not appear requisite for cytolysis; however, a complementary role cannot be excluded. Manipulation of Tumor Necrosis factor receptor subtypes on ovarian cancer cells may enhance the cytotoxic effects, thus improving the therapeutic efficacy of Tumor Necrosis factor-alpha.
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The role of Tumor Necrosis factor receptors in Tumor Necrosis factor-α - mediated cytolysis of ovarian cancer cell lines☆☆☆★
American Journal of Obstetrics and Gynecology, 1996Co-Authors: E R Kost, T J Herzog, L M Adler, S Williams, D G MutchAbstract:Abstract OBJECTIVE: Our purpose was to define the expression of Tumor Necrosis factor receptors on ovarian cancer cells and determine what role these receptors play in Tumor Necrosis factor-α - mediated cytolysis. STUDY DESIGN: Cell surface expression of Tumor Necrosis factor-α receptors was determined on ovarian cancer cell lines Caov-3, SK-OV-3, NIH : OVCAR-3, and A2780 by a Tumor Necrosis factor-α binding assay that used iodine 125 - labeled Tumor Necrosis factor-α. Monoclonal antibodies specific for the 55 to 60 kd (TR60) and 75 to 80 kd (TR80) Tumor Necrosis factor receptors were used to determine the relative density of each receptor type. To elucidate which receptor(s) was responsible for mediating the signal for cytolysis, 24-hour MTT cytolytic assays that used Tumor Necrosis factor-α and emetine were performed in the presence or absence of receptor-specific monoclonal antibodies. RESULTS: The four ovarian cell lines expressed a similar number of surface receptors, 4500 to 7000 per cell, had similar dissociation constants, 0.3 to 0.6 nmol/L, and expressed predominately the TR60 receptor subtype. Receptor function studies showed that the presence of the monoclonal antibody to the TR60 receptor completely inhibited Tumor Necrosis factor-α - mediated cytolysis, whereas the monoclonal antibody to the TR80 receptor only partially blocked cytolysis. CONCLUSIONS: Ovarian cancer cell lines express both Tumor Necrosis factor receptors, with the TR60 receptor being the dominant subtype. Tumor Necrosis factor-α - mediated cytolysis appears to be dependent on the presence of a functional TR60 receptor. The TR80 receptor does not appear requisite for cytolysis; however, a complementary role cannot be excluded. Manipulation of Tumor Necrosis factor receptor subtypes on ovarian cancer cells may enhance the cytotoxic effects, thus improving the therapeutic efficacy of Tumor Necrosis factor-α. (AM J OBSTET GYNECOL 1996;174:145-53.)
Karin Larsson - One of the best experts on this subject based on the ideXlab platform.
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Tumor Necrosis factor α and nucleus pulposus induced nerve root injury
Spine, 1998Co-Authors: Kjell Olmarker, Karin LarssonAbstract:STUDY DESIGN The effects of nucleus pulposus and various treatments to block Tumor Necrosis factor alpha activity were evaluated in an experimental set-up using immunohistochemistry and nerve conduction velocity recordings. OBJECTIVES To assess the presence of Tumor Necrosis factor alpha in pig nucleus pulposus cells, and to see if block of Tumor Necrosis factor alpha also blocks the nucleus-pulposus-induced reduction of nerve root conduction velocity. SUMMARY AND BACKGROUND DATA A meta-analysis of observed effects induced by nucleus pulposus revealed that these effects might relate to one specific cytokine-Tumor Necrosis factor alpha. METHODS Series-1: Cultured nucleus pulposus cells were stained immunohistologically with a monoclonal antibody for Tumor Necrosis factor alpha. Series-2: Nucleus pulposus was harvested from lumbar discs and applied to the sacrococcygeal cauda equina in 13 pigs autologously. Four pigs received 100 mg of doxycycline intravenously; five pigs had a blocking monoclonal antibody to Tumor Necrosis factor alpha applied locally in the nucleus pulposus, and four pigs remained nontreated, forming a control group. Three days after the application, the nerve root conduction velocity was determined over the application zone by local electrical stimulation. RESULTS Series-1: Tumor Necrosis factor alpha was found to be present in the nucleus pulposus cells. Series-2: The selective antibody to Tumor Necrosis factor alpha limited the reduction of nerve conduction velocity, although in comparison with the control group this was not statistically significant. However, treatment with doxycycline significantly blocked the nucleus-pulposus-induced reduction of conduction velocity. CONCLUSION For the first time, a specific substance, Tumor Necrosis factor alpha, has been linked to the nucleus-pulposus-induced effects of nerve roots after local application. Although the effects of this substance may be synergistic with those of other similar substances, the data of the current study may be of significant importance for the continued understanding of nucleus pulposus' biologic activity, and of possible potential use for future strategies in managing sciatica.
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Tumor Necrosis factor alpha and nucleus-pulposus-induced nerve root injury.
Spine, 1998Co-Authors: Kjell Olmarker, Karin LarssonAbstract:STUDY DESIGN The effects of nucleus pulposus and various treatments to block Tumor Necrosis factor alpha activity were evaluated in an experimental set-up using immunohistochemistry and nerve conduction velocity recordings. OBJECTIVES To assess the presence of Tumor Necrosis factor alpha in pig nucleus pulposus cells, and to see if block of Tumor Necrosis factor alpha also blocks the nucleus-pulposus-induced reduction of nerve root conduction velocity. SUMMARY AND BACKGROUND DATA A meta-analysis of observed effects induced by nucleus pulposus revealed that these effects might relate to one specific cytokine-Tumor Necrosis factor alpha. METHODS Series-1: Cultured nucleus pulposus cells were stained immunohistologically with a monoclonal antibody for Tumor Necrosis factor alpha. Series-2: Nucleus pulposus was harvested from lumbar discs and applied to the sacrococcygeal cauda equina in 13 pigs autologously. Four pigs received 100 mg of doxycycline intravenously; five pigs had a blocking monoclonal antibody to Tumor Necrosis factor alpha applied locally in the nucleus pulposus, and four pigs remained nontreated, forming a control group. Three days after the application, the nerve root conduction velocity was determined over the application zone by local electrical stimulation. RESULTS Series-1: Tumor Necrosis factor alpha was found to be present in the nucleus pulposus cells. Series-2: The selective antibody to Tumor Necrosis factor alpha limited the reduction of nerve conduction velocity, although in comparison with the control group this was not statistically significant. However, treatment with doxycycline significantly blocked the nucleus-pulposus-induced reduction of conduction velocity. CONCLUSION For the first time, a specific substance, Tumor Necrosis factor alpha, has been linked to the nucleus-pulposus-induced effects of nerve roots after local application. Although the effects of this substance may be synergistic with those of other similar substances, the data of the current study may be of significant importance for the continued understanding of nucleus pulposus' biologic activity, and of possible potential use for future strategies in managing sciatica.
Elaine Alt - One of the best experts on this subject based on the ideXlab platform.
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prevention of carbon tetrachloride induced rat liver injury by soluble Tumor Necrosis factor receptor
Gastroenterology, 1995Co-Authors: Mark J Czaja, Elaine AltAbstract:Abstract Background/Aims: Considerable indirect evidence suggests that cytokine Tumor Necrosis factor α contributes to the hepatocellular damage caused by toxic liver injury. The effects of Tumor Necrosis factor α neutralization on liver cell injury were determined in an in vivo model of toxic liver injury. Methods: The in vivo effects of Tumor Necrosis factor α were examined in carbon tetrachloride liver injury through the administration of a soluble Tumor Necrosis factor receptor to neutralize the effects of this cytokine. Results: Soluble Tumor Necrosis factor receptor treatment decreased the degree of liver injury as measured by reduced levels of serum liver enzymes and improved histology. Soluble Tumor Necrosis factor receptor administration also lowered the mortality from a lethal dose of carbon tetrachloride from 60% to 16%. Tumor Necrosis factor α neutralization had no detrimental effect on liver regeneration as determined by the timing of histone gene expression and postinjury liver weight. Conclusions: These data provide direct evidence for a role of Tumor Necrosis factor α in toxin-induced liver cell injury. In addition, these investigations suggest that soluble Tumor Necrosis factor receptor therapy may be of benefit in the treatment of human liver disease.
