The Experts below are selected from a list of 443814 Experts worldwide ranked by ideXlab platform
Rigmor Austgulen - One of the best experts on this subject based on the ideXlab platform.
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Tumor Necrosis Factor, interleukin-1, and interleukin-6 in normal human pregnancy
American Journal of Obstetrics and Gynecology, 1993Co-Authors: Sissel Linda Opsjøn, Solveig Tingulstad, Gro Wiedswang, Anders Sundan, Anders Waage, N. C. Wathen, Rigmor AustgulenAbstract:Objective: Our purpose was to investigate the cytokines, Tumor Necrosis Factor, interleukin-1, and interleukin-6 in normal human pregnancy and labor. Study design: Bioassays were used to measure these Factors in extraembryonic coelomic fluid, amniotic fluid, placenta, and maternal and cord serum. Results: Little or no Tumor Necrosis Factor, interleukin-1, or interleukin-6 was found in coelomic fluid or amniotic fluid in the first trimester. Interleukin-6 appeared in second-trimester amniotic fluid. At term Tumor Necrosis Factor was present (median 17 pg/ml) and increased with the onset of labor (median 58 pg/ml), as did interleukin-1 (median 188 to 680 pg/ml) and interleukin-6 (median 399 to 4800 pg/ml). Maternal serum interleukin-6 increased during pregnancy with a further increment with the onset of labor. Cord interleukin-6 also increased with labor but at a lower level. Conclusion: The cytokines Tumor Necrosis Factor, interleukin-1, and interleukin-6 may play a role in the onset of normal labor.
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Tumor Necrosis Factor, interleukin-1, and interleukin-6 in normal human pregnancy.
American journal of obstetrics and gynecology, 1993Co-Authors: S L Opsjłn, Solveig Tingulstad, Gro Wiedswang, Anders Sundan, Anders Waage, N. C. Wathen, Rigmor AustgulenAbstract:Our purpose was to investigate the cytokines, Tumor Necrosis Factor, interleukin-1, and interleukin-6 in normal human pregnancy and labor. Bioassays were used to measure these Factors in extraembryonic coelomic fluid, amniotic fluid, placenta, and maternal and cord serum. Little or no Tumor Necrosis Factor, interleukin-1, or interleukin-6 was found in coelomic fluid or amniotic fluid in the first trimester. Interleukin-6 appeared in second-trimester amniotic fluid. At term Tumor Necrosis Factor was present (median 17 pg/ml) and increased with the onset of labor (median 58 pg/ml), as did interleukin-1 (median 188 to 680 pg/ml) and interleukin-6 (median 399 to 4800 pg/ml). Maternal serum interleukin-6 increased during pregnancy with a further increment with the onset of labor. Cord interleukin-6 also increased with labor but at a lower level. The cytokines Tumor Necrosis Factor, interleukin-1, and interleukin-6 may play a role in the onset of normal labor.
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.)
Wlodzimierz Maslinski - One of the best experts on this subject based on the ideXlab platform.
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Laboratory changes on anti-Tumor Necrosis Factor treatment in rheumatoid arthritis.
Current opinion in rheumatology, 2003Co-Authors: Maria Ziolkowska, Wlodzimierz MaslinskiAbstract:Tumor Necrosis Factor-alpha, acting through its receptors expressed on all cells of the body, is a key mediator of inflammation and immunity. However, its overproduction may also lead to pathologic changes. The latter situation occurs often in chronic inflammatory diseases such as rheumatoid arthritis. The concept suggesting Tumor Necrosis Factor-alpha as a potential target emerged from experiments showing its key role in inducing many cytokines and mediators of inflammation. Several clinical trials targeting this cytokine in rheumatoid arthritis patients with a novel group of anti-Tumor Necrosis Factor agents demonstrated reduced synovial inflammation and inhibition of bone and cartilage degradation. In addition to the therapeutic value of anti-Tumor Necrosis Factor, analysis of laboratory changes not only proved the concept but provided new data, continuously expanding our understanding of the role of Tumor Necrosis Factor-alpha in the pathogenesis of many diseases. These laboratory measures may also help the earlier identification of rheumatoid arthritis patients who have a less satisFactory response to this therapy.
Karl Decker - One of the best experts on this subject based on the ideXlab platform.
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Regulation of the mRNA expression for Tumor Necrosis Factor-α in rat liver macrophages
Journal of hepatology, 1994Co-Authors: Marcus Grewe, Rudolf Gausling, Karin Gyufko, Rolf Hoffmann, Karl DeckerAbstract:Kupffer cells are known to produce Tumor Necrosis Factor- α upon stimulation with endotoxin or viruses. This Tumor Necrosis Factor- α synthesis is suppressed by prostaglandin E 2 or dexamethasone. Using Northern blotting and reverse transcriptase-polymerase chain reaction, it is demonstrated that endotoxin-induced Tumor Necrosis Factor- α synthesis is blocked by prostaglandin E 2 or dibutyryl 3′:5′-cyclic adenosine monophosphate on the transcriptional level. Tumor Necrosis Factor- α itself suppressed endotoxin-evoked Tumor Necrosis Factor- α mRNA expression when given in a narrow time interval with lipopolysaccharide. Interleukin-10 of human or mouse origin also inhibited the synthesis of Tumor Necrosis Factor- α mRNA and protein when given more than 2 h prior to the endotoxin challenge. The suppressive effect of prostaglandin E 2 lasted for more than 36 h while IL-10 blocked Tumor Necrosis Factor- α production for barely 24 h. Dexamethasone reduced the endotoxin-induced Tumor Necrosis Factor- α mRNA formation by approximately 50% only, although it led to nearly complete inhibition of the synthesis of the mature protein. Taken together with reverse transcriptase-polymerase chain reaction data revealing significant amounts of Tumor Necrosis Factor- α mRNA in resting Kupffer cells, an additional posttranscriptional regulation of Tumor Necrosis Factor- α synthesis has to be assumed. Tumor Necrosis Factor- α mRNA was not induced by interferon- γ , interleukin-1 β or interleukin-6 (the latter two cytokines are also synthesized by Kupffer cells), but a 24-h prestimulation of liver macrophages with interferon- γ or phorbol ester had a modest priming effect. Other substances known to stimulate rat Kupffer cells, such as phorbol ester or calcium ionophore, did not lead to the induction of Tumor Necrosis Factor- α or to an alteration of the lipopolysaccharide-induced Tumor Necrosis Factor- α mRNA synthesis at 90 min or 24 h after stimulation. Comparison with findings on Tumor Necrosis Factor- α mRNA synthesis in some macrophage-related cell lines, monocytes and freshly differentiated macrophages suggests that organ-specific differentiation of resident macrophages leads to variations in the regulation of Tumor Necrosis Factor- α mRNA production.
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Regulation of Tumor Necrosis Factor-α-mRNA synthesis and distribution of Tumor Necrosis Factor-α-mRNA synthesizing cells in rat liver during experimental endotoxemia
Journal of hepatology, 1994Co-Authors: Rolf Hoffmann, Markus Grewe, Hans-christoph Estler, Agnes Schulze-specking, Karl DeckerAbstract:Stimulated liver macrophages (Kupffer cells) are known to release a variety of inflammation-related substances, e.g. cytokines, prostanoids, and reactive oxygen intermediates. For instance, exposure of Kupffer cells in vitro to lipopolysaccharide (endotoxin) leads to a strongly enhanced synthesis of the mRNA for Tumor Necrosis Factor- α , the release of the mature protein into culture media. These events are influenced by prostanoids and corticoid hormones. Kupffer cells are thought to be the only source of Tumor Necrosis Factor- α within the hepatic sinusoid, but neither this cell specificity nor the regulatory influence of glucocorticoids or prostanoids has been confirmed in the intact organ. Using non-radioactive in situ hybridization, it was possible to obtain specific signals for Tumor Necrosis Factor- α -mRNA in individual Kupffer cells uniformly distributed (as compared to Kupffer cells detected by immunohistochemistry) throughout the liver. Kupffer cells were the only cells in the hepatic sinusoids of lipopolysaccharide-perfused livers to express mRNA for Tumor Necrosis Factor- α . Simultaneous addition of endotoxin plus dexamethasone and endotoxin and prostaglandin E 2 completely suppressed the synthesis of this mRNA. Unexpectedly, the presence of mRNA for Tumor Necrosis Factor- α was also detected in the intrahepatic bile duct epithelium of lipopolysaccharide-perfused livers. It is known that biologically active endotoxin is secreted via the bile ducts. These results seem to indicate that bile duct epithelium responds to inflammatory agents with synthesis of Tumor Necrosis Factor- α -mRNA. One must also consider new functional aspects of bile duct epithelium in chronic inflammatory diseases, e.g. primary biliary cirrhosis, chronic sclerosing cholangitis or graft-versus-host disease.
