The Experts below are selected from a list of 12 Experts worldwide ranked by ideXlab platform
S.d. Holladay - One of the best experts on this subject based on the ideXlab platform.
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Maternal immune stimulation reduces both placental morphologic damage and down-regulated placental growth-factor and cell cycle gene expression caused by urethane: are these events related to reduced Teratogenesis?
International immunopharmacology, 2003Co-Authors: L.v Sharova, A.a Sharov, P. Sura, Robert M. Gogal, Bonnie J. Smith, S.d. HolladayAbstract:Activation of the maternal immune system in mice decreased cleft palate caused by the Chemical Teratogen, urethane. Direct and indirect mechanisms for this phenomenon have been suggested, including maternal macrophages that cross the placenta to find and eliminate pre-Teratogenic cells, or maternal immune proteins (cytokines) that cross placenta to alleviate or partially alleviate toxicant-mediated effects in the developing fetus. A third mechanism to explain improved fetal developmental outcome in Teratogen-challenged pregnant mice might involve beneficial effects of immune stimulation on the placenta. In the present experiments, urethane treatment altered placental morphology and impaired placental function, the latter indicated by down-regulated activity of cell cycle genes and of genes encoding cytokines and growth factors. Maternal immune stimulation with either Freund's complete adjuvant (FCA) or interferon-gamma (IFNγ) reduced morphologic damage to the placenta caused by urethane and normalized expression of several genes that were down-regulated by urethane. Urethane treatment also shifted placental cytokine gene expression toward a T cell helper 1 (Th1) profile, while immunostimulation tended to restore a Th2 profile that may be more beneficial to pregnancy and fetal development. These data suggest that the beneficial effects of maternal immune stimulation on fetal development in Teratogen-exposed mice may, in part, result from improved placental structure and function.
L.v Sharova - One of the best experts on this subject based on the ideXlab platform.
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Maternal immune stimulation reduces both placental morphologic damage and down-regulated placental growth-factor and cell cycle gene expression caused by urethane: are these events related to reduced Teratogenesis?
International immunopharmacology, 2003Co-Authors: L.v Sharova, A.a Sharov, P. Sura, Robert M. Gogal, Bonnie J. Smith, S.d. HolladayAbstract:Activation of the maternal immune system in mice decreased cleft palate caused by the Chemical Teratogen, urethane. Direct and indirect mechanisms for this phenomenon have been suggested, including maternal macrophages that cross the placenta to find and eliminate pre-Teratogenic cells, or maternal immune proteins (cytokines) that cross placenta to alleviate or partially alleviate toxicant-mediated effects in the developing fetus. A third mechanism to explain improved fetal developmental outcome in Teratogen-challenged pregnant mice might involve beneficial effects of immune stimulation on the placenta. In the present experiments, urethane treatment altered placental morphology and impaired placental function, the latter indicated by down-regulated activity of cell cycle genes and of genes encoding cytokines and growth factors. Maternal immune stimulation with either Freund's complete adjuvant (FCA) or interferon-gamma (IFNγ) reduced morphologic damage to the placenta caused by urethane and normalized expression of several genes that were down-regulated by urethane. Urethane treatment also shifted placental cytokine gene expression toward a T cell helper 1 (Th1) profile, while immunostimulation tended to restore a Th2 profile that may be more beneficial to pregnancy and fetal development. These data suggest that the beneficial effects of maternal immune stimulation on fetal development in Teratogen-exposed mice may, in part, result from improved placental structure and function.
Charles C. Church - One of the best experts on this subject based on the ideXlab platform.
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Arrhenius thermodynamics and birth defects: Chemical Teratogen synergy. Untested, testable, and projected relevance.
Birth Defects Research Part C-embryo Today-reviews, 2013Co-Authors: Morton W. Miller, Charles C. ChurchAbstract:This article addresses the issue of hyperthermia-induced birth defects with an accompanying additional Teratogen, be it a Chemical or a physical agent (i.e., a simultaneous “combinational” exposure to two Teratogens, one of which is hyperthermia). Hyperthermia per se is a recognized human and animal Teratogen. An excellent example of such combinational exposures is an epileptic woman who becomes pregnant while taking valproic acid (VPA) to control seizures. VPA is a recognized Chemical Teratogen, and fever (hyperthermia) is not an uncommon event during pregnancy. While VPA also may occasionally induce fever as a side effect, we are concerned here with fevers arising from other, unrelated causes. There is a small but internally consistent literature on these combinational-Teratogen exposures involving hyperthermia plus a Chemical Teratogen; in each instance, the effect level has been observed to be synergistically elevated above levels induced by the separate Teratogenic components. The data were empirical. The observed synergy is, however, consistent with Arrhenius thermodynamics, a well-known Chemical rate equation. The need for information about combinational Teratogen exposures is acute; fever is a common occurrence during pregnancy; and there are many instances whereby there is also the simultaneous presence of some other Teratogen(s). Given that the rate of autism spectrum disorders in the United States was recently presented as 1 in 88 births, it seems reasonable to suspect that such combinational regimens are much more prevalent than previously thought. Our hypothesis is that synergistic birth defect levels from combinational regimens are consistent with Arrhenius thermodynamics. Birth Defects Research (Part C) 99:50–60, 2013. © 2013 Wiley Periodicals, Inc.
A.a Sharov - One of the best experts on this subject based on the ideXlab platform.
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Maternal immune stimulation reduces both placental morphologic damage and down-regulated placental growth-factor and cell cycle gene expression caused by urethane: are these events related to reduced Teratogenesis?
International immunopharmacology, 2003Co-Authors: L.v Sharova, A.a Sharov, P. Sura, Robert M. Gogal, Bonnie J. Smith, S.d. HolladayAbstract:Activation of the maternal immune system in mice decreased cleft palate caused by the Chemical Teratogen, urethane. Direct and indirect mechanisms for this phenomenon have been suggested, including maternal macrophages that cross the placenta to find and eliminate pre-Teratogenic cells, or maternal immune proteins (cytokines) that cross placenta to alleviate or partially alleviate toxicant-mediated effects in the developing fetus. A third mechanism to explain improved fetal developmental outcome in Teratogen-challenged pregnant mice might involve beneficial effects of immune stimulation on the placenta. In the present experiments, urethane treatment altered placental morphology and impaired placental function, the latter indicated by down-regulated activity of cell cycle genes and of genes encoding cytokines and growth factors. Maternal immune stimulation with either Freund's complete adjuvant (FCA) or interferon-gamma (IFNγ) reduced morphologic damage to the placenta caused by urethane and normalized expression of several genes that were down-regulated by urethane. Urethane treatment also shifted placental cytokine gene expression toward a T cell helper 1 (Th1) profile, while immunostimulation tended to restore a Th2 profile that may be more beneficial to pregnancy and fetal development. These data suggest that the beneficial effects of maternal immune stimulation on fetal development in Teratogen-exposed mice may, in part, result from improved placental structure and function.
P. Sura - One of the best experts on this subject based on the ideXlab platform.
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Maternal immune stimulation reduces both placental morphologic damage and down-regulated placental growth-factor and cell cycle gene expression caused by urethane: are these events related to reduced Teratogenesis?
International immunopharmacology, 2003Co-Authors: L.v Sharova, A.a Sharov, P. Sura, Robert M. Gogal, Bonnie J. Smith, S.d. HolladayAbstract:Activation of the maternal immune system in mice decreased cleft palate caused by the Chemical Teratogen, urethane. Direct and indirect mechanisms for this phenomenon have been suggested, including maternal macrophages that cross the placenta to find and eliminate pre-Teratogenic cells, or maternal immune proteins (cytokines) that cross placenta to alleviate or partially alleviate toxicant-mediated effects in the developing fetus. A third mechanism to explain improved fetal developmental outcome in Teratogen-challenged pregnant mice might involve beneficial effects of immune stimulation on the placenta. In the present experiments, urethane treatment altered placental morphology and impaired placental function, the latter indicated by down-regulated activity of cell cycle genes and of genes encoding cytokines and growth factors. Maternal immune stimulation with either Freund's complete adjuvant (FCA) or interferon-gamma (IFNγ) reduced morphologic damage to the placenta caused by urethane and normalized expression of several genes that were down-regulated by urethane. Urethane treatment also shifted placental cytokine gene expression toward a T cell helper 1 (Th1) profile, while immunostimulation tended to restore a Th2 profile that may be more beneficial to pregnancy and fetal development. These data suggest that the beneficial effects of maternal immune stimulation on fetal development in Teratogen-exposed mice may, in part, result from improved placental structure and function.