Academic literature on the topic 'Embryopathies'

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Journal articles on the topic "Embryopathies"

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Menegola, Elena, Maria Luisa Broccia, Mariangela Prati, Rossana Ricolfi, and Erminio Giavini. "Glutathione Status in Diabetes-Induced Embryopathies." Neonatology 69, no. 5 (1996): 293–97. http://dx.doi.org/10.1159/000244323.

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Gheysen, Willem, and Debra Kennedy. "An update on maternal medication‐related embryopathies." Prenatal Diagnosis 40, no. 9 (July 28, 2020): 1168–77. http://dx.doi.org/10.1002/pd.5764.

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Sadler, T. W., E. S. Hunter, R. E. Wynn, and L. S. Phillips. "Evidence for Multifactorial Origin of Diabetes-Induced Embryopathies." Diabetes 38, no. 1 (January 1, 1989): 70–74. http://dx.doi.org/10.2337/diab.38.1.70.

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Andersen, Stine L. "Risk of embryopathies with use of antithyroidal medications." Current Opinion in Endocrinology & Diabetes and Obesity 24, no. 5 (October 2017): 364–71. http://dx.doi.org/10.1097/med.0000000000000353.

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Sadler, T. W., E. S. Hunter, R. E. Wynn, and L. S. Phillips. "Evidence for multifactorial origin of diabetes-induced embryopathies." Diabetes 38, no. 1 (January 1, 1989): 70–74. http://dx.doi.org/10.2337/diabetes.38.1.70.

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Burton, Graham J., Joanne Hempstock, and Eric Jauniaux. "Oxygen, early embryonic metabolism and free radical-mediated embryopathies." Reproductive BioMedicine Online 6, no. 1 (January 2003): 84–96. http://dx.doi.org/10.1016/s1472-6483(10)62060-3.

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Suzuki, K., D. Matsumaru, S. Matsushita, A. Murashima, M. Ludwig, H. Reutter, and G. Yamada. "Epispadias and the associated embryopathies: genetic and developmental basis." Clinical Genetics 91, no. 2 (October 10, 2016): 247–53. http://dx.doi.org/10.1111/cge.12871.

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Torchinsky, Arkady, and Vladimir Toder. "TNFalpha in the Pathogenesis of Diabetes-Induced Embryopathies: Functions and Targets." Review of Diabetic Studies 4, no. 4 (2007): 200–209. http://dx.doi.org/10.1900/rds.2007.4.200.

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Balkan, Wayne, L. S. Phillips, Steve Goldstein, and T. W. Sadler. "Potential role of somatomedin inhibitors in the production of diabetic embryopathies." Teratology 37, no. 3 (March 1988): 271–82. http://dx.doi.org/10.1002/tera.1420370313.

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Denno, Kelly M., and T. W. Sadler. "Phenylalanine and its metabolites induce embryopathies in mouse embryos in culture." Teratology 42, no. 5 (November 1990): 565–70. http://dx.doi.org/10.1002/tera.1420420513.

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Dissertations / Theses on the topic "Embryopathies"

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Robertson, Stephen. "Identification of the gene mutated in the otopalatodigital syndromes." Thesis, University of Oxford, 2002. http://ethos.bl.uk/OrderDetails.do?uin=uk.bl.ethos.249221.

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Freitag, Walburga. "Contergan eine genealogische Studie des Zusammenhangs wissenschaftlicher Diskurse und biographischer Erfahrungen." Münster New York München Berlin Waxmann, 2003. http://www.waxmann.com/kat/1503.hml.

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Stöckel, Cornelia [Verfasser]. "Reorganisation des primären somatosensorischen Kortex bei Thalidomid-Embryopathie / vorgelegt ovn Cornelia Stöckel." 2004. http://d-nb.info/974405353/34.

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Lee, Crystal J. J. "Molecular Mechanisms and Determinants of Species Sensitivity in Thalidomide Teratogenesis." Thesis, 2012. http://hdl.handle.net/1807/36210.

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The expanding therapeutic use of thalidomide (TD) remains limited by its species-specific teratogenicity in humans and rabbits, but not rodents. The R and S isomers of TD may be selectively responsible for its respective therapeutic and teratogenic effects, but rapid in vivo racemization makes this impossible to confirm. Fluorothalidomide (FTD), a fluorinated TD analogue with stable, non-racemizing isomers, may serve as a model compound for determining stereoselective effects. In vivo, FTD was undetectable in plasma, suggesting rapid breakdown, as confirmed in vitro, where FTD hydrolyzed up to 22-fold faster than TD. Unlike TD, FTD in pregnant rabbits and mice was highly toxic and lethal to both dams and fetuses. In rabbit embryo culture, FTD initiated optic (eye) vesicle and hindbrain but not classic limb bud embryopathies. Chemical instability, potent general toxicity and absence of limb bud embryopathies make FTD an unsuitable stereoselective model for TD teratogenesis. TD teratogenesis may involve its bioactivation by embryonic prostaglandin H synthases (PHSs) to a free radical intermediate that increases embryopathic reactive oxygen species (ROS) formation. However, the teratogenic potential of rapidly formed TD hydrolysis products and the determinants of species-specific teratogenesis are unclear. For some teratogens, mouse strains that are resistant in vivo are susceptible in embryo culture, suggesting maternal and/or placental determinants of risk. However, TD and two hydrolysis products, 2-phthalimidoglutaramic acid (PGMA) and 2-phthalimidoglutaraic acid (PGA), were non-embryopathic in CD-1 mouse embryo culture. Also, mice deficient in oxoguanine glycosylase 1 (OGG1), which repairs oxidatively damaged DNA, were resistant to TD embryopathies in culture and in vivo. Therefore, murine resistance to TD teratogenesis is dependent on embryonic factors, rather than maternal/placental determinants or increased DNA repair. In contrast, rabbit embryos exposed in culture to TD, PGMA and PGA exhibited head/brain, otic (ear) vesicle and classic limb bud embryopathies, validating the first mammalian embryo culture model for TD teratogenesis and providing the first evidence of a teratogenic role for TD hydrolysis products. Pretreatment with eicosatetraynoic acid (ETYA), a dual PHS/lipoxygenase inhibitor, or phenylbutylnitrone (PBN), a free radical spin trapping agent, completely blocked TD, PGMA and PGA-initiated embryopathies, implicating a PHS-dependent, ROS-mediated embryopathic mechanism.
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Seyoum, Girma G. "Influence of zinc and methionine on the embryopathic effects of ethanol in the rat." 1994. http://hdl.handle.net/1993/18436.

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Books on the topic "Embryopathies"

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Kennedy, Julia C. Antisense evidence for NF-[kappa]B-mediated signal transduction in the mechanism of phenytoin embryopathies. Ottawa: National Library of Canada, 2002.

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N, Fitch, and Paradice B. A, eds. Pathology of the human embryo and previable fetus: An atlas. New York: Springer-Verlag, 1990.

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Kennedy, Julia C. Antisense evidence for NF-kappa B-mediated signal transduction in the mechanism of phenytoin embryopathies. 2002, 2002.

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4

Töndury, G. Embryopathien: Über die Wirkungsweise von Viren auf den menschlichen Keimling. Springer, 2012.

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5

(Editor), Michael Chapman, J. G. Grudzinskas (Editor), and T. Chard (Editor), eds. The Embryo. Springer-Verlag Berlin and Heidelberg GmbH & Co. K, 1991.

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Book chapters on the topic "Embryopathies"

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Sadler, T. W., and Ulf J. Eriksson. "Animal Models for Diabetes-Induced Embryopathies." In Issues and Reviews in Teratology, 283–304. Boston, MA: Springer US, 1988. http://dx.doi.org/10.1007/978-1-4613-0929-1_7.

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Hashiloni-Dolev, Yael. "Abortions on Embryopathic Grounds: Policy and Practice in Israel and Germany." In A Life (Un)Worthy of Living, 83–104. Dordrecht: Springer Netherlands, 2007. http://dx.doi.org/10.1007/1-4020-5218-9_5.

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"Nutritional Disorders and Toxic Embryopathies." In Pediatric Pathology, 63–66. Boca Raton, FL : CRC Press/Taylor & Francis Group, 2017. |: CRC Press, 2016. http://dx.doi.org/10.1201/9781315382531-16.

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