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Journal articles on the topic 'Embryopathies'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

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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2

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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3

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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4

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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5

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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6

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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7

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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8

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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9

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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10

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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11

Pannu, Harshbir Singh, Krishna Shiva Prakash, Rajinder Nahar R., Kona Sambha Murthy, Sethuratnam Rajan, Suresh Gururaj Rao, Rajratnam Karnan Kalyan Singh, and Kotturathu Mammen Cherian. "Surgical Treatment of Transposition of Great Arteries with Interrupted Pulmonary Artery: A Rare Association of Embryopathies." Journal of Cardiac Surgery 10, no. 3 (May 1995): 264–69. http://dx.doi.org/10.1111/j.1540-8191.1995.tb00608.x.

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12

Hunter, E. S., and T. W. Sadler. "The role of the visceral yolk sac in hyperglycemia-induced embryopathies in mouse embryos in vitro." Teratology 45, no. 2 (February 1992): 195–203. http://dx.doi.org/10.1002/tera.1420450213.

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13

Miller, Lutfiya, and Peter G. Wells. "Altered methanol embryopathies in embryo culture with mutant catalase-deficient mice and transgenic mice expressing human catalase." Toxicology and Applied Pharmacology 252, no. 1 (April 2011): 55–61. http://dx.doi.org/10.1016/j.taap.2011.01.019.

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14

Savchenko, L. V., V. I. Mikhalev, G. G. Chusova, V. I. Morgunova, and L. Yu Sashnina. "HEMATOLOGICAL AND BIOCHEMICAL INDICATORS OF COWS WHEN USING INTERFERON-TAU AND VITAMIN E FOR PREVENTION OF EMBRYOPATHIES." BULLETIN OF VETERINARY PHARMACOLOGY 2, no. 15 (2021): 52–61. http://dx.doi.org/10.17238/issn2541-8203.2021.2.52.

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15

Miller-Pinsler, Lutfiya, and Peter G. Wells. "Embryonic catalase protects against ethanol embryopathies in acatalasemic mice and transgenic human catalase-expressing mice in embryo culture." Toxicology and Applied Pharmacology 287, no. 3 (September 2015): 232–39. http://dx.doi.org/10.1016/j.taap.2015.06.007.

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16

Kasapinovic, Sonja, Gordon P. McCallum, Michael J. Wiley, and Peter G. Wells. "The peroxynitrite pathway in development: Phenytoin and benzo[a]pyrene embryopathies in inducible nitric oxide synthase knockout mice." Free Radical Biology and Medicine 37, no. 11 (December 2004): 1703–11. http://dx.doi.org/10.1016/j.freeradbiomed.2004.08.004.

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17

JESPERSEN, C., I. G. HELMUTH, and T. G. KRAUSE. "Varicella-zoster immunoglobulin treatment in pregnant women in Denmark from 2005 to 2015: descriptive epidemiology and follow-up." Epidemiology and Infection 144, no. 16 (August 18, 2016): 3426–34. http://dx.doi.org/10.1017/s0950268816001485.

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SUMMARYPrimary infection with varicella-zoster virus in pregnancy poses a risk of severe infection and embryopathies. Upon exposure, seronegative women are candidates for varicella-zoster immunoglobulin (VZIG). The aim of this paper was to describe risk factors for VZIG treatment including sources of varicella exposure and to study how many women developed clinical infection and received postpartum vaccination. We identified all pregnant women who received VZIG from December 2005 to March 2015. Additional information was obtained from Danish registers and a follow-up questionnaire. A total of 104 women were included and 88 completed the questionnaire. Significantly more women had ‘other country of origin’ than Denmark. They were more often second para (57%) and had most commonly been exposed to varicella by their own child (58%). Five women developed clinical varicella infection, and only 26·5% were vaccinated after delivery. The study concludes that few women developed infection after VZIG and none developed pneumonia. General practitioners should be particularly aware of obtaining varicella anamnesis in parous women from non-temperate countries in order to perform selective vaccination prior to pregnancy. In case of varicella exposure during pregnancy in a seronegative woman, postpartum vaccination is crucial.

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18

Shapiro, Aaron M., Lutfiya Miller-Pinsler, and Peter G. Wells. "Breast cancer 1 (BRCA1)-deficient embryos develop normally but are more susceptible to ethanol-initiated DNA damage and embryopathies." Redox Biology 7 (April 2016): 30–38. http://dx.doi.org/10.1016/j.redox.2015.11.005.

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19

Bhuller, Yadvinder, and Peter G. Wells. "A Developmental Role for Ataxia-Telangiectasia Mutated in Protecting the Embryo from Spontaneous and Phenytoin-Enhanced Embryopathies in Culture." Toxicological Sciences 93, no. 1 (June 21, 2006): 156–63. http://dx.doi.org/10.1093/toxsci/kfl045.

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20

Lee, Crystal J. J., Luisa L. Gonçalves, and Peter G. Wells. "Resistance of CD-1 and ogg1 DNA Repair–Deficient Mice to Thalidomide and Hydrolysis Product Embryopathies in Embryo Culture." Toxicological Sciences 122, no. 1 (April 19, 2011): 146–56. http://dx.doi.org/10.1093/toxsci/kfr084.

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21

Abramov, Julia P., and Peter G. Wells. "Embryonic catalase protects against endogenous and phenytoin‐enhanced DNA oxidation and embryopathies in acatalasemic and human catalase‐expressing mice." FASEB Journal 25, no. 7 (April 8, 2011): 2188–200. http://dx.doi.org/10.1096/fj.11-182444.

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22

Mathé, G. "Chromosome rearrangments: from embryopathies and cancer, to species evolution: in memoriam of Jerome Lejeune, the founder of human genetics." Biomedicine & Pharmacotherapy 48, no. 8-9 (January 1994): 333–34. http://dx.doi.org/10.1016/0753-3322(94)90046-9.

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23

Parker, Michael J., Katherine Teasdale, and Michael J. Parker. "The genetic assessment of looked after children: common reasons for referral and recent advances." Archives of Disease in Childhood 101, no. 6 (February 4, 2016): 581–84. http://dx.doi.org/10.1136/archdischild-2014-307215.

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Looked after children are recognised as generally having greater health needs than their peers. There are numerous potential causes, environmental and genetic, and the aetiology is often multifactorial. Assessments, especially clinical genetic ones, may be limited if the information available is incomplete or not shared. There have been some exciting recent advances in diagnostic genetic testing and more are on the horizon. However, we are currently only able to make a genetic diagnosis in less than half of patients, even when both parents are available for comparative testing. There may, therefore, remain an inevitable degree of residual uncertainty about the genetic contribution to a particular child's problems. There are increasing societal pressures for genetic information to be made available to individuals in general. However, there are significant considerations in carrier/predictive testing in children and we would maintain that looked after children should not be treated differently to other children in this regard, unless there is a compelling ‘best interest’ justification for so doing. Diagnostic criteria exist for fetal alcohol syndrome and other embryopathies and should be applied. Such should be considered as diagnoses of exclusion, so a child should not be prematurely labelled with these conditions, without fully assessing for the contribution of other factors, genetic or otherwise.

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24

Miller-Pinsler, Lutfiya, Amy Sharma, and Peter G. Wells. "Enhanced NADPH oxidases and reactive oxygen species in the mechanism of methanol-initiated protein oxidation and embryopathies in vivo and in embryo culture." Archives of Toxicology 90, no. 3 (March 1, 2015): 717–30. http://dx.doi.org/10.1007/s00204-015-1482-0.

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25

Ramin, Nicole, René Thieme, Sünje Fischer, Maria Schindler, Thomas Schmidt, Bernd Fischer, and Anne Navarrete Santos. "Maternal Diabetes Impairs Gastrulation and Insulin and IGF-I Receptor Expression in Rabbit Blastocysts." Endocrinology 151, no. 9 (July 14, 2010): 4158–67. http://dx.doi.org/10.1210/en.2010-0187.

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Women with type 1 diabetes are subfertile. Diabetes negatively affects pregnancy by causing early miscarriage and poor prenatal outcomes. In this study we examine consequences of maternal type 1 diabetes on early embryo development, metabolic gene expression, and the pattern of insulin receptor (IR) and IGF-I receptor (IGF-IR) distribution in rabbit blastocysts. In female rabbits, type 1 diabetes was induced by alloxan treatment. Six-day-old blastocysts were recovered and assessed for receptor distribution and metabolic gene expression. In vitro culture of blastocysts was performed in medium containing 1 mm, 10 mm, or 25 mm glucose, simulating normo- and hyperglycemic developmental condition in vitro. The fertility rate of the diabetic rabbits clearly mirrored subfertility with a drop in blastocyst numbers by 40% (13.3 blastocysts in diabetic vs. 21.9 in control females). In blastocysts onset and progression of gastrulation was delayed and expression of IR and IGF-IR and their metabolic target genes (hexokinase, phosphoenolpyruvate carboxykinase), both in vivo and in vitro, was down-regulated. The amount of apoptotic cells in the embryonic disc was increased, correlating closely with the reduced transcription of the bcl-x(L) gene. Blastocyst development is clearly impaired by type 1 diabetes during early pregnancy. Insulin-stimulated metabolic genes and IR and IGF-IR are down-regulated, resulting in reduced insulin and IGF sensitivity and a delay in development. Dysregulation of the IGF system and embryonic glucose metabolism are potential reasons for diabetogenous subfertility and embryopathies and start as soon as during the first days of life.

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26

Miller-Pinsler, Lutfiya, and Peter G. Wells. "Deficient DNA repair exacerbates ethanol-initiated DNA oxidation and embryopathies in ogg1 knockout mice: gender risk and protection by a free radical spin trapping agent." Archives of Toxicology 90, no. 2 (October 30, 2014): 415–25. http://dx.doi.org/10.1007/s00204-014-1397-1.

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27

Shabunin, Sergey, Vitaliy Mikhalev, Anatoly Nezhdanov, Vladimir Safonov, Pavel Parshin, and Polina Anipchenko. "PSVIII-16 Interferon-TAU in the pathogenesis and prevention of intrauterine growth restriction and embryonic death in dairy cows." Journal of Animal Science 98, Supplement_4 (November 3, 2020): 254–55. http://dx.doi.org/10.1093/jas/skaa278.459.

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Abstract The aim of the research was to assess the state of the hormonal and cytokine blood profiles of Holstein dairy cows during the early period of gestation with physiological formation of the embryo, its intrauterine growth restriction and death, clarify the pathogenetic mechanisms of these embryopathologies development and identify the efficacy of their prevention using recombinant bovine INFT. The dynamics of serum concentration of P4, cortisol (F) and cytokines: INFT, interleukin IL-2, tumor necrosis factor (TNFα), interferon-γ (INF-γ) at the physiological formation of the embryo (n = 9), its growth restriction (n = 9) and death (n = 8) were studied. The blood samples were obtained on the day of artificial insemination, during early blastogenesis (days 8–9), implantation of the embryo (days 15–16), the formation of primary genital organs (days 32–33), and at the end of the embryonic period of development (days 60–65). In cows with intrauterine growth restriction and embryonic death, serum concentration of P4, compared with the cows demonstrating their physiological formation, was lower by 14.0–30.1%, F - by 11.2–35.5%, INFT - by 21.0–37.7% when the content of IL-2 was exceeded by 46.5–310.5%, TNFα - by 11.7–36.2%, INF-γ - by 58.0–296.0%. A statistically significant positive correlative relationship between the content of INFT, P4, F and a negative one with the indices of the concentration of proinflammatory cytokines was found. Violation of the hormonal-cytokine balance in the organisms of fertilized animals is a universal pathogenetic mechanism for the development of early embryopathies. Injections of recombinant bovine INFT to inseminated cows during the pre- and implantation periods increased the level of progesterone production and reduced the synthesis of proinflammatory cytokines. The efficacy of insemination of cows increased by 1.96 times, the manifestation of fetal/embryonic intrauterine growth restriction syndrome decreased by 2.35 times in comparison with the control animals.

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28

Hannemann, Doreen, Reinhard Meister, Elisabeth Eléfant, Wolfgang Paulus, Thierry Vial, Minke Reuvers, Elisabeth Robert-Gnansia, et al. "Vitamin K antagonists and pregnancy outcome." Thrombosis and Haemostasis 95, no. 06 (2006): 949–57. http://dx.doi.org/10.1160/th06-02-0108.

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SummaryVitamin K antagonists (VKA) are known to act as teratogens; however, there is still uncertainty about the relative risk for birth defects and the most sensitive period. In a multi-centre (n=12), observational, prospective study we compared 666 pregnant women exposed to phenprocoumon (n=280), acenocoumarol (n=226), fluindione (n=99), warfarin (n=63) and phenindione (n=2) to a non-exposed control group (n=1,094). Data were collected by institutes collaborating in the European Network of Teratology Information Services (ENTIS) during individual risk counselling between 1988 and 2004. Main outcome measures were coumarin embryopathy and other birth defects, miscarriage rate, birth-weight, and prematurity. The rate of major birth defects after 1st trimester exposure was significantly increased (OR 3.86, 95% CI 1.86–8.00). However, there were only two coumarin embryopathies (0.6%; both phenprocoumon). Prematurity was more frequent (16.0% vs. 7.6%, OR 2.61, 95% CI 1.76–3.86), mean gestational age at delivery (37.9 vs. 39.4, p<0.001), and mean birth weight of term infants (3,166 g vs. 3,411 g; p<0.001) were lower compared to the controls. Using the methodology of survival analysis, miscarriage rate reached 42% vs. 14% (hazard ratio 3.36; 95% CI 2.28–4.93). In conclusion, use of VKA during pregnancy increases the risk of structural defects and other adverse pregnancy outcomes.The risk for coumarin embryopathy is, however, very small, in particular when therapy during the 1st trimester did not take place later than week 8 after the 1st day of the last menstrual period. Therefore, elective termination of a wanted pregnancy is not recommended if (inadvertent) exposure took place in early pregnancy. Close follow-up by the obstetrician including level II ultrasound should be recommended in any case of VKA exposure during pregnancy.

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29

SC, María, Pedro-José LE, Marina PS, and Carolina AM. "Umbilical Cord Hernia Associated with a Patent Urachus: A Case Report." Asploro Journal of Pediatrics and Child Health 2, no. 1 (January 30, 2020): 13–18. http://dx.doi.org/10.36502/2020/asjpch.6151.

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An umbilical cord hernia (UCH) is a form of abdominal wall defect, affecting 6 out of every 10,000 newborns. The persistence of urachus is an embryonic remnant that connects the bladder to the abdominal wall at the level of the umbilicus, being yet more uncommon. We reviewed the literature, searching in PubMed, under the terms “Hernia of umbilical cord”, “Congenital hernia of cord” and “Persistent Urachus”. Only a few similar cases of both pathologies associated described were found. Our main objective is to highlight the distinct clinical features, embryogenesis, prognosis and associated anomalies of two infrequent embryopathies. And to describe a infrequent case of both abnormalities presenting simultaneously. UCH are often misdiagnosed with other abdominal wall deffects, such as omphalocele, umbilical hernias, gastroschisis and umbilical cord cysts. The normal cord insertion, adequate muscle development of the abdominal wall and a wall defect less than 5cm is what differentiates it from an omphalocele. UCH has a low morbidity overall, as it is not associated with other anomalies. The most frequently observed urachal malformations are the persistence of a urachus and urachal cyst. The prenatal diagnosis of patent urachus is made by ultrasound or magnetic resonance, being easily mistaken with abdominal wall defects, confirming the diagnosis with an ultrasound at birth. The persistence of urachus may resolve spontaneously, if not, surgical resolution is recommended. Similar to a UCH, a patent urachus shows little association with other malformations. It is important to know the clinical presentation and the diagnostic perinatal methods employed for appropriate management and favorable results for both pathologies. This relies on knowing when to suspect possible associated anomalies and when complementary studies might be needed. It is also important to be aware that there is the possibility of a UCH and a patent urachus existing simultaneously.

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30

Peters, Klaus M. "Thalidomid-Embryopathie: eine vielfältige Katastrophe." Orthopädie & Rheuma 15, no. 2 (April 2012): 23–28. http://dx.doi.org/10.1007/s15002-012-0064-2.

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31

Bröcheler, J., and R. Halfmann. "Präsakrale Meningozele bei Thalidomid-Embryopathie." DMW - Deutsche Medizinische Wochenschrift 115, no. 25 (March 25, 2008): 977–79. http://dx.doi.org/10.1055/s-2008-1065108.

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32

Peters, Klaus M. "Thalidomid-Embryopathie: eine vielfältige Katastrophe." pädiatrie hautnah 26, no. 1 (February 2014): 44–47. http://dx.doi.org/10.1007/s15014-014-0309-4.

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33

MacKenzie, A., M. W. Ferguson, and P. T. Sharpe. "Hox-7 expression during murine craniofacial development." Development 113, no. 2 (October 1, 1991): 601–11. http://dx.doi.org/10.1242/dev.113.2.601.

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We have used in situ hybridisation to establish the temporal and spatial expression patterns of the mouse homeobox-containing gene; Hox-7, in the developing embryonic cranium and nervous system of the mouse between embryonic days 9.5 (E9.5) and E15.5. Hox-7 has previously been associated with areas of mesenchymal-epithelial interaction and cell migration especially in neural crest ectomesenchymal cells. Aside from the expression patterns seen in the facial anlage at E9.5, Hox-7 transcripts were also detected in the neuroepithelium including cells of the dorsal midline of the neural tube. This expression pattern persisted throughout the embryonic time span studied. At E11.5, expression of Hox-7 became obvious in the neuroepithelium of the forming tela choroida and the telencephelii in areas destined to form the choroid plexus before any atrophy of the neuroepithelium took place. High expression of Hox-7 was also present in the mesenchyme cells invading the pouch formed by the involuting choroid plexus neuroepithelium. A second major site where Hox-7 was expressed was the anlage of the anterior pituitary; the Rathke's pouch. Expression became obvious at E10.5 throughout the pouch but by E12.5 became more regionalised in areas of the pouch destined to form the pars distalis. Hox-7 was also expressed in the forming meninges and skull bone precursors from E10.5 onwards. Expression of the Hox-7 gene is also seen in the external ear, the forming eye, the nasal pits and forming Jacobson's organs. When these expression patterns are considered together with characterised human and mouse retinoic acid embryopathies and the congenital malformations seen in human children associated with deletion of chromosome 4p16.1 (Wolf-Hirschhorn syndrome), Hox-7 may be a good candidate as one of the genes involved in the initiation of the choroid plexus phenotype and its subsequent formation, the formation of the outer ear, formation of the dentition and the differentiation of the cell types of the anterior pituitary. The expression pattern of Hox-7 in the dorsal midline of the neural tube further suggests that it may also be involved in the specification of the dorsal-ventral axis of the developing nervous system.

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34

Nash, J. E., and T. V. N. Persaud. "Embryopathic risks of cigarette smoking." Experimental pathology 33, no. 2 (January 1988): 65–73. http://dx.doi.org/10.1016/s0232-1513(88)80127-0.

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35

Gröber, Uwe. "Folsäure." Zeitschrift für Orthomolekulare Medizin 15, no. 04 (December 2017): 23–27. http://dx.doi.org/10.1055/s-0043-123230.

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ZUSAMMENFASSUNGFolsäure erfüllt in seiner Wirkform Tetrahydrofolsäure essenzielle Funktionen in Zellwachstum und -teilung. Zur Verhinderung von Embryopathien durch Folsäuremangel in der Frühschwangerschaft wird die präkonzeptionelle Einnahme von Folsäure empfohlen. Im späteren Leben geht ein Mangel mit einer Risikoerhöhung für Demenz und kardiovaskuläre Komplikationen wie Schlaganfall einher. Diabetikern, Patienten mit kardiovaskulären Erkankungen und älteren Menschen sind Kontrollen des Homocysteinspiegels sowie ggf. Supplementierung von Folsäure und anderen B-Vitaminen anzuraten.

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36

Balde, M., G. Breitbach, A. Wettstein, W. Hoffmann, and G. Bastert. "Fallotsche Tetralogie nach Cumarineinnahme in der Frühschwangerschaft - eine Embryopathie?" Geburtshilfe und Frauenheilkunde 48, no. 03 (March 1988): 182–83. http://dx.doi.org/10.1055/s-2008-1035721.

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37

Reddy, A. K., S. N. Renganathan, A. E. Jayamohan, and P. M. Lakshmanan. "Gregg syndrome aka embryopathia rubeolaris: CT illustration." Case Reports 2014, jun09 1 (June 9, 2014): bcr2014204204. http://dx.doi.org/10.1136/bcr-2014-204204.

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38

Cohen, M. Michael. "Asymmetry: Molecular, biologic, embryopathic, and clinical perspectives." American Journal of Medical Genetics 101, no. 4 (2001): 292–314. http://dx.doi.org/10.1002/ajmg.1217.

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39

Merkl, M., S. Beblo, D. Wand, P. Nickel, A. Bigl, M. Landgraf, A. Merkenschlager, and M. K. Bernhard. "Cumarin-Embryopathie und palmoplantare Hyperkeratose bei einem 8-jährigen Jungen." Kinder- und Jugendmedizin 11, no. 04 (2011): 213–15. http://dx.doi.org/10.1055/s-0038-1629144.

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ZusammenfassungDie Einnahme von Cumarin (bzw. CumarinDerivaten) in der Schwangerschaft kann insbesondere im ersten Trimenon eine Embryo-pathie verursachen. Bei einem 8-jährigen Jungen wurde eine Cumarin-Embryopathie mit einer begleitenden paternal vererbten palmoplantaren Hyperkeratose diagnostiziert. Klinisch fielen insbesondere eine Mittelgesichtsdysplasie mit breiter Nasenwurzel, kleinen, tiefsitzenden Ohren, Brachy- und Syndaktylie auf. Die Handflächen und Fußsohlen zeigten eine Hyperkeratose. Eine begleitende leichte mentale Retardierung könnte auch verhal-tens- und umweltbedingte Sekundärfolge aufgrund des Kleinwuchses und der Dysmorphiezeichen sein.Bei potenziell schwangeren Frauen sollte eine Cumarin-Exposition möglichst vermieden werden. Eine therapeutische Alternative ist die (vorübergehende) Umstellung auf niedermolekulares Heparin.

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40

Schwaibold, H., Ch Wittekind, H. Schillinger, and N. Böhm. "Embryopathia und Fetopathia diabetica bei einem unreifen Totgeborenen." Klinische Pädiatrie 200, no. 02 (March 1988): 135–39. http://dx.doi.org/10.1055/s-2008-1033700.

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41

Tiboni, G. M., F. Marotta, A. P. Castigliego, and C. Rossi. "Impact of estrogen replacement on letrozole-induced embryopathic effects." Human Reproduction 24, no. 11 (July 27, 2009): 2688–92. http://dx.doi.org/10.1093/humrep/dep277.

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42

Rummler, S., R. Schulze, B. Leeder, and R. Kassem. "Die Coumarin-Embryopathie - eine erneut zu beobachtende Erkrankung des Neugeborenen? - Ein Fallbericht." Geburtshilfe und Frauenheilkunde 63, no. 01 (February 6, 2003): 70–73. http://dx.doi.org/10.1055/s-2003-37099.

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Kevekordes-Stade, B., L. Nährlich, C. Döbig, J. P. Guggenbichler, U. Mayer, and M. Fartasch. "Differentialdiagnose einer konnatalen Toxoplasmose bei Verdacht auf Embryopathie mit Pigmentstörungen der Netzhaut." Monatsschrift Kinderheilkunde 147, no. 1 (January 1999): 51–55. http://dx.doi.org/10.1007/s001120050398.

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Krämer, Johannes. "Reifes Neugeborenes mit Dysmorphiezeichen – seltene Embryopathie als vermeidbare Ursache von geistiger Behinderung." Der Gynäkologe 53, no. 4 (February 28, 2020): 265–68. http://dx.doi.org/10.1007/s00129-020-04574-7.

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Smoak, Ida W. "Embryopathie effects of the oral hypoglycemic agent chlorpropamide in cultured mouse embryos." American Journal of Obstetrics and Gynecology 169, no. 2 (August 1993): 409–14. http://dx.doi.org/10.1016/0002-9378(93)90098-4.

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Seyoum, G. G., and T. V. N. Persaud. "Can methionine and zinc prevent the embryopathic effects of alcohol?" Medical Hypotheses 34, no. 2 (February 1991): 153–56. http://dx.doi.org/10.1016/0306-9877(91)90185-2.

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Neumann, U., and Cornelia Schäfer‐Nolte. "Versuche zur induktion von embryopathien und konzentrations‐änderungen von alpha‐fetoprotein und serumalbumin beim hühnerembryo1." Avian Pathology 17, no. 2 (January 1988): 279–94. http://dx.doi.org/10.1080/03079458808436447.

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Torchinsky, Arkady, and Vladimir Toder. "Mechanisms of the embryo's response to embryopathic stressors: a focus on p53." Journal of Reproductive Immunology 85, no. 1 (May 2010): 76–80. http://dx.doi.org/10.1016/j.jri.2010.01.003.

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Smoak, Ida W., and Thomas W. Sadler. "Embryopathic effects of short-term exposure to hypoglycemia in mouse embryos in vitro." American Journal of Obstetrics and Gynecology 163, no. 2 (August 1990): 619–24. http://dx.doi.org/10.1016/0002-9378(90)91213-v.

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Smoak, I. W. "Embryopathic effects of diazoxide and the reduction of sulfonylurea-induced dysmorphogenesis in vitro." Toxicology in Vitro 8, no. 5 (October 1994): 1121–27. http://dx.doi.org/10.1016/0887-2333(94)90253-4.

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