Journal articles: 'Fetal effects'

1

Chiriboga, Claudia A. "Fetal Effects." Neurologic Clinics 11, no. 3 (August 1993): 707–28. http://dx.doi.org/10.1016/s0733-8619(18)30147-6.

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ONGUN, Hakan, Kıymet ÇELİK, and Nihal OYGÜR. "Chorioamnionitis and Its Fetal Effects." Turkiye Klinikleri Journal of Pediatrics 29, no. 3 (2020): 175–86. http://dx.doi.org/10.5336/pediatr.2020-76142.

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Hanson, James W. "Fetal hydantoin effects." Teratology 33, no. 3 (June 1986): 349–53. http://dx.doi.org/10.1002/tera.1420330314.

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4

Goldman, Jacquelin. "Fetal Alcohol Syndrome and Fetal Alcohol Effects." Journal of Clinical Child Psychology 14, no. 1 (March 1985): 82. http://dx.doi.org/10.1207/s15374424jccp1401_14.

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5

Houme, H. Eugene, and Carol L. Clericuzio. "1295 FETAL PRIMIDONE EFFECTS." Pediatric Research 19, no. 4 (April 1985): 326A. http://dx.doi.org/10.1203/00006450-198504000-01319.

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6

Woodson, R. H. "Review of Fetal Alcohol Syndrome and Fetal Alcohol Effects." Contemporary Psychology: A Journal of Reviews 30, no. 7 (July 1985): 584. http://dx.doi.org/10.1037/023959.

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7

Alvear, J., S. Andreani, P. Vargas, F. Cortes, and P. De Valdivia. "Fetal Alcohol Syndrome and Fetal Alcohol Effects, Psicomotor Development20." Pediatric Research 42, no. 6 (December 1997): 923. http://dx.doi.org/10.1203/00006450-199712000-00053.

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Frost, Mackenzie S., Aqib H. Zehri, Sean W. Limesand, William W. Hay, and Paul J. Rozance. "Differential Effects of Chronic Pulsatile versus Chronic Constant Maternal Hyperglycemia on Fetal Pancreaticβ-Cells." Journal of Pregnancy 2012 (2012): 1–8. http://dx.doi.org/10.1155/2012/812094.

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Constant maternal hyperglycemia limits, while pulsatile maternal hyperglycemia may enhance, fetal glucose-stimulated insulin secretion (GSIS) in sheep. However, the impact of such different patterns of hyperglycemia on the development of the fetalβ-cell is unknown. We measured the impact of one week of chronic constant hyperglycemia (CHG,n=6) versus pulsatile hyperglycemia (PHG,n=5) versus controls (n=7) on the percentage of the fetal pancreas staining for insulin (β-cell area), mitotic and apoptotic indices and size of fetalβ-cells, and fetal insulin secretion in sheep. Baseline insulin concentrations were higher in CHG fetuses (P<0.05) compared to controls and PHG. GSIS was lower in the CHG group (P<0.005) compared to controls and PHG. PHGβ-cell area was increased 50% (P<0.05) compared to controls and CHG. CHGβ-cell apoptosis was increased over 400% (P<0.05) compared to controls and PHG. These results indicate that late gestation constant maternal hyperglycemia leads to significantβ-cell toxicity (increased apoptosis and decreased GSIS). Furthermore, pulsatile maternal hyperglycemia increases pancreaticβ-cell area but did not increase GSIS, indicating decreasedβ-cell responsiveness. These findings demonstrate differential effects that the pattern of maternal hyperglycemia has on fetal pancreaticβ-cell development, which might contribute to later life limitation in insulin secretion.

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Saji, Haruya, Michiko Yamanaka, Akiko Hagiwara, and Rieko Ijiri. "Losartan and fetal toxic effects." Lancet 357, no. 9253 (February 2001): 363. http://dx.doi.org/10.1016/s0140-6736(00)03648-5.

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10

Froelich, M. A., T. Y. Euliano, and D. Caton. "FETAL EFFECTS OF MATERNAL ANALGOSEDATION." Anesthesiology 96, no. 4 (April 1, 2002): NA. http://dx.doi.org/10.1097/00000542-200201000-00100.

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11

Froelich, M. A., T. Y. Euliano, and D. Caton. "FETAL EFFECTS OF MATERNAL ANALGOSEDATION." Anesthesiology 96 (April 2002): 1. http://dx.doi.org/10.1097/00000542-200204001-00100.

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12

Chiriboga, Claudia A. "FETAL DRUG AND ETHANOL EFFECTS." CONTINUUM: Lifelong Learning in Neurology 10 (October 2004): 151–77. http://dx.doi.org/10.1212/01.con.0000293614.22581.30.

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13

Holmes, Lewis B. "Fetal Effects of Anticonvulsant Polytherapies." Archives of Neurology 68, no. 10 (October 1, 2011): 1275. http://dx.doi.org/10.1001/archneurol.2011.133.

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14

Lundborg, Per. "FETAL EFFECTS OF ANTIHYPERTENSIVE DRUGS." Acta Medica Scandinavica 205, S628 (April 24, 2009): 95–97. http://dx.doi.org/10.1111/j.0954-6820.1979.tb00793.x.

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15

Chiriboga, Claudia A. "Fetal Alcohol and Drug Effects." Neurologist 9, no. 6 (November 2003): 267–79. http://dx.doi.org/10.1097/01.nrl.0000094941.96358.d1.

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16

Nadel, Meryl. "Offspring With Fetal Alcohol Effects:." Alcoholism Treatment Quarterly 2, no. 1 (March 15, 1985): 105–16. http://dx.doi.org/10.1300/j020v02n01_09.

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17

Salisbury, Amy L., Kathryn L. Ponder, James F. Padbury, and Barry M. Lester. "Fetal Effects of Psychoactive Drugs." Clinics in Perinatology 36, no. 3 (September 2009): 595–619. http://dx.doi.org/10.1016/j.clp.2009.06.002.

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18

Philipps, A. F., T. S. Rosenkrantz, R. M. Clark, I. Knox, D. G. Chaffin, and J. R. Raye. "Effects of Fetal Insulin Deficiency on Growth in Fetal Lambs." Diabetes 40, no. 1 (January 1, 1991): 20–27. http://dx.doi.org/10.2337/diab.40.1.20.

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19

Philipps, A. F., T. S. Rosenkrantz, R. M. Clark, I. Knox, D. G. Chaffin, and J. R. Raye. "Effects of fetal insulin deficiency on growth in fetal lambs." Diabetes 40, no. 1 (January 1, 1991): 20–27. http://dx.doi.org/10.2337/diabetes.40.1.20.

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20

Conry, Julianne. "Neuropsychological Deficits in Fetal Alcohol Syndrome and Fetal Alcohol Effects." Alcoholism: Clinical and Experimental Research 14, no. 5 (October 1990): 650–55. http://dx.doi.org/10.1111/j.1530-0277.1990.tb01222.x.

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21

Löser. "Alcohol and pregnancy – fetal alcohol syndrome and fetal alcohol effects." Therapeutische Umschau 57, no. 4 (April 1, 2000): 246–52. http://dx.doi.org/10.1024/0040-5930.57.4.246.

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Alkoholembryopathie ist ein spezifisches polydystrophes Fehlbildungsmuster, das diagnostisch durch folgende Kriterien zu sichern ist: 1. Alkoholabhängigkeit oder -mißbrauch der Mutter in der Schwangerschaft 2. Wachstumsstörungen in Gewicht, Länge und Kopfumfang 3. Multiple Minor- und Majoranomalien als Hemmungsmißbildungen 4. Organische zerebrale und zerebelläre Veränderungen, Hirnleistungsschwächen, Wesensveränderungen und Verhaltensstörungen. Die sogenannten Alkoholeffekte («fetal alcohol effects») als Schwachformen mit überwie-gend neurotoxischen neuropsychologischen Auswirkungen sind mehrfach häufiger als das Vollbild der Alkoholembryopathie; sie bleiben meist unerkannt, werden übersehen, sind phänotypisch unspezifisch und daher schwer zu diagnostizieren. Alkohol in der Schwangerschaft ist heute der bedeutsamste Schadstoff für Embryo und Feten und eine der häufigsten Ursachen einer geistigen Entwicklungsstörung, mit langzeitigen, irreversiblen Folgen für das Kind in der Schule, der sozialen Reifung und der Lebensführung. Der Alkohol selbst und der Azetaldehyd bewirken die zytotoxischen Schäden. Eine sichere Konsumdosis der Verträglichkeit ist nicht bekannt. Die Diagnose wird nicht laborchemisch, sondern anamnestisch und klinisch gestellt. Das Risiko einer späteren Suchtentwicklung kann bei diesen Kindern auf über 20% geschätzt werden.

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22

Philipps, A. F., T. S. Rosenkrantz, M. L. Grunnet, M. E. Connolly, P. J. Porte, and J. R. Raye. "Effects of Fetal Insulin Secretory Deficiency on Metabolism in Fetal Lamb." Diabetes 35, no. 9 (September 1, 1986): 964–72. http://dx.doi.org/10.2337/diab.35.9.964.

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23

Walsh, Jennifer M., Ricardo Segurado, Rhona M. Mahony, Michael E. Foley, and Fionnuala M. McAuliffe. "The Effects of Fetal Gender on Maternal and Fetal Insulin Resistance." PLOS ONE 10, no. 9 (September 14, 2015): e0137215. http://dx.doi.org/10.1371/journal.pone.0137215.

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24

WANG, XUEGONG, LORRAINE TAFRA, RONALD BEREZNIAK, RICARDO V. LLOYD, LISA MURAIKA, and DONALD C. DAFOE. "EFFECTS OF COTRANSPLANTED FETAL LIVER ON FETAL PANCREAS ISOGRAFTS 1, 2." Transplantation 53, no. 2 (February 1992): 272–76. http://dx.doi.org/10.1097/00007890-199202010-00004.

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25

Philipps, A. F., T. S. Rosenkrantz, M. L. Grunnet, M. E. Connolly, P. J. Porte, and J. R. Raye. "Effects of fetal insulin secretory deficiency on metabolism in fetal lamb." Diabetes 35, no. 9 (September 1, 1986): 964–72. http://dx.doi.org/10.2337/diabetes.35.9.964.

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26

Malinowski, Ann Kinga, Jonathan Sen, and Mathew Sermer. "Hyperreactio Luteinalis: Maternal and Fetal Effects." Journal of Obstetrics and Gynaecology Canada 37, no. 8 (August 2015): 715–23. http://dx.doi.org/10.1016/s1701-2163(15)30176-6.

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27

Hale, R. "Effects of hypothyroidism on fetal development." ACOG Clinical Review 6, no. 5 (October 2001): 12. http://dx.doi.org/10.1016/s1085-6862(01)80058-3.

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28

Pearce, William J. "Fetal Cerebrovascular Maturation: Effects of Hypoxia." Seminars in Pediatric Neurology 28 (December 2018): 17–28. http://dx.doi.org/10.1016/j.spen.2018.05.003.

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29

Bates, Shannon M., and Jeffrey S. Ginsberg. "5 Anticoagulants in pregnancy: fetal effects." Baillière's Clinical Obstetrics and Gynaecology 11, no. 3 (September 1997): 479–88. http://dx.doi.org/10.1016/s0950-3552(97)80023-5.

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30

Riley, Edward P., Jennifer D. Thomas, Charles R. Goodlett, Anna Y. Klintsova, William T. Greenough, Basalingappa L. Hungund, F. Zhou, Y. Sari, T. Powrozek, and Ting-Kai Li. "Fetal Alcohol Effects: Mechanisms and Treatment." Alcoholism: Clinical and Experimental Research 25, s1 (May 2001): 110S—116S. http://dx.doi.org/10.1111/j.1530-0277.2001.tb02384.x.

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31

Souter, Dereck, Jane Harding, Lesley McCowan, Clare O'Donnell, Elisabeth McLeay, and Helen Baxendale. "Antenatal Indomethacin-Adverse Fetal Effects Confirmed." Australian and New Zealand Journal of Obstetrics and Gynaecology 38, no. 1 (February 1998): 11–16. http://dx.doi.org/10.1111/j.1479-828x.1998.tb02949.x.

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32

Souter, Dereck, Jane Harding, Lesley McCowan, Clare O'Donnell, Elisabeth McLeay, and Helen Baxendale. "Antenatal Indomethacin-Adverse Fetal Effects Confirmed." Australian and New Zealand Journal of Obstetrics and Gynaecology 39, no. 1 (February 1999): 11–16. http://dx.doi.org/10.1111/j.1479-828x.1999.tb03019.x.

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33

Abramowicz, Jacques S., Stanley B. Barnett, Francis A. Duck, Peter D. Edmonds, Kullervo H. Hynynen, and Marvin C. Ziskin. "Fetal Thermal Effects of Diagnostic Ultrasound." Journal of Ultrasound in Medicine 27, no. 4 (April 2008): 541–59. http://dx.doi.org/10.7863/jum.2008.27.4.541.

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34

Farrar, Henry C., and Jeffrey L. Blumer. "Fetal Effects of Maternal Drug Exposure." Annual Review of Pharmacology and Toxicology 31, no. 1 (April 1991): 525–47. http://dx.doi.org/10.1146/annurev.pa.31.040191.002521.

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35

Golub, Mari S., Farla L. Kaufman, Marlissa A. Campbell, Ling-Hong Li, and James M. Donald. "“Natural” progesterone: information on fetal effects." Birth Defects Research Part B: Developmental and Reproductive Toxicology 77, no. 5 (2006): 455–70. http://dx.doi.org/10.1002/bdrb.20089.

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36

Chawla, Deepak. "Fetal Effects of Maternal Iron Deficiency." Indian Journal of Pediatrics 82, no. 12 (October 16, 2015): 1080–81. http://dx.doi.org/10.1007/s12098-015-1904-2.

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37

Gallant, Donald M. "ETHANOL EFFECTS ON FETAL CEREBRAL CORTEX." Alcoholism: Clinical and Experimental Research 11, no. 2 (April 1987): 190. http://dx.doi.org/10.1111/j.1530-0277.1987.tb01290.x.

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38

Simamura, Eriko, Hiroki Shimada, Hiroki Shoji, Hiroki Otani, and Toshihisa Hatta. "Effects of melanocortins on fetal development." Congenital Anomalies 51, no. 2 (May 20, 2011): 47–54. http://dx.doi.org/10.1111/j.1741-4520.2011.00316.x.

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39

Zana, Michela, Francesca Magli, Alessandra Mazzucchi, Elisa Castoldi, Daniele Gibelli, Giulia Caccia, Francesca Cornacchia, Daniel A. Gaudio, Mirko Mattia, and Cristina Cattaneo. "Effects of Cremation on Fetal Bones." Journal of Forensic Sciences 62, no. 5 (January 25, 2017): 1140–44. http://dx.doi.org/10.1111/1556-4029.13414.

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40

Tabor, Bannie L., and Alex Soffici. "Cocaine effects on fetal behavioral state." American Journal of Obstetrics and Gynecology 163, no. 4 (October 1990): 1364–65. http://dx.doi.org/10.1016/0002-9378(90)90722-j.

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41

Norman, Andrew B., Michael N. Lehman, and Paul R. Sanberg. "Functional effects of fetal striatal transplants." Brain Research Bulletin 22, no. 1 (January 1989): 163–72. http://dx.doi.org/10.1016/0361-9230(89)90141-x.

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42

Lingman, Göran, and Karel Maršál. "Circulatory effects of fetal cardiac arrhythmias." Pediatric Cardiology 7, no. 2 (June 1986): 67–74. http://dx.doi.org/10.1007/bf02328953.

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43

Stonestreet, B. S., M. Goldstein, W. Oh, and J. A. Widness. "Effects of prolonged hyperinsulinemia on erythropoiesis in fetal sheep." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 257, no. 5 (November 1, 1989): R1199—R1204. http://dx.doi.org/10.1152/ajpregu.1989.257.5.r1199.

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Offspring of diabetic mothers have an increased incidence of neonatal polycythemia, decreased oxygen tension in cord blood at delivery, and elevated plasma erythropoietin levels at birth. Experimental fetal hyperinsulinemia has been associated with reduced fetal oxygen content and increased erythropoietin concentration. To test the hypothesis that prolonged fetal hyperinsulinemia results in increased fetal erythropoiesis and red cell volume during gestation, we infused insulin or placebo for 11 +/- 0.2 (+/- SE) days into chronically catheterized fetal sheep, beginning at 124 days of gestation. Indices of fetal erythropoiesis, red cell and blood volume were measured before and during the infusions. Insulin infusion resulted in increased plasma insulin, decreased plasma glucose, and decreased oxygen saturation values. The nucleated red blood cell (RBC) and RBC counts were significantly higher in the insulin- compared with the placebo-treated fetal sheep after 6-8 and 9-12 days of infusion, respectively. Although erythropoietin concentration did not differ between the groups, red cell volume expressed as a change from the base-line value was significantly higher in the insulin-treated group. We conclude that prolonged fetal hyperinsulinemia augmented erythropoiesis and red cell volume during late gestation in fetal sheep.

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44

Agnew, C. L., M. G. Ross, Y. Fujino, M. G. Ervin, L. Day, and L. K. Kullama. "Maternal/fetal dehydration: prolonged effects and responses to oral rehydration." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 264, no. 1 (January 1, 1993): R197—R203. http://dx.doi.org/10.1152/ajpregu.1993.264.1.r197.

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Dehydration induces marked alterations in maternal-fetal fluid homeostasis and accompanying fetal endocrine responses. We sought to determine if the increase in fetal plasma arginine vasopressin (AVP) levels during maternal dehydration is mediated by fetal plasma hypovolemia in addition to hyperosmolality and to examine maternal and fetal plasma atrial natriuretic factor (ANF) responses to maternal dehydration and oral rehydration. Seven pregnant ewes (127 +/- 1 day) were water deprived for 72-96 h, and five of these were orally rehydrated. Dehydration induced significant increases in maternal plasma osmolality (pOSM) (300 +/- 2 to 325 +/- 8 mosmol/kg) and AVP (3.0 +/- 0.4 to 18.9 +/- 4.0 pg/ml), and decreases in plasma ANF levels (28.1 +/- 3.1 to 19.7 +/- 3.1 pg/ml). Fetal pOSM (293 +/- 3 to 314 +/- 4 mosmol/kg), AVP (2.5 +/- 0.6 to 8.1 +/- 4.8 pg/ml), and urinary fractional sodium excretion increased significantly, whereas plasma ANF and fetal blood volume did not change. After maternal water access maternal plasma AVP decreased rapidly in comparison to the gradual decrease in maternal pOSM. Fetal plasma AVP levels did not change significantly and fetal pOSM decreased more slowly than maternal pOSM. Fetal plasma ANF increased in association with increased urine flow and glomerular filtration rate after maternal rehydration. These data indicate marked differences in fetal and maternal plasma ANF and AVP responses with dehydration-induced increases in fetal plasma AVP being secondary to plasma hyperosmolality, rather than hypovolemia. Rapid suppression of maternal plasma AVP may contribute to the slower equilibration of fetal pOSM during oral, as compared with intravenous, maternal rehydration.

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45

Leury, B. J., K. D. Chandler, A. R. Bird, and A. W. Bell. "Effects of maternal undernutrition and exercise on glucose kinetics in fetal sheep." British Journal of Nutrition 64, no. 2 (September 1990): 463–72. http://dx.doi.org/10.1079/bjn19900046.

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Fetal glucose kinetics were measured using a combination of isotope-dilution and Fick-principle methodology in single-pregnant ewes which were either well-fed throughout, or fed at 0.3–0.4 predicted energy requirement for 7–21 d during late pregnancy. All ewes were studied while standing at rest and then while walking on a treadmill at 0.7 m/s on a 10° slope for 60 min. Underfed ewes suffered major decreases in fetal total disposal rate, fetal-placental transfer and umbilical net uptake of glucose, each of which were significantly related to declines in maternal and fetal blood glucose concentrations respectively. In well-fed ewes, fetal endogenous glucose production was negligible, as indicated by the similarity between fetal utilization rate (total glucose disposal rate minus placental uptake of fetal glucose) and umbilical net uptake of glucose, and by nearly identical fetal and maternal arterial blood specific radioactivities of maternally infused D-[2-3H]glucose. By contrast, in underfed ewes, fetal utilization rate greatly exceeded umbilical net uptake of glucose, and the fetal:maternal [3H]glucose specific activity ratio declined significantly, suggesting induction of a substantial rate of fetal endogenous glucogenesis. Exercise caused increases in fetal total glucose disposal rate and glycaemia in fed and underfed ewes. In underfed ewes only, this was accompanied by increased placental uptake of fetal glucose and umbilical net glucose uptake, unchanged fetal glucose utilization and decreased fetal endogenous glucose production. It is concluded that fetal gluconeogenesis makes a major contribution to fetal glucose requirements in undernourished ewes. Increased maternal supply of fetal glucose during exercise substitutes for rather than adds to fetal endogenous glucogenesis.

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46

Meyer, B. A., S. W. Walsh, and V. M. Parisi. "Hemodynamic effects of leukotriene C4 in ovine fetus." American Journal of Physiology-Endocrinology and Metabolism 259, no. 6 (December 1, 1990): E851—E855. http://dx.doi.org/10.1152/ajpendo.1990.259.6.e851.

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Leukotrienes are synthesized during pregnancy and produce cardiovascular effects in adults. We hypothesized that leukotriene C4 would cause vasoconstriction in the fetus and placenta. Eight near-term, unanesthetized ovine fetuses were studied before and after infusion of 10 micrograms leukotriene C4 (LTC4) into the fetal vena cava. Cardiovascular monitoring of maternal and fetal arterial pressures and heart rates was performed. Fetal blood flows were measured by the radioactive-microsphere technique. Sustained elevations in systolic and diastolic blood pressure and decreased fetal heart rate began by 1 min and returned to baseline by 30 min. Arterial pH fell from 7.33 +/- 0.01 to 7.29 +/- 0.01 at 15 min (P less than 0.05) and to 7.29 +/- 0.01 at 30 min (P less than 0.05), with a significant increase in base deficit from 0.7 +/- 0.7 to 3.5 +/- 0.7 at 15 min (P less than 0.05) and to 2.9 +/- 1.0 at 30 min (P less than 0.05). Fetal PO2 and PCO2 were unchanged. Significant decreases in blood flow and resistance were seen in the umbilical placental circulation as well as in fetal skeletal muscle and intestine. Blood flow and resistance were unchanged in the renal and adrenal vascular beds. Fetal administration of LTC4 caused no changes in maternal cardiovascular parameters. These findings represent the first in vivo studies of the effects of a lipoxygenase metabolite on fetal-placental blood flow.

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47

Yilmaz, Osman, and Ayhan Şule Göncü. "Effects of nifedipine on fetal cardiac function in preterm labor." Journal of Perinatal Medicine 48, no. 7 (September 25, 2020): 723–27. http://dx.doi.org/10.1515/jpm-2020-0160.

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AbstractObjectivesTo evaluate the effects of nifedipine treatment on fetal hemodynamics and cardiac function during preterm labor. This prospective study assessed several quantitative parameters of fetal cardiac circulation and function, and found no significant changes at 48 h after nifedipine treatment. These findings suggest that tocolytic nifedipine may be safe for fetuses. It supports clinicians to use nifedipine treatment for tocolysis without any cardiac effect on the fetus.MethodsA prospective cohort study was conducted at a tertiary hospital between January 2016 and October 2017. A total of 45 pregnant women who required nifedipine for preterm labor were included in this study. Fetal Doppler ultrasound was performed and fetal systolic and diastolic function was measured prior to, and 48 h after, the first nifedipine treatment. Conventional Doppler parameters were used to evaluate fetal heart function and hemodynamic changes. Tricuspid annular plane systolic excursion, mitral annular plane systolic excursion and the sphericity index were also evaluated to assess changes in fetal cardiac morphology.ResultsNo significant changes in fetal Doppler parameters were observed following nifedipine tocolysis. There was no significant difference in the fetal cardiac function parameters of both ventricles before vs. after nifedipine treatment. Tricuspid annular plane systolic excursion, mitral annular plane systolic excursion, and sphericity index values were unchanged following nifedipine treatment.ConclusionsOral administration of nifedipine did not to alter fetal cardiac function or morphology. Fetal cardiac parameters and various Doppler indices were unchanged following nifedipine treatment. Maternal nifedipine treatment does not appear to have any significant effect on fetal cardiac function.

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48

Räsänen, Juha. "The Effects of Ritodrine Infusion on Fetal Myocardial Function and Fetal Hemodynamics." Acta Obstetricia et Gynecologica Scandinavica 69, no. 6 (January 1990): 487–92. http://dx.doi.org/10.3109/00016349009013323.

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49

Famy, Chris, Ann P. Streissguth, and Alan S. Unis. "Mental Illness in Adults With Fetal Alcohol Syndrome or Fetal Alcohol Effects." American Journal of Psychiatry 155, no. 4 (April 1998): 552–54. http://dx.doi.org/10.1176/ajp.155.4.552.

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50

Hales, David A., and Gail S. Hales. "Fetal alcohol syndrome and fetal alcohol effects: A selected list of sources." Reference Services Review 23, no. 2 (February 1995): 79–96. http://dx.doi.org/10.1108/eb049248.

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Journal articles on the topic 'Fetal effects'

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