Статті в журналах: "Prenatal events"

1

Millichap, J. Gordon. "Prenatal Events and CNS Migration Disorders." Pediatric Neurology Briefs 8, no. 12 (December 1, 1994): 94. http://dx.doi.org/10.15844/pedneurbriefs-8-12-9.

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Herbison, Carly E., Karina Allen, Monique Robinson, John Newnham, and Craig Pennell. "The impact of life stress on adult depression and anxiety is dependent on gender and timing of exposure." Development and Psychopathology 29, no. 4 (April 11, 2017): 1443–54. http://dx.doi.org/10.1017/s0954579417000372.

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AbstractThere is debate about the relative importance of timing of stressful events prenatally and over the life course and risk for subsequent depressive/anxious illness. The aim of this study was to examine the relative roles of prenatal stress and postnatal stress trajectories in predicting depression and anxiety in early adulthood in males and females. Exposure to life stress events was examined in the Western Australian Pregnancy Cohort (Raine) Study during pregnancy and ages 1, 2, 3, 5, 8, 10, 14, and 17 years. At age 20, offspring completed the Depression Anxiety Stress Scale. Prenatal stress and trajectories of stress events from age 1 to 17 were analyzed in linear regression analyses. Five postnatal stress trajectories were identified. In females, medium to high chronic stress exposure or exposure during puberty/adolescence predicted depression and anxiety symptoms while low or reduced stress exposure over the life course did not, after adjustment for relevant confounders. High stress early in pregnancy contributed to male depression/anxiety symptoms independent of postnatal stress trajectory. In females, postnatal stress trajectory was more important than prenatal stress in predicting depression/anxiety symptoms. Interventions focused on reducing and managing stress events around conception/pregnancy and exposure to chronic stress are likely to have beneficial outcomes on rates of depression and anxiety in adults.

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Aderibigbe, Y. A., Oye Gureje, and O. Omigbodun. "Postnatal Emotional Disorders in Nigerian Women." British Journal of Psychiatry 163, no. 5 (November 1993): 645–50. http://dx.doi.org/10.1192/bjp.163.5.645.

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One hundred and sixty-two women were evaluated for psychiatric morbidity in the second trimester of pregnancy and also six to eight weeks postnatally. A sizeable proportion of the women also had a second prenatal assessment in their third trimester and in the lying-in ward shortly after giving birth. Assessments were conducted with the 28-item GHQ. This was initially validated using a subsample of 106 women, taken from the original group, who were interviewed with the PAS. Thirty per cent of the women were ‘cases' at the first prenatal assessment, while only 14% were ‘cases' six to eight weeks postnatally. Thus, even though there was an overlap between prenatal and postnatal morbidity, there was also substantial difference between the groups that were symptomatic at both periods. This observation was reinforced by the low correlation between the mean GHQ scores at both periods. Both prenatal and postnatal morbidities were associated with recent adverse life events, with the latter more likely to be associated with marital and family events. This observation is in support of the view that neurotic problems, prenatally or postnatally, are caused mainly by psychosocial factors.

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4

Huttunen, Matti O., Ricardo A. Machon, and Sarnoff A. Mednick. "Prenatal Factors in the Pathogenesis of Schizophrenia." British Journal of Psychiatry 164, S23 (April 1994): 15–19. http://dx.doi.org/10.1192/s0007125000292684.

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The excess of winter–spring births among individuals suffering from schizophrenia provides strong evidence for the existence of some prenatally occurring factors in the pathogenesis of schizophrenia. Recent epidemiological findings suggest that maternal viral infections during the second trimester of pregnancy may play a crucial role in the aetiology of adult schizophrenia. A ‘two-hit window’ hypothesis of the mechanism of action of prenatal factors in the pathogenesis of schizophrenia suggests at least two time-specific prenatal aetiological events. The observed association between prenatal viral infection and increased incidence of adult schizophrenia need not be a direct cytotoxic result of the viral infection, but may be caused indirectly, for example from foetal minor cerebral haemorrhages produced by the anticoagulant effects of aspirin.

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5

Lipton, L. R., K. J. Brunst, S. Kannan, Y. M. Ni, H. B. Ganguri, R. J. Wright, and M. Bosquet Enlow. "Associations among prenatal stress, maternal antioxidant intakes in pregnancy, and child temperament at age 30 months." Journal of Developmental Origins of Health and Disease 8, no. 6 (June 27, 2017): 638–48. http://dx.doi.org/10.1017/s2040174417000411.

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Prenatal stress and prenatal nutrition each have demonstrable impact on fetal development, with implications for child neurodevelopment and behavior. However, few studies have examined their joint influences despite evidence of potential interactive effects. We examined associations among prenatal stress, prenatal antioxidant intakes, and child temperament in a sociodemographically diverse pregnancy cohort (N=137 mother–child dyads). In mid-pregnancy, mothers completed an assessment of recent negative life events as a measure of prenatal stress and an assessment of prenatal diet. When the children were 30 months of age, mothers completed the Early Childhood Behavior Questionnaire-Very Short form, which provides scores on child Negative Affectivity, Effortful Control, and Surgency/Extraversion. Linear regressions tested associations between maternal prenatal negative life events and child temperament, and effect modification by maternal prenatal antioxidant intakes (vitamins A, C, and E, magnesium, zinc, selenium, β-carotene). Analyses revealed that increased maternal prenatal negative life events were associated with higher child Negative Affectivity (β=0.08, P=0.009) but not with child Effortful Control (β=−0.03, P=0.39) or Surgency/Extraversion (β=0.04, P=0.14). Prenatal intakes of zinc and selenium modified this effect: Maternal exposure to prenatal negative life events was associated with higher child Negative Affectivity in the presence of lower intakes of zinc and selenium. Modification effects approached significance for vitamins A and C. The results suggest that the combination of elevated stress exposures and lower antioxidant intakes in pregnancy increases the likelihood of heightened child temperamental negative affectivity. Increased antioxidant intakes during pregnancy may protect against influences of prenatal stress on child temperament.

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Cocoros, Noelle M., Timothy L. Lash, Al Ozonoff, Mette Nørgaard, Alfred DeMaria, Viggo Andreasen, and Henrik Toft Sørensen. "Prenatal influenza exposure and cardiovascular events in adulthood." Influenza and Other Respiratory Viruses 8, no. 1 (November 7, 2013): 83–90. http://dx.doi.org/10.1111/irv.12202.

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7

Bergman, K. M., P. Sarkar, T. G. O'Connor, N. Modi, and V. Glover. "Prenatal stressful life events predict child cognitive outcomes." Early Human Development 83, no. 2 (February 2007): 136. http://dx.doi.org/10.1016/j.earlhumdev.2006.09.033.

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8

Quinlan-Jones, Elizabeth, Denise Williams, Charlotte Bell, Claire Miller, Carolyn Gokhale, and Mark D. Kilby. "Prenatal Detection of PIK3CA-related Overgrowth Spectrum in Cultured Amniocytes Using Long-range PCR and Next-generation Sequencing." Pediatric and Developmental Pathology 20, no. 1 (January 25, 2017): 54–57. http://dx.doi.org/10.1177/1093526616669820.

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Mutations in PIK3CA are associated with overgrowth spectrum disorders including excessive growth in some areas of the body and the central nervous system. Alterations in PIK3CA occur as somatic, postzygotic events and confer a mosaic genotype with variability in phenotypic expression being commonly observed. We describe the second reported prenatal diagnosis of a PIK3CA-related overgrowth spectrum disorder. The prenatal ultrasound features in this case enabled the presumptive, prospective diagnosis to be made which was then confirmed by genetic testing. Subsequent parental testing for mutations in PIK3CA demonstrated normal genotypes. Identification of this mutation prenatally enabled prospective information to be provided to the family and facilitated multidisciplinary perinatal management.

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9

Senter, Camilla C., Nicole R. Bush, Christine T. Loftus, Adam A. Szpiro, Annette L. Fitzpatrick, Kecia N. Carroll, Kaja Z. LeWinn, et al. "Maternal Stressful Life Events during Pregnancy and Atopic Dermatitis in Children Aged Approximately 4–6 Years." International Journal of Environmental Research and Public Health 18, no. 18 (September 15, 2021): 9696. http://dx.doi.org/10.3390/ijerph18189696.

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The prevalence of atopic dermatitis (AD) in children has steadily increased over time, yet it remains largely unknown how maternal factors during pregnancy are associated with child AD. Few studies have specifically assessed the relationship between prenatal stress and child AD, with inconsistent findings. In this prospective cohort study following 426 mother-child dyads from pregnancy to middle childhood, women reported stressful life events (SLEs) experienced during the 12 months before delivery and AD outcomes in children aged approximately 4–6 years, including current, location-specific, and ever AD. We used Poisson regression to estimate risk ratios (RRs) and corresponding 95% confidence intervals (CIs) associated with a 1-unit increase in prenatal SLEs, adjusting for potential confounders. We also assessed whether the association between prenatal SLEs and child AD was modified by child sex, history of maternal atopy, or prenatal maternal resilient coping. The mean (standard deviation) of prenatal SLEs reported in the overall sample was 1.4 (1.6), with 37.1% of women reporting none. A 1-unit increase in prenatal SLEs was not significantly associated with current AD (RR: 1.08, 95% CI: 0.89, 1.31), location-specific AD (RR: 1.09, 95% CI: 0.78, 1.52), or ever AD (RR: 0.97, 95% CI: 0.87, 1.09). We did not find evidence of effect modification. Findings from this study suggest no association between prenatal SLEs and AD in middle childhood, although larger longitudinal studies with enhanced case definition and higher variability of SLE experience may more fully inform this question.

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10

VERDOUX, HELENE, JACQUES ROPERS, DOMINIQUE COSTAGLIOLA, FRANÇOISE CLAVEL-CHAPELON, and XAVIER PAOLETTI. "Serious psychiatric outcome of subjects prenatally exposed to diethylstilboestrol in the E3N cohort study." Psychological Medicine 37, no. 9 (April 4, 2007): 1315–22. http://dx.doi.org/10.1017/s0033291707000438.

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ABSTRACTBackgroundPrenatal exposure to diethylstilboestrol (DES) may induce neurodevelopmental disturbances potentially mediating an increased risk of psychiatric disorders in exposed subjects. Most findings of an increased prevalence of psychiatric disorders in men and women prenatally exposed to DES are not easy to interpret because of selection biases.MethodInformation on hormonal treatment during pregnancy and on offspring's medical outcome was collected from women participating in the Etude Epidemiologique de femmes de la Mutuelle Générale de l'Education Nationale (E3N) prospective cohort who completed consecutive postal questionnaires on a range of medical events since 1990. Information on hormonal treatment during pregnancy was collected in 1992 and on offspring's medical outcome in 2004. The psychiatric outcome of subjects prenatally exposed to DES was compared to that of their unexposed siblings.ResultsA total of 1352 mothers with DES treatment for at least one pregnancy provided information on 1680 exposed children and 1447 unexposed siblings. After adjustment for duration of follow-up, educational level, history of obstetric complication, prenatal exposure to progestagen drugs or other hormones and parental history of psychiatric hospitalization, no association was found between prenatal exposure to DES and occurrence of strictly defined serious psychiatric outcome (suicide or psychiatric hospitalization) [adjusted odds ratio (OR) 0·8, 95% confidence interval (CI) 0·5–1·2], or of broadly defined serious psychiatric outcome (same events plus psychiatric or psychological consultation) (adjusted OR 1·0, 95% CI 0·8–1·2).ConclusionsThese findings suggest that the impact of prenatal DES exposure on foetal brain development, if any, is unlikely to increase the risk of serious psychiatric disorders.

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11

Chien, Yi-Ling, Miao-Chun Chou, Wen-Jiun Chou, Yu-Yu Wu, Wen-Che Tsai, Yen-Nan Chiu, and Susan Shur-Fen Gau. "Prenatal and perinatal risk factors and the clinical implications on autism spectrum disorder." Autism 23, no. 3 (June 28, 2018): 783–91. http://dx.doi.org/10.1177/1362361318772813.

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Prenatal and perinatal factors may increase the risk of autism spectrum disorder. However, little is known about whether unaffected siblings of probands with autism spectrum disorder also share the phenomenon and whether the prenatal/perinatal factors are related to the clinical severity of autistic symptoms. We compared the frequency of prenatal and perinatal factors among 323 probands with autism spectrum disorder (mean age ± standard deviation, 10.7 ± 3.5 years; males, 91.0%), 257 unaffected siblings (11.7 ± 4.5; 42.8%), and 1504 typically developing controls (8.9 ± 1.6 years; 53.1%); and investigated their effects on the severity of autistic symptoms. We found that probands with autism spectrum disorder and their unaffected siblings had more prenatal/perinatal events than typically developing controls with higher numbers of prenatal/perinatal factors in probands than in unaffected siblings. The prenatal/perinatal events were associated with greater stereotyped behaviors, social-emotional problems, socio-communication deficits, and overall severity. We also found that six prenatal/perinatal factors (i.e. preeclampsia, polyhydramnios, oligoamnios, placenta previa, umbilical cord knot, and gestational diabetes) were associated with the severity of autistic symptoms, particularly stereotyped behaviors and socio-communication deficits. Our findings suggest that prenatal and perinatal factors may potentially moderate the clinical expression of autism spectrum disorder. The underlying mechanism warrants further research.

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12

Hougaard, Karin S., Maibritt B. Andersen, Sanna L. Kjær, Åse M. Hansen, Thomas Werge, and Søren P. Lund. "Prenatal stress may increase vulnerability to life events: Comparison with the effects of prenatal dexamethasone." Developmental Brain Research 159, no. 1 (September 2005): 55–63. http://dx.doi.org/10.1016/j.devbrainres.2005.06.014.

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13

Buck, Catherine O., Annie Gjelsvik, Patrick M. Vivier, Karine Monteiro, and Siraj Amanullah. "Prenatal Exposure to Stressful Life Events and Infant Breastfeeding." Breastfeeding Medicine 13, no. 6 (July 2018): 426–32. http://dx.doi.org/10.1089/bfm.2017.0200.

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14

Klonoff-Cohen, Hillary S., Indu P. P., and Sharon L. Edelstein. "Prenatal and intrapartum events and sudden infant death syndrome." Paediatric and Perinatal Epidemiology 16, no. 1 (January 2002): 82–89. http://dx.doi.org/10.1046/j.1365-3016.2002.00395.x.

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15

Liu, Jie, Yuansheng Gao, Sewite Negash, Lawrence D. Longo, and J. Usha Raj. "Long-term effects of prenatal hypoxia on endothelium-dependent relaxation responses in pulmonary arteries of adult sheep." American Journal of Physiology-Lung Cellular and Molecular Physiology 296, no. 3 (March 2009): L547—L554. http://dx.doi.org/10.1152/ajplung.90333.2008.

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Chronic hypoxia during the course of pregnancy is a common insult to the fetus. However, its long-term effect on the pulmonary vasculature in adulthood has not been described. In this study, the vasorelaxation responses of conduit pulmonary arteries in adult female sheep that were chronically hypoxic as fetuses and raised postnatally at sea level were investigated. Vessel tension studies revealed that endothelium-dependent relaxation responses were attenuated in pulmonary arteries from adult sheep that experienced prenatal hypoxia. Endothelial nitric oxide synthase (eNOS) protein expression was unchanged, but eNOS activity was significantly decreased in pulmonary arteries from prenatally hypoxic sheep. Protein expression of eNOS partners, caveolin-1, calmodulin, and heat shock protein 90 (Hsp90) did not change following prenatal hypoxia. However, the association between eNOS and caveolin-1, its inhibitory binding partner, was significantly increased, whereas association between eNOS and its stimulatory partners calmodulin and Hsp90 was greatly decreased. Furthermore, phosphorylation of Ser1177 in eNOS decreased, whereas phosphorylation of Thr495 increased, in the prenatally hypoxic pulmonary arteries, events that are related to eNOS activity. These data demonstrate that prenatal hypoxia results in persistent abnormalities in endothelium-dependent relaxation responses of pulmonary arteries in adult sheep due to decreased eNOS activity resulting from altered posttranslational regulation.

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16

Chiu, Yu-Han, Mats J. Stensrud, Issa J. Dahabreh, Paolo Rinaudo, Michael P. Diamond, John Hsu, Sonia Hernández-Díaz, and Miguel A. Hernán. "The Effect of Prenatal Treatments on Offspring Events in the Presence of Competing Events." Epidemiology 31, no. 5 (September 2020): 636–43. http://dx.doi.org/10.1097/ede.0000000000001222.

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17

Dörner, G., B. Schenk, B. Schmiedel, and L. Ahrens. "Stressful Events in Prenatal Life of Bi- and Homosexual Men." Experimental and Clinical Endocrinology & Diabetes 81, no. 01 (July 17, 2009): 83–87. http://dx.doi.org/10.1055/s-0029-1210210.

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Ho, H., S. Lhotak, M. E. Solano, K. Karimi, M. K. Pincus, R. C. Austin, and P. Arck. "Prenatal stress enhances severity of atherosclerosis in the adult apolipoprotein E-deficient mouse offspring via inflammatory pathways." Journal of Developmental Origins of Health and Disease 4, no. 1 (November 1, 2012): 90–97. http://dx.doi.org/10.1017/s2040174412000608.

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Atherosclerosis is the underlying cause of cardiovascular disease and stroke. Endothelial cell dysfunctions are early events in atherosclerosis, resulting in the recruitment of circulating monocytes. The immune system can elicit an inflammatory response toward the atherosclerotic lesion, thereby accelerating lesion growth. Risk factors for atherosclerosis include hypertension, smoking, stress perception or low birth weight. As prenatal stress challenge decreases the birth weight and affects the offspring's postnatal immune response, we aimed to investigate whether prenatal stress contributes to the development of atherosclerosis in mice. Syngenic pregnant apolipoprotein E-deficient (apoE−/−) dams were exposed to sound stress on gestation days 12.5 and 14.5. The presence and size of atherosclerotic plaques in the offspring at the age of 15 weeks was evaluated by histomorphology, accompanied by flow cytometric analysis of the frequency and phenotype of monocytes/macrophages and regulatory T (Treg) cells in the blood. Further, cytokine secretion of peripheral blood lymphocytes was analyzed. In response to prenatal stress challenge, an increased frequency of large atherosclerotic plaques was detectable in apoE−/− offspring, which was particularly profound in females. Prenatal stress also resulted in alterations of the offspring's immune response, such as a decreased frequency of Treg cells in blood, alterations of macrophage populations in blood and an increased secretion of inflammatory cytokines. We provide novel evidence that prenatally stressed adult offspring show an increased severity of atherosclerosis. As Treg cells are key players in dampening inflammation, the observed increase in atherosclerosis may be due to the lack of Treg cell frequency. Future interdisciplinary research is urgently required to understand the developmental origin of prenatal stress-induced atherosclerosis. The availability of our model may facilitate and foster such research endeavors.

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Baum, Michel. "Role of the kidney in the prenatal and early postnatal programming of hypertension." American Journal of Physiology-Renal Physiology 298, no. 2 (February 2010): F235—F247. http://dx.doi.org/10.1152/ajprenal.00288.2009.

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Epidemiologic studies from several different populations have demonstrated that prenatal insults, which adversely affect fetal growth, result in an increased incidence of hypertension when the offspring reaches adulthood. It is now becoming evident that low-birth-weight infants are also at increased risk for chronic kidney disease. To determine how prenatal insults result in hypertension and chronic kidney disease, investigators have used animal models that mimic the adverse events that occur in pregnant women, such as dietary protein or total caloric deprivation, uteroplacental insufficiency, and prenatal administration of glucocorticoids. This review examines the role of the kidney in generating and maintaining an increase in blood pressure in these animal models. This review also discusses how early postnatal adverse events may have repercussions in later life. Causes for the increase in blood pressure by perinatal insults are likely multifactorial and involve a reduction in nephron number, dysregulation of the systemic and intrarenal renin-angiotensin system, increased renal sympathetic nerve activity, and increased tubular sodium transport. Understanding the mechanism for the increase in blood pressure and renal injury resulting from prenatal insults may lead to therapies that prevent hypertension and the development of chronic kidney and cardiovascular disease.

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Sobas, Magdalena. "CAUSAL EVENTS RELATED TO PRENATAL AND PERINATAL CARE ABOUT OF CIVIL LIABILITY FOR INJURIES SUFFERED BEFORE BIRTH." Roczniki Administracji i Prawa 2, no. XXI (June 30, 2021): 197–217. http://dx.doi.org/10.5604/01.3001.0015.5611.

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The issue of civil liability of injuries suffered before birth it is a multi-threaded and interdisciplinary issue. This subject covers a relatively wide range of causal events that may result in damage to the legally protected property of the victim. This study considers the potential for harm in connection with prenatal care, as well as in relation to perinatal care. The study attempts to define the ways of understanding prenatal diagnosis and to indicate the legal basis for its performance. Possible exemplary causal events related to it were also identified. Delicts related to perinatal care were distinguished as a separate category. The considerations were compared with civil liability for damage.

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Rosa, Maria José, Farida Nentin, Michelle Bosquet Enlow, Michele R. Hacker, Nastasia Pollas, Brent Coull, and Rosalind J. Wright. "Sex-specific associations between prenatal negative life events and birth outcomes." Stress 22, no. 6 (May 6, 2019): 647–53. http://dx.doi.org/10.1080/10253890.2019.1608944.

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22

Layton, J. Bradley, Anne M. Butler, Dongmei Li, Kim A. Boggess, David J. Weber, Leah J. McGrath, and Sylvia Becker-Dreps. "Prenatal Tdap immunization and risk of maternal and newborn adverse events." Vaccine 35, no. 33 (July 2017): 4072–78. http://dx.doi.org/10.1016/j.vaccine.2017.06.071.

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23

Hartwig, Isabel R. V., Peter D. Sly, Louis A. Schmidt, Ryan J. van Lieshout, John Bienenstock, Patrick G. Holt, and Petra C. Arck. "Maternal prenatal life events increase risk for atopic disorders in children." Brain, Behavior, and Immunity 29 (February 2013): S15. http://dx.doi.org/10.1016/j.bbi.2013.01.045.

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Zhu, Peng, Fangbiao Tao, Jiahu Hao, Ying Sun, and Xiaomin Jiang. "Prenatal life events stress: implications for preterm birth and infant birthweight." American Journal of Obstetrics and Gynecology 203, no. 1 (July 2010): 34.e1–34.e8. http://dx.doi.org/10.1016/j.ajog.2010.02.023.

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Varcin, Kandice J., Gail A. Alvares, Mirko Uljarević, and Andrew J. O. Whitehouse. "Prenatal maternal stress events and phenotypic outcomes in Autism Spectrum Disorder." Autism Research 10, no. 11 (July 6, 2017): 1866–77. http://dx.doi.org/10.1002/aur.1830.

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Ivanitskaya, Olga, Yulia Sologub, Yulia Tsayuk, Alexey Zagray, and Aleksei Kim. "Right atrial appendage aneurysm in a fetus—Does precise prenatal diagnosis matter?" Ultrasound 28, no. 4 (July 14, 2020): 255–59. http://dx.doi.org/10.1177/1742271x20941186.

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Introduction Congenital malformations of the right atrium—aneurysms and diverticula—are rare heart defects with only a few cases having been described prenatally. Early diagnosis of these anomalies is extremely important due to the possibility of such serious complications such as supraventricular arrhythmia, thromboembolic events and sudden death. Topic Description Although each of these anomalies is well known, there are still significant discrepancies in diagnosis. At the same time, there is no essential difference in the postnatal management of patients with right atrial aneurysms or diverticula. Treatment mode varies between centers and is selected individually depending on the presence of symptoms. Discussion We discuss the problems of terminology, ultrasound criteria and prenatal differential diagnosis, anatomic and histological features and current limitations for the accurate diagnosis of right atrial aneurysms and diverticula in utero. As a clinical example, we describe a case of right atrial appendage aneurysm diagnosed in a fetus. Conclusions Considering the prenatal diagnostic difficulties and similar management of such patients after birth, we suggest avoiding the use of exact terms in the fetus, leaving the precise diagnosis for the postnatal period.

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Hundsdoerfer, Patrick, Barbara Vetter, Brigitte Stöver, Christian Bassir, Tristess Scholz, Ingrid Grimmer, Eberhard Mönch, Sabine Ziemer, Rainer Rossi, and Andreas Kulozik. "Homozygous and double heterozygous Factor V Leiden and Factor II G20210A genotypes predispose infants to thromboembolism but are not associated with an increase of foetal loss." Thrombosis and Haemostasis 90, no. 10 (2003): 628–35. http://dx.doi.org/10.1160/th03-02-0096.

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SummaryProspective and controlled data about the individual risk profile in asymptomatic children with homozygous or double heterozygous risk genotypes for Factor V Leiden (FVL) and factor II (FII) G20210A are currently unavailable. The systematic and prospective observational study presented here was designed to determine the impact of the homozygous and double heterozygous FVL and FII G20210A genotypes on the prenatal and postnatal risk profiles of affected children. Risk infants and heterozygous controls were identified by screening of 85,304 neonates. Follow-up included the comparison of prenatal and postnatal development, ultrasonography of brain and kidneys, and a panel of independent determinants of thrombophilia. The numbers of identified or expected FVL homozygotes and double heterozygotes did not differ significantly (FVL: 116 ver-sus 91, p=0.08; FVL/FII: 94 versus 76, p=0.17), indicating the absence of a prenatal disadvantage. A prenatal advantage was suggested in FII homozygotes, whose identified number far exceeded the expected (19 versus 4, p=0.002). Clinical and/or imaging abnormalities indicated spontaneous thromboembolic events in 4 of 129 risk infants (3%) but in none of the 178 controls (p=0.02). Physical and neurological development was normal in both groups during the first 2 years of life. The risk genotypes appear to confer a significant predisposition for spontaneous thromboembolic events in infancy without impeding development within the first two years of life. Foetal risk genotypes do not cause an increased foetal loss rate. Moreover, homozygous FII G20210A appears to be associated with a prenatal advantage.

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Shaaban, Aimen F., Heung Bae Kim, Ross Milner, and Alan W. Flake. "A Kinetic Model for the Homing and Migration of Prenatally Transplanted Marrow." Blood 94, no. 9 (November 1, 1999): 3251–57. http://dx.doi.org/10.1182/blood.v94.9.3251.

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Abstract Currently little is known about the mechanisms regulating the homing and the early engraftment of prenatally transplanted hematopoietic cells due to the lack of a relevant functional assay. In this study, we have defined a reproducible kinetic profile of the homing and the early engraftment events in a murine model of prenatal stem cell transplantation. Light density mononuclear cells (LDMCs) from adult C57Pep3b and SJL/J marrow were transplanted by intraperitoneal (IP) injection into C57BL/6 fetuses (106 LDMCs/fetus) at 14 days of gestation. The fetuses were sacrificed at early time points (1.5 to 96 hours) after transplantation. Recipient fetal liver and cord blood were analyzed for donor cell frequency and donor cell phenotype by dual color flow cytometry. Pertinent findings included the following: (1) a triphasic kinetic profile exists after in utero hematopoietic stem cell (HSC) transplantation (homing of circulating donor cells, rapid reduction of donor cell frequency, and donor cell competitive equilibration); (2) homing to the fetal liver is nonselective and reflects the phenotypic profile of the donor population; and (3) the kinetics after the prenatal transplantation of congenic or fully allogeneic cells are identical. This model will facilitate a systematic analysis of the mechanisms that regulate the homing of prenatally transplanted hematopoietic cells.

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Shaaban, Aimen F., Heung Bae Kim, Ross Milner, and Alan W. Flake. "A Kinetic Model for the Homing and Migration of Prenatally Transplanted Marrow." Blood 94, no. 9 (November 1, 1999): 3251–57. http://dx.doi.org/10.1182/blood.v94.9.3251.421k10_3251_3257.

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Currently little is known about the mechanisms regulating the homing and the early engraftment of prenatally transplanted hematopoietic cells due to the lack of a relevant functional assay. In this study, we have defined a reproducible kinetic profile of the homing and the early engraftment events in a murine model of prenatal stem cell transplantation. Light density mononuclear cells (LDMCs) from adult C57Pep3b and SJL/J marrow were transplanted by intraperitoneal (IP) injection into C57BL/6 fetuses (106 LDMCs/fetus) at 14 days of gestation. The fetuses were sacrificed at early time points (1.5 to 96 hours) after transplantation. Recipient fetal liver and cord blood were analyzed for donor cell frequency and donor cell phenotype by dual color flow cytometry. Pertinent findings included the following: (1) a triphasic kinetic profile exists after in utero hematopoietic stem cell (HSC) transplantation (homing of circulating donor cells, rapid reduction of donor cell frequency, and donor cell competitive equilibration); (2) homing to the fetal liver is nonselective and reflects the phenotypic profile of the donor population; and (3) the kinetics after the prenatal transplantation of congenic or fully allogeneic cells are identical. This model will facilitate a systematic analysis of the mechanisms that regulate the homing of prenatally transplanted hematopoietic cells.

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McIntyre, Lynne, Bruna Alvarez, and Diana Marre. "“I Want to Bury It, Will You Join Me?”: The Use of Ritual in Prenatal Loss among Women in Catalonia, Spain in the Early 21st Century." Religions 13, no. 4 (April 9, 2022): 336. http://dx.doi.org/10.3390/rel13040336.

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Prenatal loss, such as miscarriage and stillbirth, may be understood as the confluence of birth and death. The most significant of life’s transitions, these events are rarely if ever expected to coincide. Although human cultures have long recognized death through ritual, it has not typically been used in cases of pregnancy loss. Interest in prenatal losses in the fields of medicine and the social sciences, as well as among the general public, has grown significantly in recent years in many countries, including Spain, as evidenced by increasing numbers of clinical protocols, academic books and articles, public events and popular media coverage. Even with this growing attention, there are still no officially sanctioned or generally accepted ways of using ritual to respond to prenatal losses in Spain. However, despite a lack of public recognition or acceptance of the use of ritual, we found that women in the autonomous community of Catalonia, in Spain, are employing ritual in various fashions, both with and without the support and acceptance of their family, friends or community, to process their losses and integrate them into their lives.

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ALLEN, NICHOLAS B., PETER M. LEWINSOHN, and JOHN R. SEELEY. "Prenatal and perinatal influences on risk for psychopathology in childhood and adolescence." Development and Psychopathology 10, no. 3 (September 1998): 513–29. http://dx.doi.org/10.1017/s0954579498001722.

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The relationship between a range of prenatal and perinatal events and risk for psychopathology in offspring was examined. Prenatal and perinatal events investigated included maternal experiences, health, and substance use during pregnancy, obstetric complications, feeding practices, and infant health during the first year of life. Offspring diagnosis was based on structured interviews conducted with 579 adolescents on two occasions. Risk for later psychopathology was associated with a number of prenatal and perinatal factors. Major depression was associated with not being breast fed and maternal emotional problems during the pregnancy. Anxiety was chiefly associated with fever and illness during the first year of life and maternal history of miscarriage and stillbirth. Disruptive behavior disorder was associated with poor maternal emotional health during the pregnancy and birth complications. Risk for substance use disorder was associated with maternal use of substances during the pregnancy. Mediating effects of maternal depression, maternal–child conflict, and physical symptoms in the child, and moderating effects of gender of child and parental education were also evaluated. The limitations of this study are discussed and future research directions are suggested.

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Trisnowiyanto, Bambang, and Yohanes Purwanto. "Faktor Risiko Prenatal Perinatal Dan Postnatal Pada Kejadian Cerebral Palsy." Interest : Jurnal Ilmu Kesehatan 8, no. 2 (November 27, 2019): 204–9. http://dx.doi.org/10.37341/interest.v8i2.177.

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Background: Cerebral Palsy (CP) is a disability disorder motor motorization is most common in children with a prevalence of 2-3 per 1000 live births. The term CP is explained as a group of movement and posture disorders that are often accompanied by impaired sensation, perception, cognition, communication, behavior, epilepsy, and secondary disorders of the musculoskeletal system. Disorders of CP occur in the immature central nervous system with non-progressive traits occurring in the prenatal, perinatal, and postnatal period. Methods: The purpose of this study is to determine how much prenatal risk factors, perinatal, and postnatal events in CP at the Kitty Center Clinic in Jakarta for 5 year (2013 - 2017). Result: An observational descriptive study, which described prenatal perinatal, and postnatal risk factors for CP events at the Kitty Center Clinic in Jakarta for a period of 5 years (2013-2017) with a total of 523 study subjects. Based on the analysis of data obtained, based on the type of CP 35% quadripelgia spastic, 36% spastic diplegia, 6% spastic hemiplegia, 9% athetosis, and 14% hypotonia. Based on sex 62% are men, and 38% are women with a ratio of 1.6: 1.0. Based on the age of the child 11% <2 years, 34% 3-6 years, 33% 7-12 years, and 22%13-18 years. Conclusion: Based on risk factors of 62% prenatal, 25% perinatal, and 12% postnatal. Prenatal risk factor is the biggest risk factor as much as 62% which causes Cerebral Palsy at the Kitty Center Clinic in Jakarta.

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Huttunen, M. O., and S. A. Mednick. "Polyvagal theory, neurodevelopment and psychiatric disorders." Irish Journal of Psychological Medicine 35, no. 1 (December 6, 2017): 9–10. http://dx.doi.org/10.1017/ipm.2017.66.

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Neurodevelopment is an area of psychiatry which has attracted huge interest in the last few decades. There is substantial evidence that perinatal events can contribute to later development of mental disorder. In the current perspective article we propose a novel polyvagal theory which attempts to link prenatal events with neurodevelopment and the later onset of psychiatric disorder.

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Robinson, Monique, Kim W. Carter, Craig E. Pennell, Peter Jacoby, Hannah C. Moore, Stephen R. Zubrick, and David Burgner. "Maternal prenatal stress exposure and sex-specific risk of severe infection in offspring." PLOS ONE 16, no. 1 (January 29, 2021): e0245747. http://dx.doi.org/10.1371/journal.pone.0245747.

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Background Maternal stressful life events during pregnancy have been associated with immune dysregulation and increased risk for asthma and atopy in offspring. Few studies have investigated whether prenatal stress is associated with increased overall or specific infectious diseases in childhood, nor explored sex differences. We sought to examine the relationship between the nature and timing of maternal stress in pregnancy and hospitalisation with infection in offspring. Methods Between 1989 and 1992, exposure data on stressful life events were collected from pregnant women (Gen1) in the Raine Study at 18 and 34 weeks’ gestation and linked to statutory state-wide hospital morbidity data. We examined associations between the number, category and timing of maternal prenatal stress events and overall and clinical groups of offspring (Gen2) infection-related hospitalisation until age 16 years, adjusting for maternal age, education, and smoking in pregnancy in addition to the presence of siblings at birth. Results Of 2,141 offspring with complete stress in pregnancy data available, 1,089 had at least one infection-related hospitalisation, with upper respiratory tract infections the most common (n = 556). Each additional stressful life event during pregnancy was associated with increased risk in male offspring for hospitalisation with all infection types. There was little evidence of these associations in girls. Conclusions Increased exposure to stressful life events in utero is associated with sex-specific infection-related hospitalisations in childhood. Prenatal stress may adversely affect early immune development for boys and increase the risk of more severe infections. Mechanistic understanding would inform preventative interventions.

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Karunanayake, Amaranath, Niranga Manjuri Devanarayana, and Shaman Rajindrajith. "Early life events in functional abdominal pain disorders in children." PLOS ONE 17, no. 11 (November 2, 2022): e0275419. http://dx.doi.org/10.1371/journal.pone.0275419.

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Objectives Functional abdominal pain disorders (FAPDs) are common gastrointestinal problems in children, and the pathophysiology is thought to be multifactorial. Adverse early life events (ELE) induce alterations in the central nervous system, perhaps predisposing individuals to develop FAPDs. We aimed to study the potential adverse ELE that are associated with FAPDs. Methods We steered a school-based survey involving 1000 children from 4 randomly selected schools. FAPDs were assessed using the translated Rome III questionnaire, and ELE were identified using a pre-tested, parental questionnaire. FAPDs were diagnosed using the Rome III criteria. Results Hundred and eighty-two (182) children had FAPDs (62.1% girls, mean age 8.5, SD 2.1). ELE of them were compared with 571 children without FAPDs (51.1% girls, mean age 8.8, SD 1.9). According to the binary logistic regression analysis, family members with abdominal pain, family member with chronic pain other than abdominal pain, prenatal maternal complications and interventional deliveries, were recognized as potential risk factors for the development of FAPDs. Breast feeding over two years has shown to reduce the prevalence of FAPDs.a. Conclusions Prenatal maternal medical problems are associated a with higher prevalence of FAPDs later in life. Prolonged breastfeeding and normal vaginal delivery could be considered as factors that reduce the vulnerability of developing FAPDs in children. Therefore, minimizing pregnancy-related complications, encouraging vaginal deliveries, and encouraging breastfeeding are potentially valuable measures to prevent FAPDs during childhood.

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Hoehn, K. Sarah, Gil Wernovsky, Jack Rychik, Zhi-yun Tian, Denise Donaghue, Melissa A. Alderfer, J. William Gaynor, Anne E. Kazak, Thomas L. Spray, and Robert M. Nelson. "Parental decision-making in congenital heart disease." Cardiology in the Young 14, no. 3 (June 2004): 309–14. http://dx.doi.org/10.1017/s1047951104003099.

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Objective:To explore whether prenatal diagnosis of congenital heart disease is associated with lower levels of parental distress and greater satisfaction with decisions about cardiothoracic surgery when compared to postnatal diagnosis.Methodology:A combined quantitative–qualitative design was used. Participants included the parents of 31 neonates (30 mothers and 22 fathers) admitted to the cardiac intensive care unit between 1 November 2001 and 1 May 2002 for repair of congenital cardiac malformations. Participants completed self-report measures of anxiety, optimism, and life events pre-operatively, and semi-structured qualitative interviews assessing satisfaction with decision-making within 1 week of the operation.Results:At the time of surgery, mothers of neonates receiving the diagnosis prenatally did not differ from mothers of neonates receiving the diagnosis postnatally on measures of anxiety, optimism, and life events. Fathers of neonates receiving the diagnosis prenatally, however, reported more optimism, lower state and trait anxiety, and fewer negative life events than fathers of neonates receiving the diagnosis postnatally. When we analyzed the interviews, we found that, regardless of the timing of the diagnosis, parents felt as though they made a genuine choice for their baby to have surgery.Conclusions:In this pilot study, fathers who learned prenatally that their child had a congenital cardiac malformation were less distressed than those who discovered this fact only postnatally. From the parental perspective, nonetheless, distress and urgency do not impair their ability to make decisions about neonatal cardiac surgery.

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Veiga-Lopez, Almudena, Wen Ye, David Phillips, Carol Herkimer, and Vasantha Padmanabhan. "DEVELOPMENTAL PROGRAMMING: PRENATAL TESTOSTERONE EXCESS DISRUPTS PERIOVULATORY SEQUENCE OF EVENTS IN SHEEP." Biology of Reproduction 77, Suppl_1 (July 1, 2007): 213. http://dx.doi.org/10.1093/biolreprod/77.s1.213.

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Buka, Stephen L., Jill M. Goldstein, Eleni Spartos, and Ming T. Tsuang. "The retrospective measurement of prenatal and perinatal events: accuracy of maternal recall." Schizophrenia Research 71, no. 2-3 (December 2004): 417–26. http://dx.doi.org/10.1016/j.schres.2004.04.004.

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Zhu, Peng, Wen Huang, Jia-Hu Hao, Kun Huang, Xiao-Min Jiang, and Fang-Biao Tao. "Time-specific effect of prenatal stressful life events on gestational weight gain." International Journal of Gynecology & Obstetrics 122, no. 3 (June 29, 2013): 207–11. http://dx.doi.org/10.1016/j.ijgo.2013.04.007.

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Palmini, Andre, Eva Andermann, and Frederick Andermann. "Prenatal Events and Genetic Factors in Epileptic Patients with Neuronal Migration Disorders." Epilepsia 35, no. 5 (September 1994): 965–73. http://dx.doi.org/10.1111/j.1528-1157.1994.tb02541.x.

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Helgeson, J., J. Wardrop, T. Boomer, E. Almasri, W. B. Paxton, J. S. Saldivar, N. Dharajiya, et al. "Clinical outcome of subchromosomal events detected by whole‐genome noninvasive prenatal testing." Prenatal Diagnosis 35, no. 10 (July 27, 2015): 999–1004. http://dx.doi.org/10.1002/pd.4640.

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Flouri, Eirini, Marta Francesconi, Emily Midouhas, and Glyn Lewis. "Prenatal and childhood adverse life events, inflammation and depressive symptoms across adolescence." Journal of Affective Disorders 260 (January 2020): 577–82. http://dx.doi.org/10.1016/j.jad.2019.09.024.

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Larsen, Tricia D., Kyle H. Sabey, Alexis J. Knutson, Tyler C. T. Gandy, Eli J. Louwagie, Lothar Lauterboeck, Kennedy S. Mdaki, and Michelle L. Baack. "Diabetic Pregnancy and Maternal High-Fat Diet Impair Mitochondrial Dynamism in the Developing Fetal Rat Heart by Sex-Specific Mechanisms." International Journal of Molecular Sciences 20, no. 12 (June 25, 2019): 3090. http://dx.doi.org/10.3390/ijms20123090.

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Infants born to diabetic or obese mothers are at greater risk of heart disease at birth and throughout life, but prevention is hindered because underlying mechanisms remain poorly understood. Using a rat model, we showed that prenatal exposure to maternal diabetes and a high-fat diet caused diastolic and systolic dysfunction, myocardial lipid accumulation, decreased respiratory capacity, and oxidative stress in newborn offspring hearts. This study aimed to determine whether mitochondrial dynamism played a role. Using confocal live-cell imaging, we examined mitochondrial dynamics in neonatal rat cardiomyocytes (NRCM) from four prenatally exposed groups: controls, diabetes, high-fat diet, and combination exposed. Cardiac expression of dynamism-related genes and proteins were compared, and gender-specific differences were evaluated. Findings show that normal NRCM have highly dynamic mitochondria with a well-balanced number of fusion and fission events. Prenatal exposure to diabetes or a high-fat diet impaired dynamism resulting in shorter, wider mitochondria. Mechanisms of impaired dynamism were gender-specific and protein regulated. Females had higher expression of fusion proteins which may confer a cardioprotective effect. Prenatally exposed male hearts had post-translational modifications known to impair dynamism and influence mitophagy-mediated cell death. This study identifies mitochondrial fusion and fission proteins as targetable, pathogenic regulators of heart health in offspring exposed to excess circulating maternal fuels.

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Bräuner, E. V., T. Koch, A. Juul, D. A. Doherty, R. Hart, and M. Hickey. "Prenatal exposure to maternal stressful life events and earlier age at menarche: the Raine Study." Human Reproduction 36, no. 7 (March 21, 2021): 1959–69. http://dx.doi.org/10.1093/humrep/deab039.

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Abstract STUDY QUESTION Is there an association between prenatal exposure to stressful life events and age at menarche, and does childhood BMI mediate this association? SUMMARY ANSWER Girls exposed to prenatal stress had a slightly earlier age at menarche, but this association did not show a dose-response effect and was not mediated by childhood offspring BMI. WHAT IS ALREADY KNOWN Prenatal stress may impact on reproductive function in females including age at menarche, but human data are very limited. High childhood BMI is known to be associated with earlier age at menarche. Only one small study has measured the association between maternal stress and age at menarche and reported that childhood BMI mediated the association between maternal stress and earlier age at menarche. However, neither maternal stress nor age at menarche was prospectively recorded and the study was limited to 31 mother–daughter pairs. STUDY DESIGN, SIZE, DURATION The Raine Study is a large prospective population-based pregnancy cohort study (n = 1414 mother–daughter pairs) continuously followed from prenatal life through to adolescence. In the present study, we examined the association between exposure to maternal stressful life events during early, late and total gestation and age at menarche in offspring using 753 mother–daughter pairs with complete case information. PARTICIPANTS/MATERIALS, SETTING, METHODS Mothers prospectively reported stressful life events during pregnancy at 18 and 34 weeks using a standardized 10-point questionnaire. Exact date of menarche was assessed using a purpose-designed questionnaire at 8, 10, 14 and 17 years of age. Complete information on exposure, outcome and confounding variables was obtained from 753 mothers–daughter pairs. Multivariate linear regression complete case analysis was used to examine associations between maternal stressful life event exposure and age at menarche. Potential selection bias was evaluated using multiple imputations (50 datasets). The mediating effects of offspring childhood BMI (ages 5, 8, or 10 years) on these associations were measured in separate sub-analyses. MAIN RESULTS AND ROLE OF CHANCE Most (580/753, 77%) daughters were exposed to at least one prenatal stressful life event. Exposure to maternal stressful life events during the entire pregnancy was associated with a non-linear earlier age at menarche. Exposure to one event and two or more psychological stressful events was associated with a 3.5 and 1.7-month earlier onset of puberty, respectively when compared to the reference group with no exposure maternal stressful life events. The estimates from multiple imputation with 50 datasets were comparable with complete case analysis confirming the existence of an underlying effect. No separate significant effects were observed for exposure during early or late gestation. The association between prenatal stressful events and age at menarche was not mediated by childhood BMI in the offspring. LIMITATIONS, REASONS FOR CAUTION Stressful life events may have affected pregnant women in different ways and self-perceived maternal stress severity may have provided a more precise estimate of gestational psychological stress. The observed non-linear U-shape of the association between maternal psychological stress and age at menarche did not reflect a dose-response. This suggests that the first exposure to prenatal stress exerts a greater effect on fetal reproductive development. A potential mechanism is via dramatic initial activation of the hypothalamic–pituitary–adrenal (HPA) axis following the first stressful life event which is greater than that observed following subsequent exposure to two or more maternal stressful life events. Whilst we adjusted for a priori chosen confounders, we cannot exclude residual confounding or confounding by factors we did not include. Maternal age at menarche was not available so the effects of familial history/genetics could not be assessed. There was a large loss due to the number of girls with no information on date of menarche and missing confounder information implying risk of selection bias and multiple imputation analyses did not fully exclude this risk (similar direction but slightly weaker estimate magnitude). WIDER IMPLICATIONS OF THE FINDINGS Menarche is a sentinel reproductive event and earlier age at menarche carries implications for psychological, social and reproductive health and for long-term risk of common non-communicable diseases. Understanding the factors regulating age at menarche has extensive health implications. This is the first population-based cohort study in humans to demonstrate that prenatal psychological stress might directly modify age at menarche. STUDY FUNDING/COMPETING INTEREST(S) Dr. Bräuner and Trine Koch’s salaries were supported by Doctor Sofus Carl Emil Friis and spouse Olga Doris Friis foundation, The Danish Cancer Society (Kræftens Bekæmpelse, RP15468, R204-A12636, Denmark) and The Danish Health Foundation (Helsefonden, F-22181-23, Denmark). Martha Hickey was funded by NHMRC Practitioner Fellowships. The funding bodies played no role in the design, collection, analysis, or interpretation of data; in the writing of the manuscript; or in the decision to submit the manuscript for publication. Dr. Hart has received personal fees in his function as the Medical Director of Fertility Specialists of Western Australia and received educational sponsorship grants from MSD, Merck-Serono and from Ferring Pharmaceuticals. Dr Hart has also received personal fees from Shareholders in Western IVF outside the submitted work. TRIAL REGISTRATION NUMBER NA.

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Burt, Melissa A., Yiu Chung Tse, Patricia Boksa, and Tak Pan Wong. "Prenatal immune activation interacts with stress and corticosterone exposure later in life to modulate N-methyl-d-aspartate receptor synaptic function and plasticity." International Journal of Neuropsychopharmacology 16, no. 8 (September 1, 2013): 1835–48. http://dx.doi.org/10.1017/s1461145713000229.

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Abstract Prenatal infection is an environmental risk factor for schizophrenia while later in life, stressful events have been associated with the onset and severity of psychosis. Recent findings on the impact of stress on the N-methyl-d-aspartate receptor (NMDAR), of which hypofunctioning is implicated in schizophrenia, suggest changes in stress-induced regulation of the glutamatergic system may be related to the pathogenesis of schizophrenia. Our study aimed to test whether prenatal immune activation could interact with stress at adolescence to alter NMDAR function. We used offspring from rat dams administered bacterial lipopolysaccharide (LPS) during pregnancy (gestational days 15 and 16), an animal model expressing schizophrenia-related behavioural phenotypes. Using electrophysiological techniques, we investigated effects of stress and the stress hormone corticosterone (Cort) on NMDAR-mediated synaptic function and long-term depression (LTD) in hippocampal CA1 slices from these adolescent (aged 28–39 d) male offspring. In prenatal LPS offspring, NMDAR-mediated synaptic function and LTD were reduced and abolished, respectively, compared to prenatal saline controls. Notably, in vivo stress and in vitro Cort treatment facilitated LTD in slices from prenatal LPS rats but not prenatal saline controls. Finally, Cort enhanced NMDAR-mediated synaptic function in slices from prenatal LPS rats only. We conclude that prenatal immune activation results in NMDAR hypofunction in the hippocampus of adolescent rats but also increases responsiveness of NMDAR-mediated synaptic function and LTD towards stress. Prenatal infection could confer susceptibility to schizophrenia through modification of hippocampal NMDAR function, with hypofunction in resting conditions and heightened responsiveness to stress, thus impacting the development of the disorder.

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Viltart, Odile, and Christel C. A. Vanbesien-Mailliot. "Impact of Prenatal Stress on Neuroendocrine Programming." Scientific World JOURNAL 7 (2007): 1493–537. http://dx.doi.org/10.1100/tsw.2007.204.

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Since life emerged on the Earth, the development of efficient strategies to cope with sudden and/or permanent changes of the environment has been virtually the unique goal pursued by every organism in order to ensure its survival and thus perpetuate the species. In this view, evolution has selected tightly regulated processes aimed at maintaining stability among internal parameters despite external changes, a process termed homeostasis. Such an internal equilibrium relies quite heavily on three interrelated physiological systems: the nervous, immune, and endocrine systems, which function as a permanently activated watching network, communicating by the mean of specialized molecules: neurotransmitters, cytokines, and hormones or neurohormones. Potential threats to homeostasis might occur as early as duringin uterolife, potentially leaving a lasting mark on the developing organism. Indeed, environmental factors exert early-life influences on the structural and functional development of individuals, giving rise to changes that can persist throughout life. This organizational phenomenon, encompassing prenatal environmental events, altered fetal growth, and development of long-term pathophysiology, has been named early-life programming. Over the past decade, increased scientific activities have been devoted to deciphering the obvious link between states of maternal stress and the behavioral, cognitive, emotional, and physiological reactivity of the progeny. This growing interest has been driven by the discovery of a tight relationship between prenatal stress and development of short- and long-term health disorders. Among factors susceptible of contributing to such a deleterious programming, nutrients and hormones, especially steroid hormones, are considered as powerful mediators of the fetal organization since they readily cross the placental barrier. In particular, variations in circulating maternal glucocorticoids are known to impact this programming strongly, notably when hormonal surges occur during sensitive periods of development, so-called developmental windows of vulnerability. Stressful events occurring during the perinatal period may impinge on various aspects of the neuroendocrine programming, subsequently amending the offspring's growth, metabolism, sexual maturation, stress responses, and immune system. Such prenatal stress-induced modifications of the phenotypic plasticity of the progeny might ultimately result in the development of long-term diseases, from metabolic syndromes to psychiatric disorders. Yet, we would like to consider the outcome of this neuroendocrine programming from an evolutionary perspective. Early stressful events during gestation might indeed shape internal parameters of the developing organisms in order to adapt the progeny to its everyday environment and thus contribute to an increased reproductive success, or fitness, of the species. Moreover, parental care, adoption, or enriched environments after birth have been shown to reverse negative long-term consequences of a disturbed gestational environment. In this view, considering the higher potential for neonatal plasticity within the brain in human beings as compared to other species, long-term consequences of prenatal stress might not be as inexorable as suggested in animal-based studies published to date.

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Meddouri, L. S., S. Bourgou, R. Fakhfakh, D. Bousnina, A. Triki, and A. Belhadj. "Recent versus long-term maternal traumatic life events: Which one impacts prenatal attachment?" European Psychiatry 64, S1 (April 2021): S209. http://dx.doi.org/10.1192/j.eurpsy.2021.556.

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IntroductionPrenatal attachment is a strong predictor of post-natal attachment. Identifying factors influencing this bond is important, especially maternal history of stressful life-events.ObjectivesDetermine which type of maternal trauma impacts prenatal attachment.Methods We conducted a transversal descriptive study in a first line clinical practice center and in an university gynecology-obstetrics department. We used Prenatal Attachment Inventory (PAI) to assess maternal-fetal attachment, the Childhood Trauma Questionnaire (CTQ) to evaluate maternal childhood stressful events and the Life-Threatening Events (LTE) to explore traumas during the past 6 months.Results For the 125 pregnant women in our study, the mean age was 30 years and 5 months with 99,2% of them married. Mean gestational age was 33 weeks +1 day. PAI’s mean score was 55,58± 10,20; CTQ‘s mean score was 36,62 ± 9,53 revealing trauma in 28%. Women admitted being victims of IPV in 49,6% with almost the half (48,38%) being exposed to two or more forms of violence. Mean score for recent traumatic events in LTE was 1,87 with 65,2% being exposed to two or more life threatening event. A correlation between the total score of PAI and CTQ was found (p=0.021) particularly subscales of physical and emotional negligence of the CTQ (p=0.023 and p=0.006). We found no statistically significant correlation neither between PAI and IPV (p=0,453) nor between PAI and LTE (p= 0,360).ConclusionsProviding an appropriate training for health care providers can enable them to detect pregnancies at risk in order to refer them to trauma-informed mental health services.

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Moshonov, Rami, Keren Hod, Bella Azaria, Ifat Abadi-Korek, Rachel Berger, and Mordechai Shohat. "Benefit versus risk of chromosomal microarray analysis performed in pregnancies with normal and positive prenatal screening results: A retrospective study." PLOS ONE 16, no. 4 (April 26, 2021): e0250734. http://dx.doi.org/10.1371/journal.pone.0250734.

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Background Most studies on chromosomal microarray analysis (CMA) and amniocentesis risks have not evaluated pregnancies with low risk for genetic diseases; therefore, the efficacy and safety of CMA and amniocentesis in this population are unclear. This study aimed to examine the benefits and risks of prenatal genetic diagnostic tests in pregnancies having low risk for chromosomal diseases. Methods and findings In this retrospective study, we used clinical data from a large database of 30,830 singleton pregnancies at gestational age 16–23 weeks who underwent amniocentesis for karyotyping with or without CMA. We collected socio-demographic, medical and obstetric information, along with prenatal screening, CMA and karyotyping results. Fetal loss events were also analysed. CMA was performed in 5,837 pregnancies with normal karyotype (CMA cohort). In this cohort, 4,174 women had normal prenatal screening results and the risk for identifying genetic abnormalities with >10% risk for intellectual disability by CMA was 1:102, with no significant difference between maternal age groups. The overall post-amniocentesis fetal loss rate was 1:1,401 for the entire cohort (n = 30,830) and 1:1,945 for the CMA cohort (n = 5,837). The main limitation of this study is the relatively short follow-up of 3 weeks, which may not have been sufficient for detecting all fetal loss events. Conclusion The low risk for post-amniocentesis fetal loss, compared to the rate of severe genetic abnormalities detected by CMA, suggests that even pregnant women with normal prenatal screening results should consider amniocentesis with CMA.

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Cortes Hidalgo, Andrea P. "Prenatal and Childhood Adverse Events and Child Brain Morphology: A Population-Based Study." Aperture Neuro 2 (January 2, 2022): 1–15. http://dx.doi.org/10.52294/apertureneuro.2022.2.icjo4459.

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Bassanini, Stefania, Kerri Hallene, Giorgio Battaglia, Adele Finardi, Stefano Santaguida, Marilyn Cipolla, and Damir Janigro. "Early cerebrovascular and parenchymal events following prenatal exposure to the putative neurotoxin methylazoxymethanol." Neurobiology of Disease 26, no. 2 (May 2007): 481–95. http://dx.doi.org/10.1016/j.nbd.2007.02.008.

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