• The Journal of the Korean dental association
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• v.10 no.7
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• pp.437-444
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• 1972

• Proceedings of the PSK Conference
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• 2003.10a
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• pp.104-105
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• 2003

Hypoxic-ischemic (H-I) encephalopathy in the prenatal and perinatal period is a major cause of morbidity and mortality and often results in cognitive impairment, seizures, and motor impairment (cerebral palsy). Many studies of neonatal H-I brain injury have utilized the well characterized Levine model in which unilateral carotid ligation is followed by exposure to hypoxia. (omitted)

• Toxicological Research
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• v.16 no.2
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• pp.117-124
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• 2000

The objective of this experiment is to investigate neurobehavioral and developmental effects of fumonisin B1 (FB1) after prenatal FB1 administration in rats. FB1 (0.8 or 1.6 mg/kg) was orally exposed to pregnant rats during gestational days 13 to 20, whereas the vehicle alone was administered to control group. Maternal and offspring body weights, physical landmarks of incisor eruption, eye opening, testes descending and vaginal opening, open field activity, running wheel activity, and complex maze performance were included as endpoints for developmental and neurobehavioral measurement. Maternal body weights were not signfficantly altered after FB1 exposure. Percentage of maternal weight gain difference between control and 1.6 mg/kg FBI groups was about 4%. Pre- and post-weanling weight of offsprings after prenatal exposure to FB1 was not signfficantly changed, suggesting that FB1 at 0.8 or 1.6 kg/kg doses may not cross the placenta. Significant gender difference in running wheel activity on postnatal days 57 to 63 and complex maze performance on postnatal days 75 to 78 was observed.

• Proceedings of the Korean Society of Applied Pharmacology
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• 1996.11a
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• pp.171-172
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• 1996

Cocaine is a powerful reinforcer that has become a popular drug of abuse in man. CNS effects that are related to the abuse of cocaine include feeling of well-being and euphoria. Brain dopamine systems are thought to mediate reinforcement and it is often assumed that cocaine's inhibition of dopamine uptake is the mechanism underlying its reinforcing effects. With increase in cocaine use among general population in recent years, adverse effects of the drug have occurred in all social strata and age groups. Therefore, it has been recognized that the epidemic of cocaine abuse is a growing major concerning public health. One of the most troubling aspects of cocaine abuse is its use by pregnant women. Drug abuse during pregnancy puts two lives at risk. Cocaine produces toxic effects on the fetus at concerntrations that are apparently nontoxic to the mother. Not only does cocaine cross the placenta via diffusion and via rapid penetration to mucous membranes, due to its high lipid solubility, but cocaine can also be found in breast milk, the effects of the cocaine can persist long after the child is born. Although it is known that prenatal cocaine exposure is associated with developmental risk to the fetus ana newborn, few studies have been conducted to assess the mechanisms whereby either short-term or long-term administration of cocaine can exert its harmful effects on the mother or the child. Therefore, it was our great interest to investigate the pharmacological and neurobehavioral changes in offspring that are prenatally exposed to cocaine.

• Biomedical Science Letters
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• v.21 no.1
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• pp.15-22
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• 2015

Dexamethasone, a synthetic glucocorticoid (GC), is clinically administered to woman at risk for premature labor to induce fetal lung maturation. However, exposure to repeated or excess GCs leads to intrauterine growth restriction (IUGR) and subsequently increases risk of psychiatric and cardio-metabolic diseases in later life through fetal programming mechanisms. GCs are key mediators of stress responses, therefore, maternal nutrient restriction or psychological stress during pregnancy also causes negative impacts on birth and neurodevelopment outcome of fetuses, and other congenital defects, such as craniofacial and skeletal abnormalities. In this study, to examine the effect of prenatal stress on fetal skeletal development, dexamethasone (1 mg/kg [DEX1] or 10 mg/kg [DEX10] maternal body weight per day) was administered intraperitoneally at gestational day 7.5~9.5 and the skeletons were prepared from embryos at day 18.5. Seven out of eighteen (39%) embryos treated with DEX10 showed axial skeletal abnormalities in either the T13 or L1 vertebrae. In addition, examination of the sternum revealed that xiphoid process, the protrusive triangular part of the lower end of the sternum, was bent more outward or inward in DEX group embryos. In conclusion, our findings suggest a possible link to the understanding of the effect of uterine environment to the fetal skeletal features.

• Development and Reproduction
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• v.19 no.4
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• pp.167-180
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• 2015

Arsenic is a toxic metalloid that exists ubiquitously in the environment, and affects global health problems due to its carcinogenicity. In most populations, the main source of arsenic exposure is the drinking water. In drinking water, chronic exposure to arsenic is associated with increased risks of various cancers including those of skin, lung, bladder, and liver, as well as numerous other non-cancer diseases including gastrointestinal and cardiovascular diseases, diabetes, and neurologic and cognitive problems. Recent emerging evidences suggest that arsenic exposure affects the reproductive and developmental toxicity. Prenatal exposure to inorganic arsenic causes adverse pregnancy outcomes and children's health problems. Some epidemiological studies have reported that arsenic exposure induces premature delivery, spontaneous abortion, and stillbirth. In animal studies, inorganic arsenic also causes fetal malformation, growth retardation, and fetal death. These toxic effects depend on dose, route and gestation periods of arsenic exposure. In males, inorganic arsenic causes reproductive dysfunctions including reductions of the testis weights, accessory sex organs weights, and epididymal sperm counts. In addition, inorganic arsenic exposure also induces alterations of spermatogenesis, reductions of testosterone and gonadotrophins, and disruptions of steroidogenesis. However, the reproductive and developmental problems following arsenic exposure are poorly understood, and the molecular mechanism of arsenic-induced reproductive toxicity remains unclear. Thus, we further investigated several possible mechanisms underlying arsenic-induced reproductive toxicity.

• Journal of Home Health Care Nursing
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• v.30 no.2
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• pp.202-215
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• 2023

Purpose: This study attempted to determine the factors related to behaviors of reducing exposure to endocrine disrupting chemicals (BRE to EDCs) in pregnancy, based on the PRECEDE model. Methods: A cross-sectional survey was conducted with participants (N=239) who met the medical records and eligibility criteria from the Women's Hospital and Public Health Center. Data were collected using a specially-designed questionnaire based on the PRECEDE model and included BRE to EDCs predisposing factors, reinforcing factors, and enabling factors. The data were analyzed using the chi-square test, independent t-test, one way ANOVA, Pearson's correlation coefficients and a hierarchical multiple regression analysis. Results: In Model I it was found that participation in prenatal education influenced the BRE to EDCs significantly; and a regression showed that the determinant variables accounted for 3.4%. In Model II, the predisposing factors of perceived barriers of BRE to EDCs and environmental self-efficacy were added. It was shown that they significantly influenced BRE to EDCs in the order named, and a regression revealed that increases in the determinant variables accounted for 22.5%. In Model III, to which enabling factors were added, the information acquisition experience of BRE to EDCs interacted significantly with BRE to EDCs and a regression showed an increase in the determinant variables accounting for 25.3%. Conclusion: The results of this study, the content of endocrine disruptors must be included in the prenatal care education program for pregnant women, and it should be composed of contents that can reduce the perceived obstacle to BRE to EDCs, enhance the environmental self-efficacy, and provide the information in regard to reducing exposure to EDCs.

• Women's Health Nursing
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• v.27 no.1
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• pp.27-39
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• 2021

Purpose: This study aimed to review recent findings from birth cohort studies on maternal and child environmental health. Methods: Birth cohort studies regarding environmental health outcomes for mothers and their children were investigated through a systematic review. A literature search was conducted in PubMed, CINAHL, the Cochrane Library, Embase, and RISS to identify published studies using the keywords using a combination of the following keywords: maternal exposure, environmental exposure, health, cohort, and birth cohort. Articles were searched and a quality appraisal using the Newcastle-Ottawa Scale for cohort studies was done. Results: A review of the 14 selected studies revealed that prenatal and early life exposure to environmental pollutants had negative impacts on physical, cognitive, and behavioral development among mothers and children up to 12 years later. Environmental pollutants included endocrine disruptors, air pollution (e.g., particulate matter), and heavy metals. Conclusion: This systematic review demonstrated that exposure to environmental pollutants negatively influences maternal and children's environmental health outcomes from pregnancy to the early years of life. Therefore, maternal health care professionals should take steps to reduce mothers' and children's exposure to environmental pollutants.

• Journal of Preventive Medicine and Public Health
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• v.37 no.4
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• pp.300-305
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• 2004

Objectives : The exposure to particulate air pollution during the pregnancy has reported to result in adverse pregnancy outcome such as low birth weight, preterm birth, still birth, and intrauterine growth retardation (IUGR). We aim to assess whether prenatal exposure of particulate matter less than 10 (m in diameter ($PM_{10}$) is associated with preterm birth in Seoul, South Korea. Methods : We included 382,100 women who delivered a singleton at 25-42 weeks of gestation between 1998 and 2000. We calculated the average PM10 exposures for each trimester period and month of pregnancy, from the first to the ninth months, based on the birth date and gestational age. We used three different models to evaluate the effect of air pollution on preterm birth; the logistic regression model, the generalized additive logistic regression model, and the proportional hazard model. Results : The monthly analysis using logistic regression model suggested that the risks of preterm birth increase with PM10 exposure between the sixth and ninth months of pregnancy and the highest risk was observed in the seventh month (adjusted odds ratio=1.07, 95% CI=1.01-1.14). We also found the similar results using generalized additive model. In the proportional hazard model, the adjusted odds ratio for preterm births due to PM10 exposure of third trimester was 1.04 (95% CI=0.96-1.13) and PM10 exposure between the seventh month and ninth months of pregnancy was associated with the preterm births. Conclusions : We found that there were consistent results when we applied the three different models. These findings suggest that air pollution exposure during the third trimester pregnancy has an adverse effect on preterm birth in South Korea.

• Toxicological Research
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• v.32 no.4
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• pp.275-280
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• 2016

Prenatal nicotine exposure over an entire pregnancy has been associated with an increased prevalence of hyperactivity, anxiety-like behavior and depression-like behavior in mature rats. However, the effects of maternal nicotine exposure in late gestation and lactation on the psychology and behavior of adolescent rat offspring are unclear. Thus, we investigated the effect of nicotine exposure during late gestation and lactation on anxiety-like and impulsive decision-making behavior in adolescent offspring of rat. Female rats were orally exposed to nicotine which is within range of plasma level of human chronic smokers during the period of third last period of gestation and lactation. When the offspring were weaned, we observed alterations in the anxiety-like behavior and decision-making ability of adolescent rat offspring using light/dark box test and T-maze delay-based cost-benefit decision-making task. The maternal consumption of nicotine reduced both the time spent in the light compartment and the number of transitions compared to nicotine-free rats. Moreover, such nicotine exposed adolescent offspring rats showed impulsive decision making which chose the instant reward in a decision-making situation. We found that nicotine exposure during late gestation and lactation induces an increase in anxiety-like and impulsive decision-making behavior at this developmental stage. These findings suggest that maternal nicotine-exposed offspring are at an increased risk of developing anxious and impulsive behavior.