• Journal of Environmental Health Sciences
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• v.46 no.4
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• pp.368-375
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• 2020

Objectives: Some animal studies have reported that methyl mercury causes developmental toxicities such as placental and fetal weight loss, but the mechanism is still unclear. This study aimed to investigate the developmental toxicities of methyl mercury, focusing on placental endocrine function and fetal growth retardation in rats. Methods: Positively same-time-mated female Sprague-Dawley rats were purchased on gestational day (GD) eight and treated with 0, 5, 10 and 20 ppm of methyl mercury (n=5) dissolved in tap water from GD eight through 19. During treatment, the drinking water (methyl mercury) intake and body weight of each pregnant rat was measured daily. On day 19, caesarean sections were performed and blood samples were collected. Developmental data such as placental and fetal weights, fetus numbers, and placental efficiency (fetal weight/placental weight) were also collected. Placental prolactin-growth hormone (PRL-GH) family, such as placental lactogen (PL) -Iv, II, and prolactin-like protein (PLP) -B, levels in serum were analyzed by ELISA. Also, placental tissues were assigned to histochemistry. Results: The mean cumulative methyl mercury exposure for the 5, 10, and 20 ppm groups were 2.37, 4.63, and 9.66 mg, respectively. The mean daily exposure of the 5, 10, and 20 ppm groups were 0.24, 0.47, and 0.97 mg, respectively. Maternal body weight increased in accordance with GD. There was no significant difference in weight gain among the experimental groups. Histopathologic changes were not observed in placental tissues among the experimental groups. However, mean placental and fetal weights were lower in the 10 and 20 ppm exposed groups compared to the control. Placental efficiency was also lower in the 10 and 20 ppm exposed groups compared to the control. Serum PL-Iv and II levels were lower in the 10 and 20 ppm exposed groups than the control, in accordance with the changing pattern of placental and fetal weights and placental efficiency. Conclusion: The inhibitory effects of methyl mercury on the serum levels of placental PRL-GH family such as PL-Iv and II may be secondary leads to the reduction of placental efficiency and fetal growth retardation in rats.

• Nutrition Research and Practice
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• v.5 no.2
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• pp.112-116
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• 2011

We investigated the effect of paternal folate status on folate content and expression of the folate transporter folate receptor ${\alpha}$ ($FR{\alpha}$) in rat placental tissues. Rats were mated after males were fed a diet containing 0 mg of folic acid/kg of diet (paternal folate-deficient, PD) or 8 mg folic acid/kg of diet (paternal folate-supplemented, PS) for 4 weeks. At 20 days of gestation, the litter size, placental weight, and fetal weight were measured, and placental folate content (n=8/group) and expression of $FR{\alpha}$ (n=10/group) were analyzed by microbiological assay and Western blot analysis, respectively. Although there was no difference observed in litter size or fetal weight, but significant reduction (10%) in the weight of the placenta was observed in the PD group compared to that in the PS group. In the PD group, placental folate content was significantly lower (by 35%), whereas $FR{\alpha}$ expression was higher (by 130%) compared to the PS group. Our results suggest that paternal folate status plays a critical role in regulating placental folate metabolism and transport.

• Parasites, Hosts and Diseases
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• v.53 no.2
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• pp.189-196
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• 2015

The sequestration of infected erythrocytes in the placenta can activate the syncytiotrophoblast to release cytokines that affect the micro-environment and influence the delivery of nutrients and oxygen to fetus. The high level of IL-10 has been reported in the intervillous space and could prevent the pathological effects. There is still no data of Th17 involvement in the pathogenesis of placental malaria. This study was conducted to reveal the influence of placental IL-17 and IL-10 levels on fetal weights in malaria placenta. Seventeen pregnant BALB/C mice were divided into control (8 pregnant mice) and treatment group (9 pregnant mice infected by Plasmodium berghei). Placental specimens stained with hematoxylin and eosin were examined to determine the level of cytoadherence by counting the infected erythrocytes in the intervillous space of placenta. Levels of IL-17 and IL-10 in the placenta were measured using ELISA. All fetuses were weighed by analytical balance. Statistical analysis using Structural Equation Modeling showed that cytoadherence caused an increased level of placental IL-17 and a decreased level of placental IL-10. Cytoadherence also caused low fetal weight. The increased level of placental IL-17 caused low fetal weight, and interestingly low fetal weight was caused by a decrease of placental IL-10. It can be concluded that low fetal weight in placental malaria is directly caused by sequestration of the parasites and indirectly by the local imbalance of IL-17 and IL-10 levels.

• Journal of Preventive Medicine and Public Health
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• v.37 no.4
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• pp.306-311
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• 2004

Background : The roles of antioxidants in the placenta and genetic susceptibility to oxidant chemicals in relation to neonatal birth weight have not been elucidated. We determined whether the level of placental manganese superoxide dismutase (MnSOD) and its genetic polymorphism plays any role in oxidative stress and neonatal birth weight. Methods : We measured placental MnSOD and determined MnSOD genetic polymorphism among 108 pregnant women who were hospitalized for delivery and their singleton live births in Korea. Main outcome measurements are maternal urinary malondialdehyde (MDA) and birth weight. Results : Maternal urinary concentrations of MDA were significantly associated with neonatal birth weight (P=0.04). The enzyme level of placental MnSOD was also significantly associated with MDA concentration (P=0.04) and neonatal birth weight (p<0.01). We observed dose-response relationships between placental MnSOD and maternal urinary MDA, and neonatal birth weight after adjusting for maternal weight, height, age, and neonatal sex. After controlling for covariates, MnSOD variant genotype increased maternal urinary MDA concentrations (p<0.01) and reduced birth weight by 149 gm (P=0.08). Conclusions : This study demonstrates that the placental level of MnSOD during pregnancy significantly affects fetal growth by reducing oxidative stress, and that genetic polymorphism of MnSOD probably modulate the effects of oxidants on fetal growth.

• Journal of Community Nutrition
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• v.6 no.2
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• pp.91-96
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• 2004

The purpose of this study was to evaluate the folate nutritional status of Korean pregnant women and to investigate the relation between folate levels of maternal-umbilical cord blood, placenta tissue, and pregnancy outcomes. The study subjects consisted of 25 pregnant women who have had normal term deliveries. Dietary folate intakes of the pregnants were estimated by semi quantitative frequency questionnaire and the serum and placenta tissue folate level was measured by microbiological analysis. The total folate intakes of the pregnant women was 655.6 ${\mu}$g/d, which was 131.1% of the Korean RDA for pregnants. Maternal serum folate level was 16.18ng/ml, which was significantly lower than that of umbilical cord blood (34.98ng/ml, p<0.05). Mean folate concentration of the placental tissue was 998.0ng/ml, which was the highest compared to maternal and umbilical cord serum level. Umbilical cord serum folate level and placental tissue folate level were highly influenced by maternal serum folate level. The umbilical cord folate levels of the infant group whose birth weight was higher than 3500g were significantly higher than the group whose birth weight was less than 3500g (p<0.05). The placental folate level was significantly higher in maternal group who showed desirable weight gain during pregnancy (11 - 14kg). In conclusion, the birth weigt was related to the umbilical cord folate level and the maternal weight gain was affected by the placental folate level.

• Biomedical Science Letters
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• v.20 no.1
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• pp.43-47
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• 2014

To understand the effect of prenatal stress on sex-specific changes in embryonic and placental growth, a synthetic glucocorticoid (dexamethasone) was administered intraperitoneally at a dosage of 1 mg/kg body weight (BW) (Dex1) or 10 mg/kg BW (Dex10) to pregnant ICR mice at the gestational days 7.5, 8.5 and 9.5 post coitum (p.c.). Embryos and placentas were then harvested at days 11.5 and 18.5 p.c., and their body weight and size were measured following the determination of sex through PCR using Sry specific primers in tail tissues. As a result, female embryos presented reduced fetal body weight and size in Dex1- and Dex10-treated groups than those of control group at the embryonic day 11.5 p.c. Interestingly, the growth seems to be recovered at day 18.5 as there was no difference in growth between control and dexamethasone treated groups. In the case of males, Dex1 induced a decrease in fetal weight in day 11.5 and this pattern was maintained until day 18.5, whereas their growth was not affected by Dex10 treatment. Placental growth showed similar patterns to fetal growth in both sexes but the extent of reduction was not statistically significant in most cases. Placental weights in Dex1- and Dex10-treated group were decreased significantly in male only. The results imply that the effect of prenatal stress is largely sex dependent due to different strategies for growth and survival in a stressful environment.

• Journal of Nutrition and Health
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• v.31 no.8
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• pp.1263-1269
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• 1998

The maintenance of adequate folate levels in the umbilical cord blood is esential for supplying tissue requirements of fetal growth. However, there is data on folate levels in the cord blood of Korean infant. The present investigation was undertaken to determine folate levels in cord blood and aassess relationships between folate levels and pregnancy outcomes. Dietary and supplementary folate intake was obtained from thirty subjects who were in the third trimester fo pregancy . The umbilical cord blood was drawn at delivery and pregnancy outcomes for the subjects were collected from their medical records. Erythrocyte and plasma folate levels in the cord blood were analyzed. The subjects were divided into two groups ; high folate (HF, $\geq$654ng/ml) and low folate (LF, <654ng/ml) groups according to erythrocyte folate levels in cord blood. Dietary folate intake and the amount of supplemental folates were not significantly different between the two experimental groups. However, infant birth weight (3540$\pm$295g) and placental weight(910$\pm$85g) for the HF group were significantly higher(p=0.0041 and p=0.109, respectively) than those for the LF group, which were 3127 $\pm$419g and 823$\pm$80g , respectively. Although it was not significant, the gestational weight gain for the HF group was 2.8kg higher than that for the LF group. Thus, the erythrocyte folate level in the cord blood was significantly related to infant birth weight and placental weight. These results confirm that a high erythrocyte folate level in the umbilical cord blood promotes both fetal and placental growth and improves gestational weight gain as well.

• Korean Journal of Community Nutrition
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• v.8 no.6
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• pp.814-821
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• 2003

The purpose of this study was to assess the maternal zinc status during pregnancy and to evaluate the relationship between the zinc concentration of maternal, umblical cord blood and placental tissue and pregnancy outcomes. Venous blood samples were drawn from 53 pregnant women just before delivery and the cord blood of their newborn babies was collected immediately after birth. In addition, placental tissues were extracted. We investigated the difference in the concentration of zinc in maternal, umbilical cord blood and placental tissue in two gestational age groups (preform delivery group [PT] and normal term delivery group [NT]) at 34.7 wk and 39.0 wk of mean gestational age, respectively). We also assessed correlations of the zinc concentration of maternal, umbilical cord blood and placental tissue. Lastly, we studied the correlations between the birth weights and the zinc concentration in the maternal, umbilical cord blood and placental tissue. The concentrations of maternal serum zinc and of umbilical cord serum zinc were significantly higher in the PT group (76.9$\pm$37.4 $\mu/dl$, 101.3$\pm$41.4 $\mu/dl$) than in those of the NT group (57.8$\pm$22.4 $\mu/dl$, 80.7$\pm$27.5 $\mu/dl$), respectively (p<0.05). The zinc concentration of the umbilical cord blood was significantly higher than that of the maternal blood in both groups (p<0.05). There was no significant correlation between the gestational age and the serum zinc concentration in the cord or the maternal serum. Our results showed that there was a negative relationship between the birth weight (r=-0.286) and the maternal serum zinc concentration. Despite there not being a significant difference, there was tendency for the highest concentrations of maternal serum zinc to be associated with the lowest birth weights. These findings support a possible relationship between the maternal zinc status and the pregnancy outcome, and suggest that zinc may play a role in the many biological processes involved in the successful outcome of a pregnancy.

• The Korean Nurse
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• v.5 no.6 s.26
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• pp.62-66
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• 1966

• Clinical and Experimental Pediatrics
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• v.63 no.2
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• pp.48-51
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• 2020

Background: The etiopathogenesis of late preterm (LPT) birth is undetermined. Placental histopathology, which reflects an adverse intrauterine environment and is reportedly associated with preterm labor and neonatal morbidities, has not been studied in LPT infants. Purpose: We investigated placental pathological lesion as markers of an adverse intrauterine environment during LPT labor. Methods: This retrospective case-control study compared placental histopathological and clinical variables between LPT and term neonates. Placental variables included chorioamnionitis, funisitis, hemorrhage, abruption, infarction, calcification, and syncytial knots. Maternal variables included age, substance abuse, pregnancyassociated diabetes mellitus and hypertension, duration of rupture of membrane, antibiotic use, and magnesium sulfate, whereas, those of neonates included gestational age, birth weight, race, sex, and Apgar scores. Standard statistical proedures were applied to analyze the data. Results: Chorioamnionitis (50% vs. 17.8%, P<0.001) and funisitis (20% vs. 4.4%, P=0.002) were more common in term infants. Placental infarction rate was insignificantly higher in LPT infants (25.6% vs. 14.3%, P=0.08). The mothers in the LPT group were older (30.4 years vs. 28.1 years, P=0.05; odds ratio [OR], 1.06; 95% confidence interval [CI], 0.998-1.12, P=0.056) and more often suffered from hypertension (28.9 vs. 12.9 %, P=0.02), and received magnesium sulfate (48.9 vs. 20%, P< 0.001; OR, 2.86; 95% CI, 1.12-7.29, P<0.05). Duration of rupture of membrane was higher in term infants (13.6 hours vs. 9.1 hours, P<0.001). Chorioamnionitis (OR, 0.33; 95% CI, 0.13-0.79; P<0.05) was associated with a lower risk of LPT delivery. Conclusion: Placental infection is not a risk factor for LPT births. There is a nonsignificant predominance of vascular anomalies in LPT placentas. Higher maternal age, magnesium sulfate therapy, and maternal hypertension are clinical risk factors for LPT labor.