• Clinical and Experimental Reproductive Medicine
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• v.25 no.2
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• pp.115-122
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• 1998

The maintenance of a viable pregnancy has long been viewed as an immunological paradox. The deveolping embryo and trophoblast are immunologically foreign to the maternal immune system due to their maternally inherited genes products and tissue-specific differentiation antigens (Hill & Anderson, 1988). Therefore, speculation has arisen that spontaneous abortion may be caused by impaired maternal immune tolerance to the semiallogenic conceptus (Hill, 1990). Loss of recall antigen has been reported in immunosuppressed transplant recipients and is associated with graft survival (Muluk et al., 1991; Schulik et al., 1994). Progesterone $(10^{-5}M)$ has immunosuppressive capabilities (Szekeres-Bartho et al., 1985). Previous study showed that fertile women, but not women with unexplained recurrent abortion (URA), lose their immune response to recall antigens when pregnant (Bermas & Hill, 1997). Therefore, we hypothesized that immunosuppressive doses of progesterone may affect proliferative response of lymphocytes to trophoblast antigen and alloantigen. Proliferative responses using $^3H$-thymidine ($^3H$-TdR) incorporation of peripheral blood mononuclear cells (PBMCs) to the irradiated allogeneic periperal blood mononuclear cells as alloantigen, trophoblast extract and Flu as recall antigen, and PHA as mitogen were serially checked in 9 women who had experienced unexplained recurrent miscarriage. Progesterone vaginal suppositories (100mg b.i.d; Utrogestan, Organon) beginning 3 days after ovulation were given to 9 women with unexplained RSA who had prior evidence of Th1 immunity to trophoblast. We checked proliferation responses to conception cycle before and after progesterone supplementation once a week through the first 7 weeks of pregnancy. All patients of alloantigen and PHA had a positive proliferation response that occmed in the baseline phase. But 4 out of 9 patients (44.4%) of trophoblast antigen and Flu antigen had a positive proliferative response. The suppression of proliferation response to each antigen were started after proliferative phase and during pregnancy cycles. Our data demonstrated that since in vivo progesterone treated PBMCs suppressed more T-lymphocyte activation and $^3H$-TdR incorporation compare to PBMCs, which are not influenced by progesterone. This data suggested that it might be influenced by immunosuppressive effect of progesterone. In conclusion, progesterone may play an important immunological role in regulating local immune response in the fetal-placental unit. Furthermore, in the 9 women given progesterone during a conception cycle, Only two (22%) repeat pregnancy losses occured in these 9 women despite loss of antigen responsiveness (one chemical pregnancy loss and one loss at 8 weeks of growth which was karyotyped as a Trisomy 4). These finding suggested that pregnancy loss due to fetal aneuploidy is not associated with immunological phenomena.

• Journal of Yeungnam Medical Science
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• v.8 no.1
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• pp.72-78
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• 1991

Ephedrine sulfate was administrated 30 healthy parturients undergoing elective repeat cesarean section under spinal anesthesia. Fifteen patients received ephedrine infusion (0.01% solution, beginning with approximately 5 mg/min) immediately after induction of spinal anesthesia to maintain maternal systolic blood pressure between 90% and 100% of the baseline systolic blood pressure (mean dose of ephedrine 31.6mg). Fifteen patients (contral group) received 20mg of ephedrine as an intravenous bolus, and additional 10mg increments, if neccessary, when systolic blood pressure decreased to 80% of the baseline systolic blood pressure (mean dose of ephedrine 26.8 mg). Nausea and/or vomiting occurred in seven women in the control group and one patient in the infusion group (p<0.001). Apgar scores, fetal blood gas tension, and time for onset of respiration was comparable in the two groups. The results suggest that prophylactic ephedrine infusion is safe and desirable in healthy parturients undergoing cesarean section under spinal anesthesia.

• Journal of English Language & Literature
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• v.57 no.1
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• pp.147-170
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• 2011

This paper elucidates the characteristics of transnational adoption, estimates the possibility of beyond-borders identity of transnational adoptees, and tries to analyze Jane Jeong Trenka's The Language of Blood in its context. Though it has been regarded as one of the most humanitarian ways of helping orphans and poor children of the world, transnational adoption, a one-way flow of children from poor Asian countries to rich white countries, has been operated under the market logic between countries. Transnational adoptees, who had been abandoned and forced to be taken away from their birth mother, and later, to fulfill the desire of white parents for a perfect family, perform an ideological labor, serving to make the heterogeneous nuclear family complete. Korean transnational adoptees, forced to transcend the borders of nation, culture, and ethnicity, experience racial conflict and alienation in white adoptive family and society. Their diaspora experience of violent dislocation creates frustration and confusion in establishing their identity as a whole being. When they return to Korea to find their birth mother and their true identity, Korean adoptees, however, are faced with other obstructing issues, such as language problem, culture conflict, and maternal nationalism. Finally, Korean transnational adoptees reject Korean nationalism discourse based on blood, and try to redefine themselves as beyond-borders subjectivities with new and fluid identities. Jane Jeong Trenka's The Language of Blood, an autobiographical novel based on her experiences as a transnational adoptee, represents a Korean adopted girl's personal, cultural, and racial conflict within her white adoptive family, and questions the image of benevolent white mother and the myth of multiculturalism. The novel further represents Jane's return to Korea to find out her true identity, and shows Jane's disappointment and alienation in her birth country due to her ignorance of language and culture. Returning to USA again, and trying to be reconciled with her American mother, Jane shows the promise of accepting her new identity capable of transcending the borders, and thus, the possibility of enlarging the category of belonging.

• Neonatal Medicine
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• v.18 no.1
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• pp.49-58
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• 2011

Purpose: The purpose of this study was to evaluate the relationship between cord blood adiponectin and insulin-like growth factor (IGF)-I and their effect on fetal growth and insulin resistance in mothers with gestational diabetes mellitus (GDM). Methods: Cord blood adiponectin and IGF-I were compared between mothers with GDM (GDM group, N=53) and controls (non-GDM group, N=101). Neonates were classified into three groups of small for gestational age (SGA, N=26), appropriate for gestational age (AGA, N=97), and large for gestational age (LGA, N=31) by birth weight. The association between cord adiponectin and IGF-I levels was evaluated in relation to maternal and neonatal clinical data. Results: Cord adiponectin was lower in the GDM group than in the non-GDM group (P<0.001). There was no significant difference in cord adiponectin among the SGA, AGA, and LGA groups in the GDM group (P=0.228). The cord adiponectin of AGA in the GDM group was significantly lower than that in the non-GDM group (P<0.001). The most powerful predictor affecting cord adiponectin was the result of maternal 75 g oral glucose tolerance test. The cord IGF-I values between the GDM group and the non-GDM group were not different (P=0.834). Neonates with the heavier birth weight had the higher cord IGF-I levels. The most powerful predictor affecting cord IGF-I was birth weight and the next was maternal parity. Conclusion: Both cord blood adiponectin and IGF-I were associated with fetal growth, but IGF-I was a more general and direct factor affecting fetal body size, and adiponectin seemed to have more association with insulin sensitivity than growth.

• Clinical and Experimental Pediatrics
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• v.51 no.5
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• pp.546-550
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• 2008

In this untreated classic phenylketonuria (PKU) case, mental retardation is severe; however, there have been individuals- like the mother of this case- who have escaped mental retardation and all the other potential sequelae of phenylketonuria, despite having high blood phenylalanine levels, and very poor dietary control. It appears that they have nearly normal brain phenylalanine levels despite high blood phenylalanine (Phe) levels. A number of studies have now demonstrated considerable variability in blood vs. brain phenylalanine levels in phenylketonuria patients. Outcome of phenylketonuria appears to be related to brain phenylalanine levels. We report a case of "undiagnosed" maternal phenylketonuria syndrome. A female infant had low birth weight (2,400 g) with microcephaly. We examined her family and discovered that her mother was an undiagnosed phenylketonuria patient with a borderline intelligence quotient (IQ). The infant's sister, six years old, was diagnosed with phenylketonuria at the age of four years was mentally retarded and had received an operation for cleft lip and palate. the sister had also had a low birth weight (2,300 g). Her sister and mother were compound heterozygotes (mother: R243Q/Y325X; sister: Y325X/P407S). The infant and father were heterozygous carriers (baby: R243Q/ -; father: P407S/ - ).

• Kidney Research and Clinical Practice
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• v.37 no.4
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• pp.356-365
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• 2018

Background: Woman kidney donors face obstetric complication risks after kidney donation, such as gestational hypertension and preeclampsia. Studies on childbirth-related complications among Asian women donors are scarce. Methods: This retrospective cohort study included woman donors aged 45 years or younger at the time of kidney donation in a single tertiary hospital between 1985 and 2014. Pregnancy associated complications were investigated using medical records and telephone questionnaires for 426 pregnancies among 225 donors. Matched non-donor controls were selected by propensity score and the maternal and fetal outcomes were compared with those of donors. Primary outcomes were differences in maternal complications, and secondary outcomes were fetal outcomes in pregnancies of the donor and control groups. Results: A total of 56 cases had post-donation pregnancies. The post-donation pregnancies group was younger at the time of donation and older at the time of delivery than the pre-donation pregnancies group, and there were no differences in primary outcomes between the groups except the proportion receiving cesarean section. Comparison of the complication risk between post-donation pregnancies and non-donor matched controls showed no significant differences in gestational hypertension, preeclampsia, or composite outcomes after propensity score matching including age at delivery, era at pregnancy, systolic blood pressure, body weight, and estimated glomerular filtration ratio (odds ratio, 0.63; 95% confidence interval, 0.19-2.14; P = 0.724). Conclusion: This study revealed that maternal and fetal outcomes between woman kidney donors and non-donor matched controls were comparable. Studies with general population pregnancy controls are warranted to compare pregnancy outcomes for donors.

• Journal of Nutrition and Health
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• v.29 no.2
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• pp.206-212
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• 1996

This study was to see if pregnant rats fed a pantothenic acid(PA) deficient diet for whole 3 weeks gestation would produce pups comparable to the normal controls, at the cost of maternal tissue PA concentration ([PA]) or coenzyme A content ([Co A]). Compared to the controls, dams fed a PA deficient diet tended to decrease weight gain, and produced pups with lower body, liver and brain weight (p<0.05). Postpartum dam's blood [PA] decreased more in PA deficient group than control (p<0.05, PA deficient : 2.52$\pm$0.66 to 0.77$\pm$0.23uM, control : 2.58$\pm$0.52 to 1.45$\pm$0.68uM), although Hb concentration did not differ between two groups. Pup's blood [PA] at birth was lower in PA deficient group than control group(1.75$\pm$0.27uM vs. 3.90$\pm$0.76uM, respectively, p<0.05) and 2-3 times that of postpartum dams in both two groups. [Co A] and [PA] in pup's tissues were 23-68% of dams in both groups, in spite of the higher [PA] in pups. These data suggest that Co A metabolism differs between pups and dams ; the pups were more adversely affected than dams by the dietary PA deficiency of dams during gestation.

• BioChip Journal
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• v.12 no.4
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• pp.304-308
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• 2018

Atopic disease is caused by a complex combination of environmental factors and genetic factors, and studies on influence of exposure to various environmental factors on atopic diseases are continuously reported. However, the exact cause of atopic dermatitis is not yet known. Our study was conducted to analyse the association of SNPs with the development of atopic disease in a small cohort. Samples were collected from the Mothers' and Children's Environmental Health (MOCEH) study and 192 cord blood DNA samples were used to identify incidence of atopy due to influence of exposure to environmental factors. Genetic elements were analysed using a precision medicine research (PMR) array designed with various SNPs for personalized medicine. Case-control analysis of atopy disease revealed 253 significant variants (p<0.0001) and SNPs on five genes (CARD11, ZNF365, KIF3A, DMRTA1, and SFMBT1) were variants identified in previous atopic studies. These results are important to confirm the genetic mutation that may lead to the onset of foetal atopy due to maternal exposure to harmful environmental factors. Our results also suggest that a small-scale genome-wide association analysis is beneficial to confirm specific variants as direct factors in the development of atopy.

• Journal of Genetic Medicine
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• v.8 no.1
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• pp.1-16
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• 2011

Owing to the risk of fetal loss associated with prenatal diagnostic procedures (amniocentesis, chorionic villus sampling), noninvasive prenatal diagnosis (NIPD) is ultimate goal of prenatal diagnosis. The discovery of circulating cell-free fetal DNA (cffDNA) in maternal plasma in 1997 has opened up new probabilities for NIPD by Dr. Lo et al. The last decade has seen great development in NIPD. Fetal sex and fetal RhD status determination by cffDNA analysis is already in clinical use in certain countries. For routine use, this test is limited by the amount of cell-free maternal DNA in blood sample, the lack of universal fetal markers, and appropriate reference materials. To improve the accuracy of detection of fetal specific sequences in maternal plasma, internal positive controls to confirm to presence of fetal DNA should be analyzed. We have developed strategies for noninvasive determination of fetal gender, and fetal RhD genotyping using cffDNA in maternal plasma, using real-time quantitative polymerase chain reaction (RT-PCR) including RASSF1A epigenetic fetal DNA marker (gender-independent) as internal positive controls, which is to be first successful study of this kind in Korea. In our study, accurate detection of fetal gender through gestational age, and fetal RhD genotyping in RhD-negative pregnant women was achieved. In this assay, we show that the assay is sensitive, easy, fast, and reliable. These developments improve the reliability of the applications of circulating fetal DNA when used in clinical practice to manage sex-linked disorders (e.g., hemophilia, Duchenne muscular dystrophy), congenital adrenal hyperplasia (CAH), RhD incompatibility, and the other noninvasive pregnant diagnostic tests on the coming soon. The study was the first successful case in Korea using cffDNA in maternal plasma, which has created a new avenue for clinical applications of NIPD.

• Clinical and Experimental Pediatrics
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• v.57 no.7
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• pp.329-332
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• 2014

3-methylcrotonyl-coenzyme A carboxylase (3MCC) deficiency is an autosomal recessive disorder in which leucine catabolism is hampered, leading to increased urinary excretion of 3-methylcrotonylglycine. In addition, 3-hydroxyisovalerylcarnitine levels increase in the blood, and the elevated levels form the basis of neonatal screening. 3MCC deficiency symptoms are variable, ranging from neonatal onset with severe neurological abnormality to a normal, asymptomatic phenotype. Although 3MCC deficiency was previously considered to be rare, it has been found to be one of the most common metabolic disorders in newborns after the neonatal screening test using tandem mass spectrometry was introduced. Additionally, asymptomatic 3MCC deficient mothers have been identified due to abnormal results of unaffected baby's neonatal screening test. Some of the 3MCC-deficient mothers show symptoms such as fatigue, myopathy, or metabolic crisis with febrile illnesses. In the current study, we identified an asymptomatic 3MCC deficient mother when she showed abnormal results during a neonatal screening test of a healthy infant.