• 대한생식의학회:학술대회논문집
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• 2002.05a
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• pp.11-17
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• 2002

Animal clones derived from somatic cells have been successfully produced in a variety of mammalian species such as sheep, cattle, mice, goats, pigs, cat and rabbits. However, there are still many unsolved problems in the present cloning technology. Somatic cell nuclear transfer has shown several developmental aberrancies including high rate of abortion in early gestation and increased perinatal death. These developmental failures of cloned embryos may arise from abnormal reprogramming of donor genome and/or incomplete cloning procedure. We have found that overall genomic methylation status of cloned bovine embryos is quite different from that of normal embryos in various genomic regions, suggesting that the developmental failures of cloned embryos may be due to incomplete reprogramming of donor genomic DNA. Many of the advances in understanding the molecular events for reprogramming of donor genome will more clarify the developmental defects of cloned embryos.

• Journal of Preventive Medicine and Public Health
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• v.9 no.1
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• pp.129-138
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• 1976

The causes and problems underlying deaths in perinatal period are often similar and might be expected to yield to same type of preventive measures. This is one of the reasons for attempting to develop a reporting of perinatal mortality and its related matters. This study aims at figuring out the biologic risk factors onto the perinatal death. Considering stillbirth and early neonatal mortality separately, considerable associations between stillbirth and reproductive history of women, are observed, ana it is found that prematurity is the the far most important factor in the early neonatal mortality.

• Clinical and Experimental Pediatrics
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• v.45 no.12
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• pp.1512-1518
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• 2002

Purpose : Twins have a higher mortality and morbidity than singletons. Co-twin with one fetal death is particularly at risk. We investigated the neonatal outcome of live co-twins when one fetus had died after the 20th gestational week, and associated risk factors. Methods : A retrospective study was performed in fifteen cases of twin pregnancy with single intrauterine fetal deaths after the 20th gestational week during the period from January 1996 to December 2000 at Chonnam University Hospital. Results : Gestational age was $33.7{\pm}3.2weeks$, birth weight was $1,992{\pm}592g$. Interval between one fetal death being detected and the delivery of a live co-twin was $32.4{\pm}29.5days$. There were 11 cases(73.3%) of premature babies less than 37 gestational weeks. Main causes of preterm delivery were preterm labor and premature rupture of membranes. Hematologic findings suggesting disseminated intravascular coagulopathy(DIC) were not found in all mothers before delivery, and was not associated with DIC and encephalomalacia of the live co-twin. Perinatal outcome of fifteen live co-twins was as follows : six were normal(40%), three were DIC(20.0%), three were encephalomalacia(20.0%), one suffered intrauterine growth retardation, there was one case of twin to twin transfusion syndrome, and one of congenital heart disease(atrial septal defect with pulmonary stenosis). The occurrence of DIC and encephalomalacia in live co-twins was not related to placental chorionicity, birth weight, gestational week, and the interval between the detection one fetal death and the delivery of a live co-twin. Conclusion : We could not find any maternal hematologic problems in twin pregnancies complicated by one fetal death. Twenty percent of live co-twins showed DIC and encephalomalacia. However, its associated risk factors were not found. We need to investigate more closely the cases of live co-twins with one intrauterine fetal death.

• Clinical and Experimental Pediatrics
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• v.46 no.6
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• pp.597-601
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• 2003

Trisomy 9 mosaic syndrome is a rarely reported chromosomal abnormality with high incidence of intrauterine growth retardation and perinatal death. Even a baby lives, he has severe mental retardation and significant malformations. The incidence and severity of malformations and mental retardation correlate with the percentage of trisomic cells in the different tissues. The characteristic craniofacial abnormalitis are narrow bifrontal diameter, up-slanted and short palpebral fissures, a prominent nasal bridge with a short root, a prominent lip covering a receding lower lip, low-set, posteriorly rotated, and misshapen ears. Ventricular septal defect is a main cardiac abnormality. Bony hypoplasia and dislocated hips have been frequently reported. Central nervous system, hepatobiliary, gastrointestinal and genitourinary abnormalities also had been reported. The authors report a baby who had characteristic abnormalities of trisomy 9 mosaicism with narrow temples, up-slanted palpebral fissures, a bulbous nose, thin and protruding upper lip, low set and malformed ears, hyperextended wrist and overlapping fingers. Cytogenetic analysis performed to confirm the chromosomal abnormality revealed trisomy 9, low level mosaic type.

• Journal of mucopolysaccharidosis and rare diseases
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• v.2 no.1
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• pp.19-22
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• 2016

Purpose: Mucolipidosis type II (ML II), also known as I-cell disease is an autosomal recessive inherited disorder of lysosomal enzyme transport caused by a deficiency of the uridine diphosphate (UDP)-N-acetylglucosamine:lysosomal enzyme N-acetylglucosamine-1-phosphotransferase (GlcNAc-phosphotransferase). Clinical manifestations are skeletal abnormalities, mental retardation, cardiac disease, and respiratory complications. A severely and rapidity progressive clinical course leads to death before 10 years of age. Methods/Results: In this study we diagnosed three cases of prenatal ML II in two different at-risk families. We compared two procedures -biochemical analysis and molecular analysis - for the prenatal diagnosis of ML II. Both methods require an invasive procedure to obtain specimens for the diagnosis. Biochemical analysis requires obtaining cell cultures from amniotic fluid for more than two weeks, and would result in a late diagnosis at 19 to 22 weeks of gestation. Molecular genetic testing by direct sequence analysis is usually possible when mutations are confirmed in the proband. Molecular analysis has an advantage in that it can be performed during the first-trimester. Conclusion: Molecular diagnosis is a preferable method when a prompt decision is necessary.

• Toxicological Research
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• v.12 no.2
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• pp.203-211
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• 1996

Methanol has been widely used as an industrial solvent and environmental exposure to methanol would be expected to be increasing. In humans, methanol causes metabolic acidosis and damage to ocular system, and can lead to death in severe and untreated case. Clinical symptoms are attributed to accumulation of forrnic acid which is a metabolic product of methanol. In humans and primates, formic acid is accumulated after methanol intake but not in rodents due to the rapid metabolism of methanol. Neverthless, the developmental and reproductive toxicity were reported in rodents. Previous reports showed that perinatal exposure to ethanol produces a variety of damage in human central nervous system by direct neurotoxicity. This suggests that the mechanism of toxic symptoms by methanol in rodents might mimic that of ethanol in human. In the present study I hypothesized that methanol can also induce toxicity in neuronal cells. For the study, primary culture of rat hippocampal neurons and glias were empolyed. Hippocampal cells were prepared from the embryonic day-17 fetuses and maintained up to 7 days. Effect of methanol (10, 100, 500 and 1000 mM) on neurite outgrowth and cell viability was investigated at 0, 18 and 24 hours following methanol treatment. To study the changes in proliferation of glial cells, protein content was measured at 7 days. Neuronal cell viability in culture was not altered during 0-24 hours after methanol treatment. 10 and 100 mM methanol treatment significantly enhanced neurite outgrowth between 18-24 hours. 7-day exposure to 10 or 100 mM methanol significantly increased protein contents but that to 1000 mM methanol decreased in culture. In conclusion, methanol may have a variety of effects on growing and differentiation of neurons and glial cells in hippocampus. Treatment with low concentration of methanol caused that neurite outgrowth was enhanced during 18-24 hours and the numbers of glial cell were increased for 7 days. High concentration of methanol brought about decreased protein contents. At present, the mechanism responsible for the methanol- induced enhancement of neurite outgrowth is not clear. Further studies are required to delineate the mechanism possibly by employing molecular biological techniques.

• Korea journal of population studies
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• v.11 no.1
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• pp.76-86
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• 1988

The primary objective of this study was to estimate the level of infant mortality rate and to find the cause of infant deaths prevailed in 1981~86 from vital registration data. In the course of that undertaking we have considered the non-registered portion of infant deaths especially for the non-registered portion of neonatal deaths. The main reason is that deaths occurring in the neonatal period and prior to the registration of the birth leave little incentive for the registration of either the birth or the death. From several ad-hoc survey's results and other countries' experiences it was, however, found that the proportion of neonatal deaths was 69.3%, the proportion of deaths in the period of first month in infanty was 7%, and the proportion of deaths in the period of 2 months and over in infancy was 23.7% respectivily. Thus, adoption the hypothesis that post-neonatal mortality is completly registered, we obtained the extimated number of infant deaths. Attempt to test the hypothesis was also made using the Brougeois- Pichats's function. The result was that the registered number of deaths in the post-neonatal period is almost compatible with the expected number. The major finding in this study was that the level of infant mortality rate in Korea was 19 per thousand live births in 1981 and 13 in 1986. This level of 1986 was almost identical with the level of Japan in 1970. It was also found that there was a difference in the level of infant mortality rate between sexes during 1981-83 but the difference was disappeared in 1985-86. Looking into the cause of infant deaths, it was found from registration that 21.2% of all infant deaths was due to congenital snomalies, 11.5% was due to pneumonia and 5.1% was due to the conditions originating in the perinatal period in that order. This pattern seems to be different with that of U.S.A., Japan and France. However, if we consider the non-registered neo-natal deaths, the order of the cause of infant deaths in Korea will be the same as compared countries. Finally, every efforts should should be made to obtain a good quality of data on infant mortality, making the non-registered events reported completely through hospitals.

• The Korean Nurse
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• v.30 no.3
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• pp.49-65
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• 1991

This study was carried out to assess the problems with the pregnant women, and check out the risk-factors in the high-risk pregnancies, using a simplified antepartum risk-scoring system, which was revised from Edwards' scoring system to be suitable for Korean situaition. This instrument was included 4 categories, demographic, obstetric, medical and miscellaneous factors. This survey was based on the 1300 pregnant women who were admitted, $x^2$-test, F-test, Pearsons correation, using statistical package SAS in NAS computer system, KIST. The results of the study were as follows; 1. 1313 infants were deliveried of these 560 infants(42.7%) were born to mothers with risk-scores > 7, and 753 infants(57.3%) were born to mothers risk-scores <7. 2. Maternal age" parity, education level, of the demographic factors were significant relation statistically to identify the high risk pregnancies($X^2$=20.88, 42.87, 15.60 P < 0.01). 3. C-section, post term, incompetent cervix, uterine anomaly, polyhydramnios, congenital anomaly, sensitized RH negative, abortion, preeclampsia, excessive size infant, premature, low birth weight infanl, abnormal presentation, perinatal loss, multiple pregnancy, of the obstetric factors were significant relation statistically to identify the high risk-pregnancies. ($X^2$ = 175.96, 87.5, 16.28, 21.78, 9.46, 8. 10, 6.75, 22.9, 64.84, 6.93, 361.43, 185.55, 78.65, 45.52, P < 0.01). 4. Abnormal nutrition, anemia, UTI, other medicalcondition(pulmonary disease, severe influenza), heart disease, V.D., of the miscellaneous and medical factors, were significant relation statistically to identify the high risk-pregnancies. 5. Premature, low birth weight infant, contracted pelvis, abnormal presentation, of the risk factors were significantly related with Apgar score at 1 '||'&'||' 5 minute after birth and neonatal body weight. 6. Apgar score at 1 '||'&'||' 5 minute after, birth and neonatal body weight were significantly negative correlated with risk-score. 7. There were statistically significant difference between risk-score and Apgar score at 1 '||'&'||' 5 minute after birth, 3 group(0-3, 4-6, above 7), and neonatal body weight, 2 group(below 2.5kg, the other group) (F=104.65, 96.61, 284.92, P<0.01). 8. Apgar score at 1 '||'&'||' 5 minute after birth(below 7), and neonatal body weight(below 2.5kg), were significant relation statistically with risk score.($x^2$=65.99, 60.88, 177.07, P<0.01) were 60.8 %, 60% . 9. Correct classifications of morbid infants(l '||'&'||' 5 minute Apgar score < 7) were 77.8%, 83.8% and that of nonmorbid infants(l '||'&'||' 5 minute Apgar score > 7) were 60.8%, 60%. 10. There were statistically significant difference between dislribution of maternal risk-score among the morbid infants(l '||'&'||' 5 minute Apgar score < 7) and non morbid infants(l '||'&'||' 5 minute Apgar score> 7) ($x^2$=64.8, 58.8, P < 0.001). 11. There were statistically significant difference between distribution of morbid infants(l '||'&'||' 5 minute Apgar score < 7) and fetal death. 12. The predictivity for classifying high.risk cases was 12 % and for classifying low-risk cases was 98.3 % in 5 minute Apgar score. Suggestions for further studies are as follows; 1. Contineous prospective studies, using this newly revised scoring system are strongly recommended in the stetric service. 2. Besides risk facto~s used in this study, assessmenl of risks by factors in another scoring system and paralled studies related to perinatal outcome are strongly recommended.

• Biomolecules & Therapeutics
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• v.26 no.5
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• pp.439-445
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• 2018

T-type calcium channels are low voltage-activated calcium channels that evoke small and transient calcium currents. Recently, T-type calcium channels have been implicated in neurodevelopmental disorders such as autism spectrum disorder and neural tube defects. However, their function during embryonic development is largely unknown. Here, we investigated the function and expression of T-type calcium channels in embryonic neural progenitor cells (NPCs). First, we compared the expression of T-type calcium channel subtypes (CaV3.1, 3.2, and 3.3) in NPCs and differentiated neural cells (neurons and astrocytes). We detected all subtypes in neurons but not in astrocytes. In NPCs, CaV3.1 was the dominant subtype, whereas CaV3.2 was weakly expressed, and CaV3.3 was not detected. Next, we determined CaV3.1 expression levels in the cortex during early brain development. Expression levels of CaV3.1 in the embryonic period were transiently decreased during the perinatal period and increased at postnatal day 11. We then pharmacologically blocked T-type calcium channels to determine the effects in neuronal cells. The blockade of T-type calcium channels reduced cell viability, and induced apoptotic cell death in NPCs but not in differentiated astrocytes. Furthermore, blocking T-type calcium channels rapidly reduced AKT-phosphorylation (Ser473) and $GSK3{\beta}$-phosphorylation (Ser9). Our results suggest that T-type calcium channels play essential roles in maintaining NPC viability, and T-type calcium channel blockers are toxic to embryonic neural cells, and may potentially be responsible for neurodevelopmental disorders.

• Neonatal Medicine
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• v.18 no.2
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• pp.221-227
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• 2011

Purpose: The objectives were to identify the characteristics of neonates with hydrops fetalis, and to identify the risk factors associated with mortality. Methods: A retrospective review of AMC (Asan Medical Center) dataset was performed from January 1990 to June 2009. The characteristics of 71 patients with hydrops fetalis were investigated and they were divided into two groups: the survived group and the expired group. Various perinatal and neonatal factors in two groups were compared to find out risk factors associated with mortality based on univariate analysis, followed by multiple regression analyses (SPSS version 18.0). Results: Of those 71 neonates (average gestational age: 33 weeks, birth weight: 2.6 kg), 38 survived, 33 died, resulting in overall mortality rate of 46.5%. The most common etiology was idiopathic followed by chylothorax, cardiac anomalies, twin-to-twin transfusion, meconium peritonitis, cardiac arrythmias, and congenital infections. Factors that were associated independently with mortality in logistic regression analyses were low 5-minutes Apgar score, hyaline membrane disease and delayed in achieving 50th percentile ideal body weight for appropriate gestational age by 10 days. Conclusion: In this study, 5-minutes Apgar score, hyaline membrane disease and delayed in achieving 50th percentile ideal body weight for appropriate gestational age by 10 days were significant risk factors associated with mortality in hydrops fetalis. Therefore, the risk of death among neonates with hydrops fetalis depends on the illness immediately after birth and severity of hydrops fetalis. Informations from this study may prove useful in prediction of prognosis to neonates with hydrops fetalis.