• Anatomy and Cell Biology
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• v.57 no.3
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• pp.400-407
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• 2024

Intrauterine alcohol exposure delays bone maturation and intensifies osteoporosis and fracture risk. As most studies emphasize the neurological aspects of intrauterine alcohol exposure, there is a lack of research on the implications pertaining to osseous tissue. Previous studies investigated these effects in fetuses, with limited studies on postnatal life. Postnatal studies are crucial since peak bone growth occurs during adolescence. This study aimed at assessing the effects of prenatal alcohol exposure on the humerus proximal and distal growth plate chondrocytes in 3-week-old rats. Sprague Dawley rats (n=9) were assigned to either the ethanol group (n=3), saline (n=3), and untreated (n=3) group and time-mated. Once pregnant, as confirmed by the presence of a copulation plug, the former 2 groups were treated with 0.015 ml/g of 25.2% ethanol and 0.9% saline. The untreated group received no treatment. The left humeri belonging to 6 pups per group were used. Serial sections were cut with a microtome at 5 ㎛ thickness. These sections were stained with haematoxylin and eosin for assessment of normal morphology or immunolabeled with anti-Ki-67 and transforming growth factor β-1 (TGFβ-1) antibody. Prenatal alcohol exposure adversely effected the growth plate sizes and the number of cells in the proliferative zone. Fewer TGFβ-1 immunopositive and proliferative chondrocytes were found using the anti-Ki-67 antibody. This may explain the growth retardation in offspring exposed to gestational alcohol, showing that gestational alcohol exposure inhibits cell proliferation, aiding the diminished stature.

• Animal cells and systems
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• v.6 no.3
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• pp.247-252
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• 2002

The effect of paraquat (PQ, 1,1＇-dimethyl-4,4＇-bipyridium) on the histogene-sis and glycoconjugates (GCs) properties of the pyloric region of the stomach in a perinatal rat was examined by histological and histochemical methods. Oral administration of PQ (9 mg/kg per day in 0.2 mL of D.W.) on 7 to 14 days of gestation revealed growth retardation with significant reductions in the length of pyloric gland and their pit. As for histochemical properties of GCs in the pyloric region of the stomach, the PQ-treated rats showed some differences, such as delayed initial appearance of the sulfated GCs and lectin affinities compared with the vehicle group. These different GCs properties in the surface and gastric pit were usually detected in the fetal rats and more prominent and evident differences were revealed in the gland epithelium of the early postnatal rat. These results suggest that maternal PQ administration causes intrauterine growth retardation asso-ciated with delayed histogenesis and GCs immaturation of pyloric mucosa in developing rat.

• Clinical and Experimental Pediatrics
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• v.45 no.5
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• pp.646-653
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• 2002

Purpose : The incidence of type 2 diabetes mellitus in children has been increasing worldwide recently, which is thought to be related to the increasing prevalence of obesity. We investigated to evaluate the incidence and the characteristics of type 2 diabetes mellitus in children and also analysed the relationship between intrauterine growth retardation and type 2 diabetes mellitus. Methods : We investigated 25 children diagnosed as type 2 diabetes mellitus between March 1990 and December 2000. The analysis was performed retrospectively with medical records based on the clinical characteristics and laborotory findings. Results : Incidence of type 1 and type 2 diabetes mellitus in children has been increasing since 1990. We demonstrated an increase in the percentage of type 2 diabetes mellitus children from 5.3% in 1990 to 21.0% in 2000. Sixty eight percent of patients(17/25) were classified as obese group. Initial symptoms at first visit were polyuria, polydipsia and polyphagia 48%(12/25), asymptomatic glycosuria 40% (10/25), weight loss 8%(2/25) and obesity 4%(1/25). The mean age at diagnosis was $12.9{\pm}1.8$ years. 64%(16/25) of patients had positive family history of type 2 diabetes mellitus. Autoanti-bodies were positive in 18.1%(4/22) of patients. Twenty eight percent (7/25) of patients had an associated disease and two patients had fatty liver in association with obesity. Treatment consisted of diet, exercise, education and oral hypoglycemic agents. Three patients were treated with insulin as well as oral hypoglycemic agents because of poor blood glucose control. Long-term diabetic complications occurred in 4 patients. Intrauterine growth retardtion was found in 34.6%(9/25); 88.9% (8/9) of these patients were non-obese group. Conclusion : The increase in the incidence of type 2 diabetes mellitus in children is thought to be related to the increasing prevalence of obesity. The non-obese group of patients might be associated with intrauterine growth retardation.

• Journal of Genetic Medicine
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• v.16 no.1
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• pp.23-26
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• 2019

Thrombophilia refers to inherited or acquired hemostatic disorders that result in a predisposition to blood clot formation. When combined with the hypercoagulable state that is characteristic of pregnancy, there is an increased risk of severe and recurrent pregnancy complications. Activated protein C resistance caused by factor V Leiden (FVL) mutation is known to be the most common cause of inherited thrombophilia in Caucasian population. FVL mutation has been related to pregnancy complications associated with hypercoagulation, e.g. miscarriage, intrauterine fetal demise, placental abruption, and intrauterine growth retardation. Although the FVL mutation is easily detected using molecular DNA techniques, patients who are heterozygous for this disorder often remain asymptomatic until they develop a concurrent prothrombotic condition. Because there are potentially serious effects of FVL mutation for pregnancy, and because effective treatment strategies exist, early detection and treatment of this condition might be considered.

• Korean Journal of Agricultural Science
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• v.43 no.1
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• pp.72-79
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• 2016

It has long been known that nutritional and environmental influences during the early developmental period affect the biological mechanisms which determine animal metabolism. This phenomenon, termed 'metabolic imprinting', can cause subtle but long-lasting responses to prenatal and postnatal nutrition and even be passed onto the next generation. A large amount of research data shows that nutrient availability, in terms of quantity as well as quality, during the early developing stages can decrease the number of newborn piglets and their body weight and increase their susceptibility to death before weaning. However, investigation of potential mechanisms of 'the metabolic imprinting' effect have been scant. Therefore, it remains unknown which factors are responsible for embryonic and early postnatal nutrition and which factors are major determinants of body weight and number of new born piglets. Intrauterine undernutrition, for example, was studied using a rat model providing dams 50% restricted nutrients during pregnancy and the results showed significant decreases in birth weight of newborns. This response may be a characteristic of a subset of modulations in embryonic development which is caused by the metabolic imprinting. Underlying mechanisms of intrauterine undernutrition and growth retardation can be explained in part by epigenetics. Epigenetics modulate animal phenotypes without changes in DNA sequences. Epigenetic modifications include DNA methylation, chromatin modification and small non-coding RNA-associated gene silencing. Precise mechanisms must be identified at the morphologic, cellular, and molecular levels by using interdisciplinary nutrigenomics approaches to increase pig production. Experimental approaches for explaining these potential mechanisms will be discussed in this review.

• The Journal of Pediatrics of Korean Medicine
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• v.25 no.2
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• pp.111-120
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• 2011

Objectives: The purpose of this study is to estimate genetic and environmental factors, which can affect Idiopathic true Precocious puberty, and to evaluate the clinical and endocrinologic characteristics. Methods: Retrospective and Comparative analysis of 76 children (72 girls and 4 boys) has been diagnosed with idiopathic true precocious puberty, and treated with GnRHa from December 2008 to July 2011. Results: 1. The Average chronological age (CA. yr) of children diagnosed with idiopathic true precocious puberty was $8.40{\pm}0.81$ (girls), $9.93{\pm}0.12$ (boys). 2. The Average height & weight percentile (%ile) of the girls diagnosed with idiopathic true precocious puberty was $67.38{\pm}22.04$, $67.69{\pm}23.20$. 3. The girls' mothers have diagnosed with idiopathic true precocious puberty, and they were shorter than the average. This shows that mother's small height and idiopathic true precocious puberty are closely related to each other. 4. BMI percentile (%ile) of girls diagnosed with idiopathic true precocious puberty was $63.26{\pm}24.86$. 23.6% of children were diagnosed with overweight or obesity. This result shows that obesity and idiopathic true precocious puberty are proportionally related. 5. Birth weights (kg) of the children diagnosed with idiopathic true precocious puberty were $3.16{\pm}0.43$ (girls), $3.15{\pm}0.38$ (boys). 8.3% of children were diagnosed with Intrauterine growth retardation. 6. The Average bone ages (BA. yr) of the children diagnosed with idiopathic true precocious puberty were $10.51{\pm}0.99$ (girls), $12.10{\pm}0.97$ (boys). The Average BA-CA was $2.11{\pm}0.81$ (girls), $2.00{\pm}0.87$ (boys). 7. The Average predicted adults' height (PAH. cm) of the children diagnosed with idiopathic true precocious puberty was $151.61{\pm}4.00$ (girls), $163.50{\pm}2.15$ (boys). The Average MPH-PAH was $6.84{\pm}4.91$ (girls), $6.00{\pm}5.35$ (boys). 8. 23.6% of the children treated with GnRHa were co-treated with Growth Hormone. Conclusions: Estimated factors which cause Idiopathic true precocious puberty are mother's small height, obesity, and Intrauterine growth retardation. However, the studies of Oriental Medicine for Idiopathic true precocious puberty were lacking. Further clinical and experimental researches are needed.

• Development and Reproduction
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• v.22 no.2
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• pp.199-203
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• 2018

Although trisomy 16 is commonly detected in spontaneous abortions and accounts for over 30% of cases of autosomal trisomy detected after spontaneous abortion, trisomy 16 mosaicism is rarely detected by amniocentesis in the second trimester. Here, we report a case of level III trisomy 16 mosaicism (47,XX,+16[8]/46,XX[31]) diagnosed by cytogenetic analysis of independently cultured amniotic fluid cells. The female baby was delivered at full term with low birth weight and intrauterine growth retardation, and interestingly, her karyotype was normal (46,XX). Given the difficulty in predicting the outcomes of fetuses with this mosaicism, it is recommended to inform the possibility of mosaicisms including this trisomy 16 mosaicism during prenatal genetic diagnosis and genetic counseling for parents.

• Journal of Genetic Medicine
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• v.18 no.1
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• pp.60-63
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• 2021

Gabriel-de Vries syndrome, caused by the mutation of YY1, is a newly defined genetic syndrome characterized by developmental delay, facial dysmorphism, and intrauterine growth retardation. A 7-month-old girl presented developmental delay and subtle facial dysmorphism including facial asymmetry, micrognathia, and low-set ears. Whole exome sequencing identified a de novo heterozygous missense variant in the YY1 (c.1220A>G; p.His407Arg) gene. Here, we examined the clinical and genetic characteristics of an infant with a novel likely pathogenic variant of YY1. This case expands the phenotypic spectrum of Gabriel-de Vries syndrome.

• Clinical and Experimental Reproductive Medicine
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• v.41 no.3
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• pp.97-107
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• 2014

The placenta is a temporary fetomaternal organ capable of supporting fetal growth and development during pregnancy. In particular, abnormal development and dysfunction of the placenta due to cha nges in the proliferation, differentiation, cell death, and invasion of trophoblasts induce several gynecological diseases as well as abnormal fetal development. Autophagy is a catalytic process that maintains cellular structures by recycling building blocks derived from damaged microorganelles or proteins resulting from digestion in lysosomes. Additionally, autophagy is necessary to maintain homeostasis during cellular growth, development, and differentiation, and to protect cells from nutritional deficiencies or factors related to metabolism inhibition. Induced autophagy by various environmental factors has a dual role: it facilitates cellular survival in normal conditions, but the cascade of cellular death is accelerated by over-activated autophagy. Therefore, cellular death by autophagy has been known as programmed cell death type II. Autophagy causes or inhibits cellular death via the other mechanism, apoptosis, which is programmed cell death type I. Recently, it has been reported that autophagy increases in placenta-related obstetrical diseases such as preeclampsia and intrauterine growth retardation, although the mechanisms are still unclear. In particular, abnormal autophagic mechanisms prevent trophoblast invasion and inhibit trophoblast functions. Therefore, the objectives of this review are to examine the characteristics and functions of autophagy and to investigate the role of autophagy in the placenta and the trophoblast as a regulator of cell 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.