• Journal of Life Science
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• v.15 no.6 s.73
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• pp.979-986
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• 2005

Lead (Pb) exposure during development can produce neurological deficits. In this study, the effect of Pb exposure during neonatal development via lactation on anxiety of brain function was investigated. Long-Evans strain rats were raised through two generations. At the birth of the second generation, the dams were subdivided into two groups and supplied drinking water containing either $0.2\%$ Pb (Pb-treated group) or sodium (Na, Control group) acetate until weaning. Rats were sacrificed at 3 (weaning) and 11 weeks (maturity) for brain Pb and fatty acid analysis. Motor activity and elevated plus maze tests were initiated at 9 weeks. The brains in the Pb-treated group at weaning and maturity contained 1486$\pm$98 and $270{\pm}46$ ng Pb/g, respectively The control group showed the background level of Pb ($3.7{\pm}1.0_{ng}$ Pb/g) in both ages. The alterations in brain fatty acid composition induced by Pb exposure were more evident in 3 wks old than 11 wks old. For example, in 3 wks old, the percentages of $18:2_{n-6}$, $20:2_{n-6}$ and $18:2_{n-6}$ were decreased in the Pb-treated group with an increase in $20:4_{n-6}$ In motor activity test, there was a tendency of hyperactivity in the Pb-treated group compared with the control group but the difference was not significant. In elevated plus maze test, the Pb-treated group showed fewer numbers of visits to the open arms (P < 0.05), indicating that Pb exposure may lead to anxiogenic effect.

• Clinical and Experimental Pediatrics
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• v.52 no.11
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• pp.1221-1227
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• 2009

Purpose:To identify the risk factors for poor neurodevelopmental outcomes in high-risk neonates. Methods:We studied 94 infants admitted to the neonatal intensive care unit at the Sanggye Paik Hospital between January 2002 and November 2005 and evaluated the follow-up data. The following events were considered as risk factors: ${\leq}32$ weeks of gestation, very low birth weight, Apgar scores of less than 5, neonatal resuscitation, neonatal seizure, congenital infection, and abnormalities in cranial ultrasound or magnetic resonance imaging (MRI). The infants who had any one of these risk factors were included. They were evaluated at their mean corrected age of 13.84${\pm}$8.03 months. Mental and Psychomotor Developmental Indices (MDI, PDI) were determined by a clinical psychologist using the Bayley Scales of Infant Development II. Results:The mean MDI and PDI of all the patients were 96.28${\pm}$26.70 and 94.00${\pm}$22.80, respectively. Abnormalities on cranial ultrasound or MRI were significant predictors of both low MDI (P<0.05) and low PDI (P<0.001). These abnormalities showed a stronger association with low PDI than with low MDI. The infants with periventricular leukomalacia had the lowest MDI and PDI ($70.10{\pm}28.68$ and $69.70{\pm}24.91$, respectively). Apgar score at 1 minute and very low birth weight were also significant predictors for low PDI (P<0.05, P<0.05, respectively). Conclusion:Image findings with cranial ultrasound or MRI were the strongest predictors of neurodevelopmental outcome. Periventricular leukomalacia was the best predictive factor for mental and psychomotor development.

• Neonatal Medicine
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• v.18 no.2
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• pp.165-176
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• 2011

The pathologic hallmark of new bronchopulmonary dysplasia (BPD) is an arrest in alveolarization and vascular development. Alveoli are the fully mature gas-exchange units and alveolarization denotes the process through which the developing lung attains its fully mature structure. In human, alveolarization is mainly a postnatal event and begins in utero around 35 postmenstrual weeks and continues to 2 postnatal years. Beginning of respiration with very immature lungs as a result of preterm delivery renders the immature lung to be exposed to various injuries such as mechanical stretch, hyperoxia, infection/inflammation and leads to a disruption of normal alveolarization process, which is a main pathologic finding of BPD. Better understanding of the control mechanisms of normal alveolarization process should help us to figure out the pathophysiology of BPD and discover effective preventive or therapeutic measures for BPD. In this review, the pathologic evolution of BPD from 'old' to 'new' BPD, the detailed mechanisms of normal alveolarization, and the factors that disrupt normal alveolarization will be discussed.

• Neonatal Medicine
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• v.25 no.3
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• pp.91-95
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• 2018

Bronchopulmonary dysplasia-associated pulmonary hypertension (BPD-PH) is increasingly being recognized as a cause of morbidity and mortality in preterm infants. Recently, BPD-PH has also been shown to have additional long-term negative effects on neurodevelopmental outcomes and right ventricular function. Several significant risk factors associated with the development of BPD-PH have been identified. A screening strategy for BPD-PH is needed for infants presenting more than one risk factor. In addition, an early echocardiogram within 14 days of age may be a useful tool to identify infants at high-risk for BPD-PH. We have reviewed recent progress in research concerning clinical characteristics, presentation, and outcomes of BPD-PH and have suggested direction for future studies.

• Clinical and Experimental Pediatrics
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• v.48 no.8
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• pp.806-812
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• 2005

Repair mechanisms in the postnatal and mature central nervous system(CNS) have long been thought to be very limited. However recent works have shown that the mature CSN contains neural progenitors, precursors, and stem cells that are capable of generating new neurons, astrocytes, and oligodendrocytes especially in germinative areas such as the subventricular zone of the lateral ventricles, the dentate gyrus of the hippocampus. These findings raise the possibilities for the development of novel neural repair strategies via mobilization and replacement for dying neurons of neural stem cells in situ. Indeed recent reports have provided evidences that endogenous stem cells are activated in response to various injuries, and in some injury models, limited neuronal replacement occurs in the CNS. Here, current understandings for endogenous neurogenesis and induction neurogeneis in postnatal CNS including neonatal brain are summarized and discussed.

• Bulletin of Food Technology
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• v.18 no.3
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• pp.45-61
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• 2005

The first cases of neonatal meningitis believed to have been caused by Enterobacter sakazakii were reported in 1961. Prompted by several subsequent outbreaks of E. sakazakii infections in neonates and an increasing number of neonates in intensive care units being fed rehydrated powdered infant formula, considered to be a source of the pathogen, public health authorities and researchers are exploring ways to eliminate the bacterium or control its growth in dry infant formula, processing environments and formula preparation areas in hospitals. Reviewed here are advances in taxonomy and classification of E. sakazakii, methods of detecting, isolating and typing the bacterium, antibiotic resistance, clinical etilogy and pathogenicity. Outbreaks of E. sakazakii infections in neonates and adults are summarized. Reports on the presence of E. sakazakii in clinical settings, the environment and foods and food processing facilities are reviewed.

• Applied Microscopy
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• v.24 no.4
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• pp.32-40
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• 1994

This study was undertaken to study the morphological changes of rat synapses during early postnatal periods. Neonatal rats were grouped by 1st, 2nd, 3rd, 4th and 6th postnatal weeks, and we observed the ultrastructural pattern of the synapses in the external plexiform layer of olfactory bulbs by electron microscopy. The results were as follows; 1. The numbers of synapses, lengths of synaptic thickenings and amounts of synaptic vesicles were markedly increased in the external plexiform layer during four postnatal weeks. 2. There was a tendency of increasing the proportion of the asymmetric synapse and the curved synapses during maturation. From the above results, it is suggested that the size of synapse is increasing during maturation, and at the same time the asymmetric synapses are formed from the symmetric type and the curved synapses are from the plane type.

• Journal of Interdisciplinary Genomics
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• v.3 no.2
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• pp.30-34
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• 2021

Campomelic dysplasia (CD) is a rare genetic disorder characterized by multiple skeletal anomalies and the abnormal development of male reproductive organs. To date, the SOX9 gene is the only known causal gene for CD, and approximately 90 causative mutations in SOX9 have been identified worldwide. CD is diagnosed based on clinical characteristics of skeletal dysplasia (e.g., short bowed long bones, kyphoscoliosis, bell-shaped thoracic cage with 11 pairs of ribs, and hypoplastic scapulars), typical facial features of Pierre Robin sequence with cleft palate, and gonadal dysgenesis in 46,XY individuals. Most patients with CD exhibit life-threatening respiratory failure owing to laryngotracheomalacia and hypoplastic thorax during the neonatal period. Although fatal complications decrease after infancy, several medical conditions continue to require proper management. A better understanding of this rare but lethal condition may lead to more appropriate treatments for patients.

• Journal of Korean Neurosurgical Society
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• v.64 no.3
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• pp.406-413
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• 2021

Sacrococcygeal teratoma (SCT) is an extragonadal germ cell tumor (GCT) that develops in the fetal and neonatal periods. SCT is a type I GCT in which only teratoma and yolk sac tumors arise from extragonadal sites. SCT is the most common type I GCT and is believed to originate through epigenetic reprogramming of early primordial germ cells migrating from the yolk sac to the gonadal ridges. Fetal SCT diagnosed in utero presents many obstetrical problems. For high-risk fetuses, fetal interventions (devascularization and debulking) are under development. Most patients with SCT are operated on after birth. Complete surgical resection is the key for tumor control, and the anatomical location of the tumor determines the surgical approaches. Incomplete resection and malignant histology are risk factors for recurrence. Approximately 10-15% of patients have a tumor recurrence, which is frequently of malignant histology. Long-term surveillance with monitoring of serum alpha fetoprotein and magnetic resonance imaging is required. Survivors of SCT may suffer anorectal, urological, and sexual sequelae later in their life, and comprehensive evaluation and care are required.

• BMB Reports
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• v.56 no.9
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• pp.469-481
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• 2023

The gut microbiome is widely recognized as a dynamic organ with a profound influence on human physiology and pathology. Extensive epidemiological and longitudinal cohort studies have provided compelling evidence that disruptions in the early-life microbiome can have long-lasting health implications. Various factors before, during, and after birth contribute to shaping the composition and function of the neonatal and infant microbiome. While these alterations can be partially restored over time, metabolic phenotypes may persist, necessitating research to identify the critical period for early intervention to achieve phenotypic recovery beyond microbiome composition. In this review, we provide current understanding of changes in the gut microbiota throughout life and the various factors affecting these changes. Specifically, we highlight the profound impact of early-life gut microbiota disruption on the development of diseases later in life and discuss perspectives on efforts to recover from such disruptions.