• Neonatal Medicine
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• 제18권2호
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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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• 제25권3호
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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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• 제48권8호
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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.

• 식품기술
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• 제18권3호
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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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• 제24권4호
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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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• 제3권2호
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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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• 제64권3호
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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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• 제56권9호
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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.

• Clinical and Experimental Pediatrics
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• 제54권2호
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• pp.55-63
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• 2011

Prader-Willi syndrome (PWS) is a complex multisystem genetic disorder that is caused by the lack of expression of paternally inherited imprinted genes on chromosome 15q11-q13. This syndrome has a characteristic phenotype including severe neonatal hypotonia, early-onset hyperphagia, development of morbid obesity, short stature, hypogonadism, learning disabilities, behavioral problems, and psychiatric problems. PWS is an example of a genetic condition caused by genomic imprinting. It can occur via 3 main mechanisms that lead to the absence of expression of paternally inherited genes in the 15q11.2-q13 region: paternal microdeletion, maternal uniparental disomy, and an imprinting defect. Over 99% of PWS cases can be diagnosed using DNA methylation analysis. Early diagnosis of PWS is important for effective long-term management. Growth hormone (GH) treatment improves the growth, physical phenotype, and body composition of patients with PWS. In recent years, GH treatment in infants has been shown to have beneficial effects on the growth and neurological development of patients diagnosed during infancy. There is a clear need for an integrated multidisciplinary approach to facilitate early diagnosis and optimize management to improve quality of life, prevent complications, and prolong life expectancy in patients with PWS.

• 아동학회지
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• 제25권5호
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• pp.147-161
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• 2004

This study was designed to explore developmental evaluation in healthy full-term, at risk preterm and full-term infants. Specifically the purposes of the study were to investigate Psychomotor Developmental Index(PDI) and Mental Developmental Index(MDI) based on Bayley Scales of Infant Development(1993). The subjects were 72 infants, 24 each for healthy full-term infants, 24 each for at risk preterm infants and 24 each for at risk full-term infants such as having neonatal asphyxia, hypoxic ischemic brain damage, respiratory distress syndrome. The data were analyzed through Kruskal-Wallis test and correlations to examine healthy full-term, at risk pre-term and at risk full-term infants. Results showed that there were significant differences among healthy full-term, at risk pre-term and at risk full-term infants in PDI and MDI. On the correlation with PDI and MDI, infants showed significant correlations. Early interventions for developmental improvement are required for functional outcome in these infants.