• 생명과학회지
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• 제15권6호
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• pp.979-986
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• 2005

수유기 동안 납의 투여는 급격한 체중의 변화를 유발하여 3주령 및 11주령 쥐의 경우 납을 투여한 군이 대조군에 비해 각각 50% 및 26% 체중 감소를 보였으나 뇌의 무게에는 유의적 변화를 관찰 할 수 없었다. 납 투여는 뇌 지방산 조성 변화에 큰 영향을 주지 않았지만 특히 AA와 DPAn-6와 같은 고도의 불포화 지방산 함량의 증가를 유발하였다. Motor ac-tivity 실험에서 납 투여군의 경우 대조군에 비하여 주어진 시간 내에서 움직이는 시간과 움직인 거리가 긴 것으로 보아 운동 활동성이 큰 것으로 여겨지나 두 군 간에 유의적 차이는 없었다. Elevated plus maze 실험에서 실험 1일째의 경우 open arm에 머무른 시간에는 유의적 차이가 없었으나 2일째에는 두 군에서 현저히 open arm에 머무른 시간이 감소하였으며 납 투여군의 경우 대조군에 비하여 머무른 시간이 감소하는 경향이었으나 통계적 유의성은 없었다. Open arm에 들어가는 횟수를 관찰한 결과, 실험 1일째의 경우 open arm에 들어가는 횟수가 납 투여군에서 유의적으로 적었고 2일째에는 두 군에서 모두 open arm에 들어가는 횟수가 감소하였으며 대조군에 비해 납을 투여한 쥐의 경우가 유의적으로 낮은 횟수로 open arm에 들어갔음을 관찰 할 수 있었다. 이상의 결과로부터 수유기 동안의 납 투여는 성숙 동물의 불안감을 증가시키는 효과를 나타내었다.

• Clinical and Experimental Pediatrics
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• 제52권11호
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• pp.1221-1227
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• 2009

목 적:신생아 집중치료술이 발달함에 따라 미숙아 및 극소 저체중 출생아 등의 고위험 신생아의 생존율이 크게 향상되었다. 따라서 이러한 고위험 신생아의 생존율 향상과 더불어 생존 환아에서 발육 지연, 뇌성마비, 청력 저하 등 신경학적 발달 이상을 보이는 환아의 수도 증가하여 이들 환아들의 이상을 보다 조기에 발견하기 위해 추적 관찰의 필요성이 증대되고 있다. 저자들은 신생아 집중 치료실에서 치료 후 퇴원한 환아 중 위험한 주산기 인자들로 인하여 발달 이상의 위험도가 상대적으로 높아 고위험 신생아로 추적 관리를 받고 있는 환아에서 Bayley 발달 검사를 이용하여 발달 이상의 위험 인자를 확인하기 위하여 연구를 시행하였다. 방 법:2002년 1월부터 2005년 11월까지 인제대학교 의과대학 상계백병원 신생아 집중 치료실에 입원하였던 신생아 중에서 퇴원 후 외래에서 추적 관리하였던 환아 중 Bayley 발달 검사를 시행한 94례를 대상으로 하였다. 연구 대상은 32주 미만의 재태 연령, 극소 저체중 출생아, 5점 이하의 Apgar 점수, 뇌 초음파 및 자기 공명 검사상 뇌실 내 출혈 혹은 뇌실주위 백색질 연화증 등의 이상, 신생아 소생술을 시행한 경우, 신생아 경련 또는 선천성 감염 중 한 가지 이상의 요인이 있었던 환아이다. 대상 환아들의 발달 검사로 Bayley 발달 검사(Bayley Scales of Infant Development II)를 임상심리치료사가 시행하였고, MDI와 PDI를 분석에 이용하였다. 결 과:뇌 초음파 및 자기 공명 검사는 MDI, PDI와 각각 통계적인 연관성을 보였으며(P<0.05, P<0.001), 뇌실주위 백색질 연화증의 경우 MDI는 $70.10{\pm}28.68$, PDI는 $69.70{\pm}24.91$로 의미 있게 낮은 점수를 보였다. MDI보다 PDI가 뇌의 영상학적 검사 소견과 상관관계가 더 큰 것으로 나타났다. PDI는 1분 Apgar 점수 및 극소 저체중 출생아와도 유의한 상관관계가 있었다(P<0.05, P<0.05). Bayley 발달 검사 결과는 성별, 재태 연령, 신생아 소생술 여부, 신생아 경련과 유의한 연관성이 없었다. 결 론:신생아 집중 치료실에서 치료받은 고위험 신생아를 추적 관찰하며 Bayley 발달 검사를 시행하였을 때, 검사 결과에 독립적으로 영향을 미치는 위험 인자는 뇌의 영상학적 검사 소견, 1분 Apgar 점수 및 극소 저체중 출생아였다. 그 중 뇌의 영상학적 검사 소견상 이상이 있는 경우 발달 장애의 가능성이 가장 높고, 그 외의 위험 요인에 대해서도 주기적인 추적 관찰이 중요할 것으로 생각된다.

• 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.