• Clinical and Experimental Pediatrics
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• 제53권12호
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• pp.979-984
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• 2010

Recent progress in neonatal medicine has enabled survival of many extremely low-birth-weight infants. Prenatal steroids, surfactants, and non-invasive ventilation have helped reduce the incidence of the classical form of bronchopulmonary dysplasia characterized by marked fibrosis and emphysema. However, a new form of bronchopulmonary dysplasia marked by arrest of alveolarization remains a complication in the postnatal course of extremely low-birth-weight infants. To better understand this challenging complication, detailed alveolarization mechanisms should be delineated. Proper alveolarization involves the temporal and spatial coordination of a number of cells, mediators, and genes. Cross-talk between the mesenchyme and the epithelium through soluble and diffusible factors are key processes of alveolarization. Lung interstitial cells derived from the mesenchyme play a crucial role in alveolarization. Peak alveolar formation coincides with intense lung interstitial cell proliferation. Myofibroblasts are essential for secondary septation, a critical process of alveolarization, and localize to the front lines of alveologenesis. The differentiation and migration of myofibroblasts are strictly controlled by various mediators and genes. Disruption of this finely controlled mechanism leads to abnormal alveolarization. Since arrest in alveolarization is a hallmark of a new form of bronchopulmonary dysplasia, knowledge regarding the role of lung interstitial cells during alveolarization and their control mechanism will enable us to find more specific therapeutic strategies for bronchopulmonary dysplasia. In this review, the role of lung interstitial cells during alveolarization and control mechanisms of their differentiation and migration will be discussed.

• 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.

• 환경생물
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• 제21권3호
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• pp.297-302
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• 2003

This study was designed to determine whether selenium (Se) nutrition affects pulmonary glutathione peroxidase and alveolarization in the neonatal rat. Twenty-four female Sprague Dawley rats were bred and fed a semipurified Se-deficient (0.04 ppm, Se-) or a Se-adequate (0.5 ppm, Se+) diet through pregnancy and lactation. Pulmonary DNA synthesis was slightly higher in Se+ pups than in Se- pups on d 6 and d 9 of lactation, but significant difference was not found. As pulmonary alveolarization progressed, mean air space size decreased and internal surface area and lung volume increased. No difference in pulmonary alveolarization was found between Se- and Se+ pups by age. Pulmonary Se concentration was higher in Se+ pups than in Se- pups at all age. Glutathione peroxidase activity in lung tissur reflected Se status and was lower in Se- pups than in Se+ pups. In conclusion, selenium has no significant effect on alveolarization of neonatal lungs. but it is necessary for adequate supply of pulmonary antioxidant, glutathione peroxidase.

• Clinical and Experimental Pediatrics
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• 제64권1호
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• pp.37-43
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• 2021

Background: Animal studies have shown that a leukocyte influx precedes the development of bronchopulmonary dysplasia (BPD) in premature sheep. The CXC chemokine receptor 2 (CXCR2) pathway has been implicated in the pathogenesis of BPD because of the predominance of CXCR2 ligands in tracheal aspirates of preterm infants who later developed BPD. Purpose: To test the effect of CXCR2 antagonist on postnatal systemic and pulmonary inflammation and alveolarization in a newborn Sprague-Dawley rat model of BPD. Methods: Lipopolysaccharide (LPS) was injected intraperitoneally (i.p.) into the newborn rats on postnatal day 1 (P1), P3, and P5 to induce systemic inflammation and inhibit alveolarization. In the same time with LPS administration, CXCR2 antagonist (SB-265610) or vehicle was injected i.p. to investigate whether CXCR2 antagonist can alleviate the detrimental effect of LPS on alveolarization by attenuating inflammation. On P7 and P14, bronchoalveolar lavage fluid (BALF) and peripheral blood (PB) were collected from the pups. To assess alveolarization, mean cord length and alveolar surface area were measured on 4 random nonoverlapping fields per animal in 2 distal lung sections at ×100 magnification. Results: Early postnatal LPS administration significantly increased neutrophil counts in BALF and PB and inhibited alveolarization, which was indicated by a greater mean cord length and lesser alveolar surface area. CXCR2 antagonist significantly attenuated the increase of neutrophil counts in BALF and PB and restored alveolarization as indicated by a decreased mean cord length and increased alveolar surface area in rat pups exposed to early postnatal systemic LPS. Conclusion: CXCR2 antagonist preserved alveolarization by alleviating pulmonary and systemic inflammation induced by early postnatal systemic LPS administration. These results suggest that CXCR2 antagonist can be considered a potential therapeutic agent for BPD that results from disrupted alveolarization induced by inflammation.

• 음성과학
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• 제8권4호
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• pp.109-118
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• 2001

This study was designed to evaluate the phonological characteristics in profound hearing-impaired children. 10 males and 10 females participated in this study and all were prelingually hearing impaired. 7 children were educated at deaf school and 13 children at general elementary school with private clinic. Their hearing levels were more than 95dB HL and did not appear any wave by ABR. The results can be summarized as following: The articulation accuracy of hearing impaired children was 54.19% and most distinguished phonological patterns of the hearing impaired children were alveolarization and stop assimilation. The accurate articulation phonation was significantly different from education system between deaf school and general school. The error articulation degrees in profound hearing impaired children at general school seemed meaningfully smaller than those in hearing impaired children at deaf school.

• 말소리와 음성과학
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• 제7권2호
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• pp.19-28
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• 2015

This study investigated final consonant error characteristics at word-medial position in children with functional articulation disorder. Data was collected from 11 children with functional articulation and 11 normal children, ages 4 to 5. The speech samples were collected from a naming test. Seventy-five words with every possible bi-consonants matrix at the word-medial position were used. The results of this study were as follows : First, percentage of correct word-medial final consonants of functional articulation disorder was lower than normal children. Second, there were significant differences between two groups in omission, substitution and assimilation error. Children with functional articulation disorder showed a high frequency of omission and regressive assimilation error, especially alveolarization in regressive assimilation error most. However, normal children showed a high frequency of regressive assimilation error, especially bilabialization in regressive assimilation error most. Finally, the results of error analysis according to articulation manner, articulation place and phonation type of consonants of initial consonant at word-medial, both functional articulation disorder and normal children showed a high error rate in stop sound-stop sound condition. The error rate of final consonant at word-medial position was high when initial consonant at word-medial position was alveolar sound and alveopalatal sound. Futhermore, when initial sounds were fortis and aspirated sounds, more errors occurred than linis sound was initial sound. The results of this study provided practical error characteristics of final consonant at word-medial position in children with speech sound disorder.

• Neonatal Medicine
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• 제15권1호
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• pp.22-31
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• 2008

목 적 : 기관지폐이형성증은 미숙한 폐에서의 혈관과 폐포발달의 저해로 특징 질 수 있다. 폐 발달의 결과를 고려하면 줄기세포의 투여로 자가 회복기전을 이용한 폐 발달의 촉진의 가능성은 유망하고 이로 폐 기관지이 형성의 유병률과 합병증을 줄일 수 있다. 강화된 Green fluorescent protein (EGFP)를 표기인자로 표시한 줄기세포를 비 EGFP 마우스에 주사하여 생착 여부를 보고자 하였다. 방 법 : VEGFR2 억제제인 SU1498을 생후 3일된 마우스에 주사하여 폐포발달이 저해된 모형을 만들었다. 생후 4일에 $1{\times}10^6$ EGFP 양성 줄기세포를 복강 내로 주입하였다. 줄기세포를 투여한 폐의 형태학적인 분석과 면역염색을 시행 하였고, 주입된 줄기 세포의 생착을 확인하기 위해서 동일초점 현미경으로 분석하였다. 결 과 : SU1498을 주사한 신생마우스에서 폐포 표면적과 평균 폐포 용적이 감소되었다. 폐 발달이 억제된 마우스 모형에서 주입한 EGFP 양성 줄기세포가 발견 되었고, 내피세포와 외피세포로 분화함을 공초점 현미경으로 확인하였다. 결 론 : 주입된 EGFP 양성 줄기세포가 혈관생성억제제를 이용하여 만든 마우스의 폐 발달 저해 모형에서 생착 하여 내피세포와 외피세포로 분화함을 확인하였다.