Wnt信号通路与支气管肺发育不良

Wnt信号通路是一条在进化上保守的信号传导途径,主要由经典的Wnt/β-catenin途径和非经典的Wnt/平面细胞极性途径及Wnt/Ca2+途径组成,该通路从多个水平参与肺发育及多种肺部疾病过程.支气管肺发育不良(bronchopulmonary dysplasia,BPD)是在肺发育不成熟基础上由于炎症损伤及损伤后肺纤维化异常修复所导致的慢性肺疾病.该文就Wnt信号通路与肺发育、肺部炎症和肺纤维化的关系作一综述,以期揭示Wnt信号通路与BPD之间的可能联系,为BPD的防治提供新的切入点.     

细胞信号通路与支气管肺发育不良

支气管肺发育不良( bronchopulmonary dysplasia,BPD)是目前早产儿最常见的并发症之一,已成为新生儿重症监护病房最为棘手的问题之一。 BPD的分子机制极其复杂,发病过程需要诸多信号传导通路的共同参与。该文就丝裂素活化蛋白激酶信号通路、核因子-κB通路、转化生长因子通路、Wnt通路、mTOR通路等与BPD的可能关系予以综述。     

肺发育和肺损伤-新型支气管肺发育不良

近年基于接受机械通气治疗早产儿的病理表现、支气管肺发育不良 (ＢＰＤ)流行病变化特点、及实验模型研究的最新结果 ,提出“新ＢＰＤ”的概念。以前认为ＢＰＤ的病理生理特征是 :严重的气道上皮发育不良及损伤、气道平滑肌增生、肺实质纤维化及局限性肺气肿。这些损害是由于机     

支气管肺发育不良

支气管肺发育不良（ＢＰＤ）由Ｎｏｒｔｈｗａｙ在１９６７年首次提出［１］,是继发于机械通气的一种慢性肺疾病,主要见于早产儿呼吸窘迫综合征（ＲＤＳ）,亦可见于其他疾病需长期机械通气治疗的新生儿。随着极低出生体重儿（ＶＬＢＷ）成活率的提高和机械通气的普遍开展,ＢＰＤ的发病率也随之升高,有关ＢＰＤ的研究取得了很大进展,死亡率有所下降,但仍是危害婴幼儿健康的一种严重疾病。本文将近年来ＢＰＤ的研究进展作一综述。 一、病因及发病机制１．肺发育不成熟：胎儿气道分支形成在孕２４周,此后肺泡逐渐形成,孕３０～４０周…     

氧化应激与支气管肺发育不良研究进展

支气管肺发育不良( bronchopulmonary dysplasia,BPD)是早产儿重要疾病.BPD的病因及发病机制复杂,高浓度吸氧引起的BPD与机体氧化和抗氧化失衡有关.氧化应激与炎症反应过程关系密切,二者相互影响并在BPD的发生发展中起重要作用.活性氧作为第二信使调节大量与细胞增殖、凋亡和炎症反应相关的核转录因子活性,这可能是氧化应激从基因水平促进BPD发生发展的重要机制.目前BPD的防治仍处于探索阶段.该文探讨高浓度氧疗引起的氧化应激和炎症反应与BPD的内在联系及BPD的抗氧化防治措施.     

早产儿支气管肺发育不良的防治

随着围生医学的发展,早产儿存活率上升,支气管肺发育不良(bronchopulmonary dysplasia,BPD)发病率也逐年增高.BPD是一种由多因素引发的慢性肺疾病,其病因及发病机制复杂,早期病死率高,晚期伴有呼吸系统,甚至神经系统的不良结局,严重影响早产儿存活率及生活质量.该文就BPD的防治进展作一综述.     

支气管肺发育不良的研究进展

支气管肺发育不良是由于发育不成熟等多种因素共同作用下致肺泡和肺内血管发育受阻的一种慢性肺疾患，是由于早产、治疗损伤、感染和炎症等多种因素共同作用的结果。该病需采用综合的方法来预防和治疗，包括产前糖皮质激素的应用、合适的呼吸及营养支持、防治感染、抗炎及抗氧化治疗等。要想找到更有效的防治方法，需加强基础和临床研究，特别是对肺发育和该病发生机制的研究。     

Ureaplasma and bronchopulmonary dysplasia

Advances in neonatal intensive care have greatly improved survival rates for children born in a very early stage of lung development (i.e. less than 26 weeks of gestation). In these premature babies, even low levels of oxygen and methods of minimally invasive ventilation may disrupt the growth of the distal airways, a condition described as “new” bronchopulmonary dysplasia (BPD).Ureaplasma infection can occur in utero or in the perinatal period in premature infants, in some of which the infection with these organisms triggers an important lung pro-inflammatory and pro-fibrotic response, and may increase the risk of developing BPD. The inflammation may be worsened by exposure to oxygen and mechanical ventilation. At present, clinical studies have not clarified the role of Ureaplasma in the pathogenesis of BPD and there is insufficient evidence to determine whether antibiotic treatment of Ureaplasma has influence on the development of BPD and its comorbidities.Future research in the context of well-designed and controlled clinical trials of adequate statistical power should focus on how to determine whether the treatment of Ureaplasma decreases lung inflammation, reduces rates of BPD, and improves long-term neurodevelopment.     

支气管肺发育不良早产儿1岁和2岁时体积描记肺功能的随访研究

目的 探讨支气管肺发育不良 (BPD)早产儿的远期肺功能。 方法 以2012年1月至2013年12月在复旦大学附属儿科医院新生儿病房住院的胎龄≤ 32周、出生体重≤ 1 500 g的BPD早产儿为BPD组,以同期住院非BPD早产儿按1∶1匹配为对照组,于纠正年龄1岁和2岁时召回随访,行体积描记（体描）肺功能检测,分析早产儿BPD及不同严重度BPD在纠正年龄1岁和2岁时肺功能状况。 结果 149例BPD早产儿和与之匹配的149例非BPD早产儿进入文本分析,1岁和2岁时召回随访,BPD组37例（轻中度22例,重度15例）和25例（轻中度15例,重度10例）,非BPD组33例和10例。在纠正年龄1岁及2岁时,BPD组公斤体重残气量（FRCp/kg）、达峰时间比（TPTEF/TE）、达峰容积比（VPTEF/VE）、肺内剩余25%潮气量时潮气呼气流速（TEF25）显著低于非BPD组,公斤体重有效气道阻力（Reff/kg）显著高于非BPD组。在纠正年龄1岁时,重度BPD亚组FRCp/kg 、TPTEF/TE显著低于轻中度BPD亚组, Reff/kg显著高于轻中度BPD亚组;在纠正年龄2岁时,重度BPD亚组VPTEF/VE显著低于轻中度BPD亚组,Reff/kg显著高于轻中度BPD亚组。 结论 BPD早产儿存在功能残气量降低及小气道阻塞,以重度BPD患儿更为明显。     

Cathepsin K expression is diminished in infants with bronchopulmonary dysplasia

The expression of a potent collagenolytic enzyme, cathepsin K, was measured in repeated tracheal aspirate samples from premature infants with and without a chronic lung disorder, bronchopulmonary dysplasia (BPD). At 9–13 d, but not before, cathepsin K expression was significantly lower in the lungs of premature infants developing BPD. Conclusion: Insufficient pulmonary cathepsin K in BPD may predispose premature lungs to pulmonary fibrosis.     

Incidence and prediction of bronchopulmonary dysplasia in a cohort of premature infants

Farstad T, Bratlid D. Incidence and prediction of bronchopulmonary dysplasia in a cohort of premature infants. Acta Pzdiatr 1994;83:19–24. Stockholm. ISSN 0803–5253
A prospective study on the incidence of bronchopulmonary dysplasia (BPD) in premature infants is reported. A cohort of premature infants with gestational ages 32 weeks, treated during 1989, was followed for one year. Of a total study population of 117 infants, 23 (19.6%) developed BPD, defined as oxygen dependence at 28 postnatal days. However, only 15 infants (12.8%) needed supplementary oxygen at the age of 36 gestational weeks and 5 infants (4.2%) needed supplementary oxygen periodically at one year of age. BPD was found to account for a significant part of both the total and late mortality in the cohort. Measurements of pulmonary mechanics were performed at 3 ± 1 and 12(13) ± 1 days of life in a subgroup of 26 infants with RDS who required assisted ventilation for 4 days or longer. No significant difference in lung compliance or resistance could be found during the first examination between infants who later devleoped BPD and infants with RDS only. At the second examination, infants who later developed BPD had significantly lower lung compliance (0.48 ± 0.23 ml/cmH₂O) than infants in the RDS group (1.50 ± 0.72 ml/cmH₂O) (p<0.001). Measurements of pulmonary mechanics could be of importance for early prediction of infants at risk of BPD.     

Persistent acquired lobar overinflation complicating bronchopulmonary dysplasia

Persistent acquired lobar overinflation (PALO) may complicate bronchopulmonary dysplasia (BPD). From infants admitted to the regional neonatal intensive care unit or who had been followed up at the chronic lung disease clinic in Liverpool over a 6.5-year period, 11 children with BPD and PALO were identified and details of their neonatal and subsequent outcome obtained. Their median gestational age was 29 weeks (range 24–33) and median birth weight was 1317 g (range 676–1968 g). All had received ventilatory support for severe neonatal respiratory distress syndrome for a median of 26 days (range 5–86). The median age the acquired lobar overinflation was detected was 82 days (range 45–424 days). Nine patients required continued neonatal or paediatric intensive care re-admission for deteriorating respiratory function. Six children have subsequently died at a median age of 9.5 months (range 6.5–20). Five patients underwent bronchoscopy, four suggesting the presence of bronchomalacia. Three patients had ventilation-perfusion scans all showing that the overinflated lobe had no mismatch defect unlike other areas of the lung. Conclusion The place of specific therapies for persistent acquired lobar overinflation is unclear. Surgery to remove the overinflated lobe in such cases may be inappropriate and the outcome of this complication of bronchopulmonary dysplasia appears to be poor. Received: 6 August 1998 / Accepted: 3 March 1999     

CD105在高氧肺损伤小鼠肺内表达水平及意义

目的探讨吸入中浓度氧新生小鼠血清和肺部血管内皮细胞膜抗原CD105表达水平及意义,寻求高氧肺损伤新生小鼠肺微血管发育可能的机制。方法清洁级4日龄昆明小鼠50只,随机分为观察组、对照组各25只。观察组置于氧箱中(FiO2:0.6),对照组置于空气中(FiO2:0.21),建立高氧肺损伤小鼠模型,每组分别于实验第0(实验开始时)、7、14、21、28天时随机选取5只小鼠留取血标本及肺组织,HE染色观察肺组织病理形态,酶联免疫吸附法检测血中CD105含量,免疫组化染色法检测肺组织CD105表达水平,并分析血清CD105浓度与肺组织CD105表达量的相关性。结果观察组HE染色下正常肺泡结构消失、肺泡融合、肺泡间隔增厚,肺泡炎和肺组织纤维化增加,放射状肺泡计数较对照组明显减少(P<0.01),随着吸氧时间延长,CD105的表达水平呈逐渐增高趋势,实验第7、14、21、28天观察组血清CD105浓度和肺组织CD105表达水平均高于对照组,血清(ng/L):[7天:(346.4±14.7)比(265.7±2.0),14天:(400.2±20.1)比(266.3±3.2),21天:(505.1±6.1)比(267.1±5.8),28天:(451.9±10.0)比(268.6±4.5),P<0.01];肺组织累积光密度值:[7天:(2.24±0.15)比(1.19±0.14),14天:(3.42±0.20)比(1.20±0.11),21天:(4.35±0.18)比(1.16±0.18),28天:(4.04±0.12)比(1.17±0.14),P<0.01],且观察组CD105在血清中与肺组织中的表达水平呈正相关(r=0.973,P<0.001)。结论 CD105可能代替传统的血管内皮生长因子和血管生成素-1,成为氧疗通气诱导血管重塑的重要血管生长因子。