肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的相关性研究

目的：研究肺表面活性物质蛋白（SP）B基因单核苷酸多态性分布以及与新生儿呼吸窘迫综合征（RDS）的关系。方法：选择88例RDS早产儿和未并发RDS的早产儿103例作为研究对象,采用DNA提取试剂盒提取DNA,应用聚合酶联反应-限制性片段长度多态性技术检测SP-B-18A/C、SP-B 1580C/T两个位点的单核苷酸多态性,分析两个位点多态性与RDS的关系。结果：SP-B -18A/C、SP-B 1580C/T两个位点在病例组和对照组中均存在多态性,与未并发RDS的早产儿对照组比较,RDS患儿SP-B 1580C/T位点基因型以CC型明显增多,（χ2=12.26,P0.05）。结论：SP-B 1580 位点C/T多态性与RDS有关,SP-B 1580C/T可能是RDS的易感基因,携带SP-B 1580位点C等位基因的个体患RDS的风险增加。SP-B-18A/C与RDS无关。     

内蒙古西部地区汉族新生儿呼吸窘迫综合征与SP-B外显子7区域R236C位点的相关性研究

目的通过检测和分析肺表面活性物质蛋白B基因外显子7(exon7)区域上是否存在基因变异,探讨其与内蒙古西部地区汉族新生儿呼吸窘迫综合征(NRDS)发病的关系。方法采用病例对照研究方法,选择祖上三代都居住在内蒙古西部地区的汉族NRDS患儿47例作为病例组,选择同民族和同群体中未发生NRDS的新生儿47例为对照组。通过PCR基因分析技术检测SP-B基因外显子7区域上有无突变,以及SP-B外显子7(R236C)位点的基因型、等位基因分布。结果在内蒙古西部地区汉族新生儿中,SP-B基因外显子7区域无突变发生;SP-B外显子7(R236C)位点基因型均可检出两种基因型(CC、CT),两组中均未检出TT基因型。病例组CC和CT基因型频率分别为72%和28%,C等位基因频率为85%,T等位基因频率为15%。对照组此两种基因型分别为85%和15%,C等位基因频率为93%,T等位基因频率为7%。病例组与对照组此位点基因多态性相比等位基因及基因型频率在两组之间差异无统计学意义(P0.05)。结论内蒙古西部地区汉族NRDS患儿的SP-B基因第7外显子未发现基因突变。未发现SP-B基因外显子7(R236C)位点基因多态性与该地区汉族NRDS的发生有明显相关性。     

武汉汉族新生儿肺表面活性物质蛋白B基因多态性频率分布

目的了解武汉汉族新生儿肺表面活性物质蛋白B(SP-B)基因多态性频率分布。方法采用PCR-限制性片段长度多态性分析技术和基因测序技术对武汉汉族新生儿286例(男205例,女81例)进行SP-B 1580C/T位点基因型频率检测,并将武汉汉族新生儿SP-B 1580C/T等位基因频率与德国高加索人、美国白种人及日本人比较。结果武汉汉族新生儿SP-B 1580位点基因型CC、CT、TT频率分别为44.8%、47.6%和7.6%,等位基因C和T频率分别为68.5%和31.5%;不同性别、出生体质量、胎龄新生儿SP-B 1580位点的基因型及等位基因频率比较均无统计学差异。武汉汉族新生儿SP-B 1580等位基因频率与德国高加索人和美国白种人相比均有统计学差异(Pa<0.01),但与日本人比较差异无统计学意义。结论武汉汉族新生儿SP-B 1580基因型及等位基因频率在不同性别、出生体质量、胎龄中无明显关联。不同种族人群SP-B 1580C/T基因多态性分布存在明显差异。     

肺表面活性物质蛋白B基因多态性与早产儿支气管肺发育不良的相关性

目的 研究肺表面活性物质蛋白B(Sp-B)基因单核苷酸多态性的分布及其与早产儿支气管肺发育不良(BPD)的关系.方法 采用前瞻性研究方法,选择42例BPD早产儿(BPD组)和65例非BPD早产儿(对照组)作为研究对象,应用PCR-限制性片段长度多态性技术检测SP-B-18A/C、SP-B 1580C/T、SP-B8714G/C位点的单核甘酸多态性,分析3个位点多态性与BPD的关系.结果 BPD组和对照组SP-B-18A/C基因型频率CC、AC、AA分别为35.7％、52.4％、11.9％和32.3％、47.7％、20.0％;SP-B 8714G/C:CC、GC、GG分别为26.2％、54.8％、19.0％和27.7％、58.5％、13.8％;1580C/T基因型CC、CT、TT分别为66.7％、26.2％、7.1％和40.0％、47.7％、12.3％.BPD组和对照组SP-B-18A/C等位基因:C位基因、A等位基因分别为61.9％、38.1％和56.2％、43.8％;SP-B 8714G/C:G等位基因、C等位基因分别为53.6％、46.8％和56.9％、43.1％;SP-B 1580C/T:C等位基因、T等位基因分别为79.8％、20.2％和63.8％、36.2％.SP-B-18A/C、SP-B1580C/T、SP-B 8714G/C 3个位点均存在多态性,与对照组比较,BPD患儿SP-B 1580C/T位点基因型以CC明显增多(x2=7.26,P＜0.05),C等位基因分布频率显著增高(x2=6.17,P＜0.05),携带C等位基因的个体患BPD的风险是非携带者的2.23倍(OR=2.23,95％CI:1.18～4.24).SP-B-18A/C、SP-B 8714G/C位点的基因型和等位基因分布频率均无明显变化,差异均无统计学意义(P均＞0.05).结论 SP-B 1580C/T多态性与BPD有关,SP-B 1580C/T可能是BPD的易感基因,携带SP-B 1580C等位基因的个体患BPD的风险增加.SP-B-18A/C、SP-B 8714G/C与BPD无关.     

SP-B 外显子4（T131I）位点与蒙古族新生儿呼吸窘迫综合征相关性研究

目的探讨SP-B外显子4(T131I)位点与内蒙古西部地区新生儿呼吸窘迫综合征(NRDS)易感性的关系。方法采用病例对照研究方法,选择于2009年9月-2016年2月住院诊断为NRDS的蒙古族早产儿86例作为病例组,选择同期未发生NRDS的蒙古族早产儿86例作为对照组。应用聚合酶链反应-单链构象多态(PCR-SSCP)分析技术及基因测序技术检测SP-B基因exon4区域上有无突变,以及T131I位点的基因型、等位基因分布。结果在所有研究对象中,SP-B基因exon 4区域无突变发生,T131I位点基因型均可检出3种基因型,即CC、CT、TT,病例组所占比例分别为58.1%、27.9%、14.0%,对照组分别为40.7%、43.0%、16.3%,两组基因型分布的差异无统计学意义(χ2=5.57,P=0.062);病例组C等位基因频率为80.2%,高于对照组(64.0%),差异有统计学意义(χ~2=11.33,P0.001)。结论 SP-B基因外显子4(T131I)位点基因多态性可能是蒙古族NRDS易感基因之一。     

肺表面活性物质蛋白-C基因186位点多态性与内蒙古地区蒙古族与汉族新生儿呼吸窘迫综合征相关性分析

目的：研究肺表面活性物质蛋白( surfactant protein,SP)-C基因多态性,以186位点为重,研究内蒙古地区蒙古族与汉族新生儿呼吸窘迫综合征( respiratory distress syndrome of newborn, NRDS)的相关性,分析两族是否具有基因位点差异性。方法选择151例NRDS患儿( NRDS组)与151例正常新生儿(对照组)作为研究对象,应用PCR及基因分析技术检测186位点,分析其多态性与NRDS的关系。结果在内蒙古地区,不论蒙古族还是汉族,SP-C基因186位点基因型均可检出3种基因型：即AA、AG及GG型。其中,蒙古族NRDS组和对照组患儿此3种基因型频率分别为：19.6％、33.3％、47.1％和23.5％、27.5％、49.0％,NRDS组和对照组A等位基因频率分别为36.3％和37.3％, G等位基因频率分别为63.7％和62.7％。汉族 NRDS 患儿和对照组此3种基因型频率分别为：14.0％、28.0％、58.0％和10.0％、30.0％、60.0％, NRDS 组和对照组患儿 A 等位基因频率分别为28.0％和25.0％,G等位基因频率分别为72.0％和75.0％。内蒙古地区蒙古族与汉族NRDS患儿SP-C基因型及等位基因频率在不同性别、出生体重、胎龄、分娩方式等中无明显关联( P>0.05)。对比蒙古族与汉族NRDS患儿在SP-C基因186位点上基因型和等位基因分布,并未发现SP-C基因186位点多态性具有种族上的统计学差异( P>0.05)。结论内蒙古地区NRDS患儿SP-C 186位点基因多态性无明显的种族相关性。     

肺表面活性物质蛋白-C基因遗传多态性与内蒙古地区蒙古族新生儿呼吸窘迫综合征的相关性研究

目的：研究肺表面活性物质蛋白( surfactant protein,SP)-C基因多态性,尤以外显子4(T138N)、5(S186N)位点为重与内蒙古地区蒙古族新生儿呼吸窘迫综合征(neonatal respiratory distress syndrome,NRDS)的关系。方法采用前瞻性研究方法,选择51例NRDS患儿(病例组)与51例正常新生儿(对照组)作为研究对象,应用PCR基因分析技术检测候选基因SP-C外显子4和5有无突变现象,并检测外显子4(T138N)、5(S186N)位点基因多态性,分析多态性与NRDS的关系。结果 SP-C外显子4和5未发现基因突变现象。在内蒙古地区蒙古族,SP-C外显子4(T138N)位点均可检出3种基因型：即AA、AC及CC型,SP-C外显子4(T138N)位点基因多态性病例组与对照组相比差异无统计学意义(χ2=0．454,P=0．797)。外显子5(S186N)位点可检出3种基因型：即AA、AG及GG型,SP-C外显子5(S186N)位点基因多态性病例组与对照组相比差异无统计学意义(χ2=0．493,P=0．782)。结论内蒙古地区蒙古族新生儿SP-C基因型及等位基因频率与性别、出生体重、胎龄、生产方式等无明显关联。内蒙古地区蒙古族NRDS患儿的SP-C外显子4和5未发现基因突变现象。 SP-C基因外显子4(T138N)、外显子5(S186N)位点基因多态性未发现与内蒙古地区蒙古族NRDS患儿有相关性。     

汉族新生儿呼吸窘迫综合征 ABCA3 基因多态性频率分布

目的探讨ABCA3外显子10(ABCA3 exon10)基因多态性与内蒙古西部地区汉族新生儿呼吸窘迫综合征(NRDS)发病的相关性。方法收集2014年9月—2016年9月住院汉族NRDS患儿53例作为病例组,同时间段、同民族、同群体中53例非NRDS汉族新生儿作为对照组;提取两组基因组DNA,聚合酶链式反应(PCR)扩增ABCA3 exon10,对扩增产物进行直接测序,并分析比较。结果在ABCA3外显子10的rs13332514(F353F)位点存在单个碱基点突变CT,密码子由TTC变为TTT,第353编码位点氨基酸未发生改变。病例组和对照组均存在该位点的点突变,病例组的变异率为30.2%,高于对照组(13.2%),差异有统计学意义(P0.05)。NRDS组在ABCA 3 exon 10的rs 13332514(F353F)位点检测出3种基因型(CC、CT和TT),频率分别为69.8%、20.8%和9.4%,C等位基因频率80.2%,T等位基因频率19.8%。对照组检出2种基因型(CC和CT),频率分别为86.8%和13.2%;C等位基因频率93.4%,T等位基因频率6.6%。病例组T等位基因型频率高于对照组,差异有统计学意义(P0.05)。结论 ABCA3 exon10的rs13332514(F353F)位点存在单个碱基点突变CT,该位点变异可能与内蒙古西部地区汉族新生儿发生NRDS有关,等位基因T可能增加NRDS的易感性。     

肺表面活性物质蛋白B基因多态性与新生儿呼吸窘迫综合征易感性的研究

目的 探讨肺泡表面活性物质蛋白B（SPB）基因多态性与新生儿呼吸窘迫综合征易感性的关系。方法 收集华中科技大学同济医学院附属同济医院的新生儿呼吸窘迫综合征（NRDS）诊断病例为病例组,并按1∶2比例收集胎龄和出生体重相匹配的无明显感染症状早产儿为对照组。应用聚合酶链反应 限制性片段长度多态（PCR RFLP）分析技术及基因测序技术检测SPB 18A/C及SPB1580C/T多态性,观察两组间基因型频率和等位基因频率的差异。并复习文献比较本研究汉族与其他种族人群等位基因频率的差异。结果 2008至2010年NRDS组91例,对照组182名进入分析。 ①SPB－18A/C基因在NRDS组AA,AC,CC基因型频率分别为11.0%、40.7%和48.4%,对照组分别为6.6%、31.3%和62.1%;两组基因型频率差异无统计学意义（P>0.05）;NRDS组A等位基因频率显著高于对照组（31.3% vs 22.3%）。②SPB1580C/T基因在NRDS组TT、TC和CC基因型频率分别为5.5%、63.7%和45.1%,对照组分别为30.8%、6.6%和48.4%;两组基因型频率差异无统计学意义（P>0.05）;NRDS组C等位基因频率显著高于对照组（79.1% vs 70.9%）。③本研究汉族人、美国人、巴西人和丹麦人SPB1580等位基因C频率分别为79%、35%、41%和46%,差异有统计学意义（P<0.05）,与日本人群等位基因C频率（72%）差异无统计学意义（P>0.05）;本研究汉族人、巴西人、美国人和丹麦人SPB－18等位基因A频率分别为31%、58%、57%和61%,差异有统计学意义（P<0.05）。结论 本研究汉族人群SPB－18A/C及SPB1580C/T基因多态性是NRDS的危险因素。不同种族人群SPB1580C/T和SPB－18A/C基因多态性分布存在明显差异。     

儿童特发性间质性肺疾病与肺表面活性物质-B基因多态性的相关性研究

目的 探讨肺表面活性物质(surfactant protein,SP)-B外显子4(T131I)位点的基因多态性与儿童特发性间质性肺疾病的相关性.方法 收集2013年10月至2016年9月在深圳市儿童医院和广西医科大学附属第一医院住院诊断为特发性间质性肺疾病的患儿共67例为病例组,选择同期与特发性间质性肺疾病无关的因呼吸道感染在深圳市儿童医院住院的102例患儿为对照组,采用SP-B全外显子和侧翼区高通量测序法对所有病例采集的标本进行检测,分析外显子4(T131I)位点的基因型和等位基因分布.结果 病例组和对照组SP-B基因外显子 4(T131I)位点的基因型均可检出3 种,CC、CT及TT型,病例组所占比例分别为67.16%、25.37%、7.46%,对照组分别为56.86%、35.29%、7.84%,两组基因型分布的差异无统计学意义(χ2=1.981,P=0.371);病例组C等位基因频率为79.85%,对照组为74.51%,差异无统计学意义(χ2=1.288,P=0.256).对照组SP-B基因外显子 4(T131I)位点的基因突变频率为43.14%(44/102),与人类基因组千人人群数据库基因突变频率平均值52.00%比较,差异无统计学意义(P>0.05);与欧洲千人人群数据库基因突变频率53.88%、南亚千人人群数据库基因突变频率45.50%和美洲整体人群数据库基因突变频率41.93%比较,差异无统计学意义(P>0.05),而与东亚千人人群数据库基因突变频率26.39%和非洲千人人群数据库基因突变频率80.18%比较,差异有统计学意义(P<0.05).结论 SP-B 基因外显子4(T131I)位点的基因多态性与儿童特发性间质性肺疾病易感性不存在相关性,外显子4(T131I)位点的基因突变频率与种族人群和地域具有一定的差异性.     

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??Objective To investigate the characteristics of SP-B gene exon 7 mutation of neonatal respiratory distress syndrome??NRDS?? in the Han nationality and the Mongol nationality. Methods The prospective study method was used. Eighty-five infants with NRDS??the NRDS group?? and eighty-four infants without NRDS??the control group?? were selected as the research objects in June 2013- June 2015 in Inner Mongolia Medical University-Affiliated Hospital. In these cases?? there were 55 cases with RDS??the NRDS group?? and 58 cases without RDS??the control group?? in the han nationality?? in the Mongol nationality there were 30 cases with RDS??the NRDS group?? and 26 cases without RDS??the control group??. We extracted DNA and PCR gene analysis was used to detect candidate genes on exon 7 of SP-B. Results Between the NRDS group and the control group of children?? gender?? gestational age?? birth weight?? birth way and whether to promote lung mature regularly had no significant correlation ??P??0.05??. Gene mutations were not found on exon 7 of SP-B in these two groups. Conclusion There is no mutation on SP-B gene exon 7 in this study.There is no difference on SP-B gene exon 7 between the Mongolian and the Han nationality in the Inner Mongolia area.     

Surfactant protein (SP) B associations and interactions with SP-A in white and black subjects with respiratory distress syndrome

BACKGROUND: The etiology of respiratory distress syndrome (RDS) is multifactorial and/or multigenic. Surfactant protein A (SP-A) and/or SP-B genetic variants have been identified as risk or protection factors for RDS. METHODS: We genotyped subjects with and without RDS for the SP-B intron 4 size variants (invariant (inv), deletion (del), insertion (ins) and for four (-18 (A/C), 1013 (A/C), 1580 (C/T), 9306 (A/G)) SP-B single nucleotide polymorphisms (SNP), to study case-control associations in black and white subjects. We also determined whether specific SP-B variants interact with RDS susceptibility or protective SP-A variants to enhance or reduce risk for RDS. RESULTS: Based on odds ratio: (1) the SP-B intron 4 del variant in white subjects is more of an RDS risk factor for males and for subjects of 28 weeks 相似文献   

Polymorphisms of surfactant protein B encoding gene: modifiers of the course of neonatal respiratory distress syndrome?

Surfactant protein B (SP-B) is a lipophilic protein and plays a major role in lung mechanics. Polymorphisms of surfactant protein A, another component of the surfactant system, have been previously described to be a risk factor for respiratory distress syndrome (RDS) and bronchopulmonary dysplasia (BPD) in preterms. The aim of this prospective study was to determine whether polymorphisms within intron 4 of the SP-B gene are related to the incidence, severity and complications of RDS in Caucasian newborns. In order to identify SP-B intron 4 polymorphisms, we analysed genomic DNA by means of polymerase chain reaction, fragment length and sequence analysis in 140 preterms and 58 healthy term neonates. The frequency of intron 4 variations did not differ between preterms and terms. A total of 111 preterms with the intron 4 wild type (group 1) and 29 preterms carrying the genetic variations (group 2) did not differ in gestational age, gender distribution and birth weight. Compared to group 1, the overall incidence of RDS (75.7% versus 93.1%, P < 0.05), the frequency of severe RDS (28.4% versus 55.2%, P < 0.01) and BPD (21.6% versus 48.3%, P < 0.01) were all higher in group 2. The median duration of oxygen dependency (4 days versus 17 days, P < 0.05) and the need for surfactant administration were also higher in group 2 than in group 1 (43.2% versus 72.4%, P < 0.01). Duration of mechanical ventilation and rate of chronic lung disease at 36 weeks were comparable in both groups. CONCLUSION: we suggest that polymorphisms in intron 4 of the surfactant protein B gene independently modify the course of neonatal respiratory distress syndrome.     

新生儿呼吸窘迫综合征SP-A基因多态性的研究

目的：探讨新生儿呼吸窘迫综合征(respiratory distress syndrome,RDS)肺表面活性蛋白的基因表达特点已成为RDS发病机制的研究热点,目前国内尚无有关报道。该文旨在探讨中国早产儿SP-A基因型的表达特点,以及SP-A等位基因与RDS风险的相关性,从基因水平探讨RDS发病机制,以便更好的预防和治疗。方法：选择已确诊RDS的早产儿为实验组,因早产寄养的新生儿为对照组,取抗凝静脉血2 mL,采用SSCP方法检测SP-A基因6A2、6A3、1A0、1A1。结果：SP-A1等位基因6A2、6A3的分布频率在RDS组分别为0.50、0.056,在对照组分别为0.214、0.107;SP-A2等位基因1A0、1A1的分布频率在RDS组分别为0.722、0.667, 在对照组分别为0.679、0.821。两组比较SP-A1等位基因6A2在RDS组有过表达现象（P<0.05）,而6A3有低表达倾向（P>0.05）;而SP-A2等位基因1A0、1A1的分布频率两组无显著差异（P>0.05）。在胎龄<32周的早产儿SP-A等位基因两组之间比较差异无显著性;而在>32周的早产儿,SP-A1等位基因6A2在RDS组有过表达现象（分布频率0.56,0.15,P<0.05）。男婴等位基因6A2在RDS组有过表达倾向（P>0.05）。结论：在该组正常早产儿人群中SP-A1等位基因6A2、6A3均为低频率分布,SP-A2等位基因1A0与1A1均为高频率分布,1A0、1A1的高表达为该组早产儿基因分布的特点;在 RDS患儿中,SP-A1等位基因6A2有高表达,提示6A2可能为RDS的易感基因。     

Inflammatory and anti-inflammatory responsiveness of surfactant proteins in fetal and neonatal rabbit lung

Spontaneous preterm birth due to intrauterine infection is associated with increased concentrations of cytokines in amniotic fluid and in the airways at birth. Intra-amniotic IL-1 induces fetal lung maturity, consistent with the decrease in the incidence of respiratory distress syndrome (RDS) in intrauterine inflammation. On the other hand, antenatal corticosteroid decreases the incidence of RDS in infants born prematurely. The aim of the present study was to investigate the interaction between IL-1 and glucocorticoid in the expression of the surfactant proteins SP-A, -B, and -C. Lung explants from rabbit fetuses at 22 (immature), 27 (transitional), and 30 (mature) d of gestation (term, 30-31 d) and on d 1 after term birth were cultured with dexamethasone (Dx), IL-1alpha, or vehicle in the presence or absence of actinomycin D. According to the present results, IL-1alpha and Dx additively increased the expression of SP-A and SP-B on d 22. Later in gestation, SP-B and SP-C were suppressed by IL-1, whereas glucocorticoid tended to increase the expression of SP-B and SP-C and prevented the IL-1-induced suppression of SP. IL-1alpha and steroid interactively increased the stability of SP mRNA compared with the single agonist, possibly explaining the additive effects on the SP mRNA levels. The present results reveal beneficial additive effects of glucocorticoid and cytokine on lung surfactant. They may explain some of the acute beneficial effects of glucocorticoid therapy in chorioamnionitis before premature birth and in inflammatory lung disease after birth.     

肺表面活性物质结合蛋白基因的克隆

从正常人肺组织抽提总ＲＮＡ，通过反转录－聚合酶链反应（ＲＴ－ＰＣＲ）技术，扩增出肺表面活性物质结合蛋白（ＳＰ－Ｂ、ＳＰ－Ｃ）基因片段，分别为２４０ｂｐ、１１０ｂｐ。又通过ＰＣＲ产物的回收、克隆、连接、转化、酶解以及ＤＮＡ序列分析，证明所克隆的基因片段与已发表的人成熟ＳＰ－Ｂ、Ｃ的ｃＤＮＡ序列完全一致，未发现有任何突变。提示本研究为利用基因工程手段得到ＳＰ及其与人工合成磷脂重组成有效的外源性肺表面活性物质奠定了基础，同时也证明ＲＴ－ＰＣＲ技术是很有效的ｃＤＮＡ克隆化手段，具有简便快捷的优点。     

Surfactant composition and function in a primate model of infant chronic lung disease: effects of inhaled nitric oxide

Bronchopulmonary dysplasia, or chronic lung disease (CLD), of premature infants involves injury from hyperoxia and mechanical ventilation to an immature lung. We examined surfactant and nitric oxide (NO), which are developmentally deficient in premature infants, in the baboon model of developing CLD. Fetuses were delivered at 125 d gestation and were managed for 14 d with ventilation and oxygen prn without (controls) or with inhaled NO at 5 ppm. Compared with term infants, premature control infants had reduced maximal lung volume, decreased tissue content of surfactant proteins SP-A, -B, and -C, abnormal lavage surfactant as assessed by pulsating bubble surfactometer, and a low concentration of SP-B/phospholipid. NO treatment significantly increased maximal lung volume and tissue SP-A and SP-C, reduced recovery of lavage surfactant by 33%, decreased the total protein:phospholipid ratio of surfactant by 50%, and had no effect on phospholipid composition or SP content except for SP-C (50%). In both treatment groups, levels of SP-B and SP-C in surfactant were negatively correlated with STmin, with a 5-fold greater SP efficiency for NO versus control animals. By contrast, lung volume and compliance were not correlated with surfactant function. We conclude that surfactant is often dysfunctional in developing CLD secondary to SP-B deficiency. NO treatment improves the apparent ability of hydrophobic SP to promote low surface tension, perhaps secondary to less protein inactivation of surfactant, and improves lung volume by a process unrelated to surfactant function.