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中华妇幼临床医学杂志(电子版)

Chinese Journal of Obstetrics & Gynecology and Pediatrics(Electronic Edition) ›› 2019, Vol. 15 ›› Issue (03): 283 -291. doi: 10.3877/cma.j.issn.1673-5250.2019.03.008

Special Issue: ；

Original Article

Screening of bronchopulmonary dysplasia susceptibility genes in preterm infants of Zhuang nationality

Yan Li1, Qiufen Wei1, Xiaofang Guo1, Qi Yang2, Xinnian Pan1,†(), Danhua Meng1, Wei Tan1   

  1. 1. Department of Neonatology, Maternal & Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning 530003, Guangxi Zhuang Autonomous Region, China
    2. Genetics and Metabolism Center, Maternal & Child Health Hospital of Guangxi Zhuang Autonomous Region, Nanning 530003, Guangxi Zhuang Autonomous Region, China
  • Received:2018-10-12 Revised:2019-03-13 Published:2019-06-01
  • Corresponding author: Xinnian Pan
  • About author:
    Corresponding author: Pan Xinnian, Email:
  • Supported by:
    Health and Family Planning Commission Self-financing Research Project of Guangxi Zhuang Autonomous Region(Z2016085, Z20170787, Z20170788); Yu Miao Plan Project of Maternal & Child Health Hospital of Guangxi Zhuang Autonomous Region(GXWCH-YMJH-2017003)
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Objective

To investigate possible susceptibility genes of bronchopulmonary dysplasia (BPD) and their features in preterm infants of Zhuang nationality in Guangxi Zhuang Autonomous Region.

Methods

A total of 50 preterm infants (Zhuang nationality) with gestational age≤ 32 weeks and birth weight ≤ 1 500 g who were treated in Maternal & Child Health Hospital of Guangxi Zhuang Autonomous Region from January 2016 to January 2018, were enrolled into this study. According to whether preterm infants diagnosed as BPD during hospital stay, they were divided into BPD group (n=36, BPD preterm infants) and control group (n=14, non-BPD preterm infants). Peripheral venous blood samples with 2 mL were sampled from all preterm infants within 12 h after admission to perform Sanger gene sequencing. Twenty-four BPD related susceptible candidate genes were selected base on domestic and foreign literatures. Firstly, Hardy-Weinberg equilibrium test was performed to select BPD related susceptibility genes with hereditary stability in preterm infants of Zhuang nationality in this study. Then, the genotype distribution differences of selected BPD related susceptibility genes in preterm infants of Zhuang nationality under different conditions were compared using chi-square test to select susceptibility genes related to BPD occurrence and its severity degree in preterm infants of Zhuang nationality. Finally, to analyze the association between susceptibility genes and occurrence of BPD, the differences of genotype distribution and allele frequency (AF) of BPD susceptibility genes were compared between two groups using chi-square test. This study was in line with the requirements of World Medical Association Declaration of Helsinki revised in 2013, and informed contents were obtained from all guardians of preterm infants.

Results

① Among 24 BPD related susceptibility genetic loci in preterm infants of Zhuang nationality, the genotype distribution of 17 genes consistent with Hardy-Weinberg equilibrium (P>0.05), which had population representation in preterm infants of this study, and were chosen as candidate genes. ② Among these 17 analyzed genes, the genetic polymorphism of vascular endothelial growth factor (VEGF)-2578 and toll-like receptors (TLR)-5 genes may associated with the occurrence of BPD in preterm infants of Zhuang nationality (P<0.05), no genetic locus was found to associated with the severity of BPD (P>0.05). ③ There were significant differences between two groups in genotype distribution and AF of VEGF-2578 or TLR-5 genetic locus (VEGF-2578 genetic locus: χ2=0.350, P=0.030; χ2=9.040, P=0.003. TLR-5 genetic locus: χ2=0.378, P=0.016; χ2=8.268, P=0.004). In BPD group, CC genotype proportion in all genotypes of VEGF-2578 genetic locus and TT genotype proportion in all genotypes of TLR-5 genetic locus were significantly higher than those of control group (80.6% vs 42.9%, 83.3% vs 42.9%); and the AF of C allele of VEGF-2578 genetic locus and AF of T allele of TLR-5 genetic locus were significantly higher than those of control group (87.5% vs 60.7%, 88.9% vs 64.3%).

Conclusions

The genetic loci polymorphisms of VEGF-2578 and TLR-5 genes might be associated with the occurrence of BPD in preterm infants of Zhuang nationality. The CC genotype of VEGF-2578 genetic locus and TT genotype of TLR-5 genetic locus might be the susceptible genotype of BPD in preterm infants of Zhuang nationality. The carrier of C allele of VEFG-2578 gene or T allele of TLR-5 gene of Zhuang nationality might at higher risk of BPD.

Key words: Bronchopulmonary dysplasia, Genetic testing, Genotype, Gene frequency, Susceptibility gene, Zhuang nationality, Infant, premature
表1 与壮族早产儿支气管肺发育不良可能相关的24个候选易感基因位点扩增引物序列
序号 基因位点 正向引物 反向引物
1 SPOCK2(rs1245560) 5′-GCAGGACAGTCTTTGGGTTG-3′ 5′-AGGCAGCTTAGAGACCACTG-3′
2 SPA1-AA19(rs1059047) 5′-ACTCCATGACTGACCACCTT-3′ 5′-ACTCACAGATGGTCAGTCGG-3′
3 SPA1-AA50(rs1136450) 5′-ACGTTGGATGCAGATGGGCCTCCTGAAAAG-3′ 5′-ACGTTGGATGTGCGAAGTGAAGGACGTTTG-3′
4 SPA1-AA62(rs833061) 5′-ACGTTGGATGAATCCTGGAGTGACCCCTG-3′ 5′-ACGTTGGATGAGTGAGGACGTGTGTGTCTG-3′
5 SPA1-AA133(rs1059057) 5′-ACGTTGGATGAGAGACAAAGTGGTCAGTGG-3′ 5′-ACGTTGGATGGATTCCTTGGGACAGCAATG-3′
6 SPA1-AA219(rs4253527) 5′-ACGTTGGATGGAACTCACAGATGGTCAGTC-3′ 5′-ACGTTGGATGAGACTTCCGCTACTCAGACG-3′
7 SPB18(rs2077079) 5′-GACAAACACTGAGGTCGCTG-3′ 5′-CTCAGTGAGTGGTGGAGCTG-3′
8 SPB1013(rs3024798) 5′-ACGTTGGATGCTAAGAGAACCTCCCCATTG-3′ 5′-ACGTTGGATGACTCTTGGCATAGGTCATCC-3′
9 SPB1580(rs1130866) 5′-CATGATGCCAGGTGTGTAGC-3′ 5′-TTTGTGTCTGGCCGGCTT-3′
10 SPB9306(rs7316) 5′-GGCAAGCTTTCTTCCTCGAG-3′ 5′-TCGGCCTTCTGAGTAGTTGG-3′
11 VEGF-460(rs833061) 5′-TGGAGCGAGCAGCGTCTTCG-3′ 5′-CAGGGCCTGAGAGCCGTTCC-3′
12 VEGF-2578(rs699947) 5′-GGATGGGGCTGACTAGGTAAGC-3′ 5′-AGCCCCCTTTTCCTCCAAC-3′
13 VEGF＋405(rs2010963) 5′-TGCCATTCCCCACTTGAATC-3′ 5′-GAAGCGAGAACAGCCCAGAA-3′
14 DAG1-N494H(rs1457319153) 5′-CCTCACCGCCTACTCGTATT -3′ 5′- GCAGTTTCAGGGTCAGCTTC -3′
15 TNFα(rs1799724) 5′-GTATGGGGACCCCCCCTTAA-3′ 5′-GACCCGGAGACTCATAATGC-3′
16 TLR-4(rs4986790) 5′-TGTATTCAAGGTCTGGCTGGT-3′ 5′-GCATTCCCACCTTTGTTGGA-3′
17 TLR-5(rs5744168) 5′-ACGGACTTGACAACCTCCAA-3′ 5′-TCTGGAGATGAGGTACCCGT-3′
18 TLR-10(rs11096955) 5′-GGTAAGGCTTATCTTGACCACA-3′ 5′-GACGAGTTGTTTAAAAGGACT-3′
19 MIF-173(rs755622) 5′-ACTAAGAAAGACCCGAGG-3′ 5′-GGGGCACGTTGGTGTTTAC-3′
20 TIRAP-2054(rs8177374) 5′-CAAGTACCAGATGCTGCAGG-3′ 5′-CCGACAGCCTTTTCCAGAAG-3′
21 IL-18RAP(rs3771150) 5′-GGGGCCCATCTTAAGCTGAT-3′ 5′-TGTTGCTCTGAGACCACGAT-3′
22 IL-18R1(rs3771171) 5′-ACGGGTAGTAGAGAATACAGCC-3′ 5′-TCTTCTATGCTCCTGGGTGTC-3′
23 MMP16C/T(rs2664352) 5′-TTCCTCCCCTGAACTCCAAC-3′ 5′-TGGAGAGTGTCTGGGGAAAC-3′
24 MMP16A/G(rs2664349) 5′-AACAGGAAAGGGAGGTGAGG-3′ 5′-ACAAAAGCCCTTCCCATTGC-3′
表2 2组壮族早产儿一般临床资料比较
组别 例数 男性[例数(%)] 胎龄(周，±s) 出生体重(g，±s) 呼吸支持治疗方式[例数(%)]
生后3 d内机械通气 非侵入性呼吸支持
BPD组 36 28(77.8) 29.3±1.7 1 300±90 21(58.3) 15(41.7)
对照组 14 11(78.6) 30.1±1.2 1 310±110 8(57.1) 6(42.9)
检验值 ? χ2＝0.009 t＝－1.687 t＝0.414 χ2＝0.006
P值 ? 0.951 0.098 0.681 0.939
表3 符合Hardy-Weinberg平衡定律的与壮族早产儿支气管肺发育不良可能相关的17对等位基因的Hardy-Weinberg平衡检验结果
候选基因 χ2值 P值 候选基因 χ2值 P值 候选基因 χ2值 P值
SPA1-AA50 2.124 0.156 VEGF＋405 0.123 0.732 TIRAP-2054 1.756 0.180
SPA1-AA133 1.243 0.299 DAG1-N494H 1.424 0.244 IL-18RAP 2.624 0.102
SPB18 3.326 0.068 TNFα 3.452 0.071 IL-18R1 2.262 0.145
SPB1580 0.324 0.523 TLR-4 1.859 0.173 MMP16C/T 1.895 0.172
SPB9306 0.130 0.726 TLR-5 0.089 0.425 MMP16A/G 0.562 0.446
VEGF-2578 0.067 0.789 TLR-10 0.142 0.698 ? ? ?
表4 与壮族早产儿支气管肺发育不良发生有关的候选基因筛选结果[例数(%)]
发生BPD 例数 SPA1-AA50基因基因型分布 SPA1-AA133基因基因型分布 SPB18基因基因型分布
CC CG GG AA AG GG AA AC CC
是 36 17(47.2) 13(36.1) 6(16.7) 16(44.5) 12(33.3) 8(22.2) 14(38.9) 13(36.1) 9(25.0)
否 14 7(50.0) 5(35.7) 2(14.3) 6(42.8) 4(28.6) 4(28.6) 5(35.7) 6(42.9) 3(21.4)
χ2值 ? 0.032 0.070 0.063
P值 ? 0.974 0.884 0.904
发生BPD 例数 SPB1580基因基因型分布 SPB9306基因基因型分布 VEGF-2578基因基因型分布
CC CG GG AA AG GG CC AC AA
是 36 13(36.1) 12(33.3) 11(30.6) 12(33.3) 15(41.7) 9(25.0) 29(80.6) 5(13.8) 2(5.6)
否 14 5(35.7) 6(42.9) 3(21.4) 6(42.9) 5(35.7) 3(21.4) 6(42.9) 5(35.7) 3(21.4)
χ2值 ? 0.105 0.089 0.350
P值 ? 0.758 0.820 0.030
发生BPD 例数 VEGF＋405基因基因型分布 DAG1-N494H基因基因型分布 TNFα基因基因型分布
CC CG GG AA AG GG CC CT TT
是 36 19(52.8) 12(33.3) 5(13.9) 20(55.6) 12(33.3) 4(11.1) 16(44.4) 9(25.0) 11(30.6)
否 14 7(50.0) 3(21.4) 4(28.6) 7(50.0) 2(14.3) 5(35.7) 4(28.6) 6(42.8) 4(28.6)
χ2值 ? 0.181 0.295 0.182
P值 ? 0.428 0.093 0.423
发生BPD 例数 TLR-4基因基因型分布 TLR-5基因基因型分布 TLR-10基因基因型分布
AA AG GG CC CT TT AA AC CC
是 36 22(61.1) 10(27.8) 4(11.1) 2(5.6) 4(11.1) 30(83.3) 21(58.3) 8(22.2) 7(19.5)
否 14 6(42.9) 3(21.4) 5(35.7) 2(14.2) 6(42.9) 6(42.9) 7(50.0) 4(28.6) 3(21.4)
χ2值 ? 0.277 0.378 0.079
P值 ? 0.126 0.016 0.855
发生BPD 例数 TIRAP-2054基因基因型分布 IL-18RAP基因基因型分布 IL-18R1基因基因型分布
CC CT TT CC CT TT AA AG GG
是 36 20(55.6) 12(33.3) 4(11.1) 15(41.7) 14(38.9) 7(19.4) 23(63.9) 9(25.0) 4(11.1)
否 14 8(57.1) 2(14.3) 4(28.6) 5(35.7) 6(42.9) 3(21.4) 7(50.0) 5(35.7) 2(14.3)
χ2值 ? 0.246 0.054 0.127
P值 ? 0.199 0.928 0.663
发生BPD 例数 MMP16C/T基因基因型分布 MMP16A/G基因基因型分布
CC CT TT AA AG GG
是 36 17(47.2) 12(33.3) 7(19.5) 24(66.7) 7(19.4) 5(13.9)
否 14 5(35.7) 6(42.9) 3(21.4) 7(50.0) 3(21.4) 4(28.6)
χ2值 ? 0.107 0.180
P值 ? 0.749 0.432
表5 与壮族早产儿支气管肺发育不良严重程度有关的候选基因筛选结果[例数(%)]
BPD严重程度 例数 SPA1-AA50基因基因型分布 SPA1-AA133基因基因型分布 SPB18基因基因型分布
CC CG GG AA AG GG AA AC CC
轻度 20 9(45.0) 6(30.0) 5(25.0) 8(40.0) 7(35.0) 5(25.0) 6(30.0) 7(35.0) 7(35.0)
中度 10 5(50.0) 5(50.0) 0(0) 6(60.0) 4(40.0) 0(0) 5(50.0) 4(40.0) 1(10.0)
重度 6 3(50.0) 2(33.3) 1(16.7) 2(33.3) 1(16.7) 3(50.0) 3(50.0) 2(33.3) 1(16.7)
χ2值 ? 0.290 0.373 0.271
P值 ? 0.509 0.213 0.585
BPD严重程度 例数 SPB1580基因基因型分布 SPB9306基因基因型分布 VEGF-2578基因基因型分布
CC CG GG AA AG GG CC AC AA
轻度 20 6(30.0) 6(30.0) 8(40.0) 5(25.0) 7(35.0) 8(40.0) 1(5.0) 3(15.0) 16(80.0)
中度 10 5(50.0) 3(30.0) 2(20.0) 4(40.0) 5(50.0) 1(10.0) 1(10.0) 1(10.0) 8(80.0)
重度 6 2(33.3) 3(50.0) 1(16.7) 3(50.0) 3(50.0) 0(0) 0(0) 1(16.7) 5(83.3)
χ2值 ? 0.263 0.371 0.153
P值 ? 0.613 0.220 0.929
BPD严重程度 例数 VEGF＋405基因基因型分布 DAG1-N494H基因基因型分布 TNFα基因基因型分布
CC CG GG AA AG GG CC CT TT
轻度 20 10(50.0) 8(40.0) 2(10.0) 12(60.0) 6(30.0) 2(10.0) 9(45.0) 5(25.0) 6(30.0)
中度 10 5(50.0) 3(30.0) 2(20.0) 5(50.0) 3(30.0) 2(20.0) 4(40.0) 2(20.0) 4(40.0)
重度 6 4(66.6) 1(16.7) 1(16.7) 3(50.0) 3(50.0) 0(0) 3(50.0) 2(33.3) 1(16.7)
χ2值 ? 0.205 0.238 0.167
P值 ? 0.812 0.706 0.906
BPD严重程度 例数 TLR-4基因基因型分布 TLR-5基因基因型分布 TLR-10基因基因型分布
AA AG GG CC CT TT AA AC CC
轻度 20 11(55.0) 5(25.0) 4(20.0) 1(5.0) 1(5.0) 18(90.0) 13(65.0) 4(20.0) 3(15.0)
中度 10 7(70.0) 3(30.0) 0(0) 1(10.0) 2(20.0) 7(70.0) 5(50.0) 3(30.0) 2(20.0)
重度 6 4(66.7) 2(33.3) 0(0) 0(0) 1(16.7) 5(83.3) 3(50.0) 1(16.7) 2(33.3)
χ2值 ? 0.302 0.258 0.203
P值 ? 0.460 0.632 0.819
BPD严重程度 例数 TIRAP-2054基因基因型分布 IL-18RAP基因基因型分布 IL-18R1基因基因型分布
CC CT TT CC CT TT AA AG GG
轻度 20 11(55.0) 6(30.0) 3(15.0) 6(30.0) 9(45.0) 5(25.0) 13(65.0) 5(25.0) 2(10.0)
中度 10 6(60.0) 3(30.0) 1(10.0) 5(50.0) 3(30.0) 2(20.0) 7(70.0) 2(20.0) 1(10.0)
重度 6 3(50.0) 3(50.0) 0(0) 4(66.7) 2(33.3) 0(0) 3(50.0) 2(33.3) 1(16.7)
χ2值 ? 0.208 0.303 0.139
P值 ? 0.805 0.456 0.950
BPD严重程度 例数 MMP16C/T基因基因型分布 MMP16A/G基因基因型分布
CC CT TT AA AG GG
轻度 20 9(45.0) 5(25.0) 6(30.0) 14(70.0) 3(15.0) 3(15.0)
中度 10 5(50.0) 4(40.0) 1(10.0) 7(70.0) 2(20.0) 1(10.0)
重度 6 3(50.0) 3(50.0) 0(0) 3(50.0) 2(33.3) 1(16.7)
χ2值 ? 0.311 0.184
P值 ? 0.424 0.868
表6 2组早产儿VEGF-2578及TLR-5位点基因型分布及等位基因频率比较
组别 例数 VEGF-2578位点基因型分布 VEGF-2578位点AF TLR-5位点基因型分布 TLR-5位点AF
CC AC AA C A TT TC CC T C
BPD组 36 29(80.6) 5(13.8) 2(5.6) 63(87.5) 9(12.5) 30(83.3) 4(11.1) 2(5.6) 64(88.9) 8(11.1)
对照组 14 6(42.9) 5(35.7) 3(21.4) 17(60.7) 11(39.3) 6(42.9) 6(42.9) 2(14.2) 18(64.3) 10(35.7)
χ2值 ? 0.350 9.040 0.378 8.268
P值 ? 0.030 0.003 0.016 0.004
[1]
钟美珍，白海涛，刘登礼，等. 早产儿支气管肺发育不良危险因素前瞻性队列研究[J]. 中国新生儿科杂志，2011, 26(6): 377-382.
[2]
李燕，韦秋芬，潘新年，等. 早产儿支气管肺发育不良严重程度的影响因素[J]. 中国当代儿科杂志，2014, 16(10): 1014-1018.
[3]
Lavoie PM, Pham C, Jang KL. Heritability of bronchopulmonary dysplasia, defined according to the consensus statement of the national institutes of health[J]. Pediatrics, 2008, 122(3): 479-485.
[4]
赵堃，农绍汉，余宇晖，等. 汉族早产儿支气管肺发育不良易感基因筛查[J]. 中华实用儿科临床杂志，2015, 30(4): 254-257.
[5]
邵肖梅，叶鸿瑁，丘小汕. 实用新生儿学[M]. 4版. 北京：人民卫生出版社，2011: 416-422.
[6]
Hadchouel A, Durrmeyer X, Bouzigon E, et al. Identification of SPOCK2 as a susceptibility gene for bronchopulmonary dysplasia[J]. Am J Respir Crit Care Med, 2011, 184(10): 1164-1170.
[7]
Concolino P, Capoluongo E, Santonocito C, et al. Genetic analysis of the dystroglycan gene in bronchopulmonary dysplasia affected premature newborns[J]. Clin Chim Acta, 2007, 378(1-2): 164-167.
[8]
Kwinta P, Bik-Multanowski M, Mitkowska Z, et al. Genetic risk factors of bronchopulmonary dysplasia[J]. Pediatr Res, 2008, 64(6): 682-688.
[9]
Prencipe G, Auriti C, Inglese R, et al. A polymorphism in the macrophage migration inhibitory factor promoter is associated with bronchopulmonary dysplasia[J]. Pediatr Res, 2011, 69(2): 142-147.
[10]
Ryckman KK, Dagle JM, Kelsey K, et al. Genetic associations of surfactant protein D and angiotensin-converting enzyme with lung disease in preterm neonates[J]. J Perinatol, 2012, 32(5): 349-355.
[11]
Sampath V, Garland JS, Le M, et al. A TLR5 (g.1174C>T) variant that encodes a stop codon (R392X) is associated with bronchopulmonary dysplasia[J]. Pediatr Pulmonol, 2012, 47(5): 460-468.
[12]
Kumral A, Tuzun F, Yesilirmak DC, et al. Genetic basis of apnoea of prematurity and caffeine treatment response: role of adenosine receptor polymorphisms: genetic basis of apnoea of prematurity[J]. Acta Paediatr, 2012, 101(7): e299-e303.
[13]
Cakmak BC, Calkavur S, Ozkinay F, et al. Association between bronchopulmonary dysplasia and MBL2 and IL1-RN polymorphisms[J]. Pediatr Int, 2012, 54(6): 863-868.
[14]
Elhawary NA, Tayeb MT, Abdel-Ghafar S, et al. TNF-238 polymorphism may predict bronchopulmonary dysplasia among preterm infants in the Egyptian population[J]. Pediatr Pulmonol, 2013, 48(7): 699-706.
[15]
Ali S, Hirschfeld AF, Mayer ML, et al. Functional genetic variation in NFKBIA and susceptibility to childhood asthma, bronchiolitis, and bronchopulmonary dysplasia[J]. J Immunol, 2013, 190(8): 3949-3958.
[16]
Rezvani M, Wilde J, Vitt P, et al. Association of a FGFR-4 gene polymorphism with bronchopulmonary dysplasia and neonatal respiratory distress[J]. Dis Markers, 2013, 35(6): 633-640.
[17]
张佳，常立文，李文斌，等. 新生儿肺泡表面活性物质蛋白A1基因多态性与支气管肺发育不良相关性研究[J]. 中国实用儿科杂志，2011, 26(5): 358-360.
[18]
卢维城，向伟，郑旭，等. 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[J]. 中华实用儿科临床杂志，2013, 28(2): 118-121.
[19]
Rova M, Haataja R, Marttila R, et al. Data mining and multiparameter analysis of lung surfactant protein genes in bronchopulmonary dysplasia[J]. Hum Mol Genet, 2004, 13(11): 1095-1104.
[20]
Hadchouel A, Decobert F, Franco-Montoya ML, et al. Matrix metalloproteinase gene polymorphisms and bronchopulmonary dysplasia: identification of MMP16 as a new player in lung development[J]. PLoS One, 2008, 3(9): e3188.
[21]
周玉容，常立文，李文斌，等. 武汉汉族新生儿中肺表面活性物质蛋白D基因多态性及其与支气管肺发育不良相关性分析[J]. 中国病理生理杂志，2011, 27(5): 968-971.
[22]
袁文浩，常立文，李文斌，等. 血管内皮生长因子基因多态性与支气管肺发育不良相关性研究[J]. 中国实用儿科杂志，2012, 27(9): 682-685.
[23]
常立文，李文斌. 早产儿高氧肺损伤的基础研究与临床[J]. 中华围产医学杂志，2009, 12(3): 161-162.
[24]
Malash AH, Ali AA, Samy RM, et al. Association of TLR polymorphisms with bronchopulmonary dysplasia[J]. Gene, 2016, 592(1): 23-28.
[25]
高原，刘花兰，包云光，等. 支气管肺发育不良早产儿肝细胞生长因子、血管内皮生长因子水平变化及其相关性[J/CD]. 中华妇幼临床医学杂志(电子版), 2015, 11(3): 342-346.
[26]
Huusko JM, Mahlman M, Karjalainen MK, et al. Polymorphisms of the gene encoding Kit ligand are associated with bronchopulmonary dysplasia[J]. Pediatr Pulmonol, 2015, 50(3): 260-270.
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