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[Association between GSTP1 gene polymorphisms and susceptibility to noise-induced hearing loss].

Identifieur interne : 000008 ( Main/Exploration ); précédent : 000007; suivant : 000009

[Association between GSTP1 gene polymorphisms and susceptibility to noise-induced hearing loss].

Auteurs : L L Yuan [République populaire de Chine] ; G S Chen [République populaire de Chine] ; J. Jiao [République populaire de Chine] ; W H Zhou [République populaire de Chine] ; H. Wu [République populaire de Chine] ; G Z Gu [République populaire de Chine] ; H L Zhang [République populaire de Chine] ; Y X Zheng [République populaire de Chine] ; S F Yu [République populaire de Chine]

Source :

RBID : pubmed:32306671

Descripteurs français

English descriptors

Abstract

Objective: To investigate the association between the single nucleotide polymorphisms (SNPS) at rs1695 and rs6591256 in glutathione S-transferase P1 (GSTP1) gene and susceptibility to noise-induced hearing loss in Chinese Han workers exposed to noise. Methods: Using the 1: 1 nested case-control study and taking 6297 workers exposed to noise in a steel plant in Henan province as the cohort study population in July 2019, we screened those who have been exposed to noise for ≥3 years and whose binaural high frequency (3000, 4000, 6000 Hz) average hearing threshold is ≥40 dB (A) into the case group. The control group was selected according to the matching criteria of the same sex, same type of work, and the age difference was not more than 5 years old, and the working age difference was not more than 2 years. 276 subjects were selected into the case group and the control group respectively. The medium and high throughout single nucleotide polymorphism typing technology (SNPscanTM technology) was used to detect the polymorphism of three nucleotide sites of GSR gene, and conditional logistic regression was used to analyze the relationship between single nucleotide polymorphism (SNP) and NIHL, and the relationship between different polymorphic sites and the risk of NIHL after adjusting covariates. After stratification with different cumulative noise exposure (CNE) , Conditional logistic regression analysis was used to analysis the risk of NIHL at different loci. Results: The mean and standard deviation of age of the selected subjects was (40.28±8.00) , the mean and standard deviation of noise-exposed working years was (18.7±8.92) years. The range of noise exposure levels and comulative noise exposure were 80.05-93.35dB (A) and 86.83-107.92 dB (A) ·year, respectively. Compared with the control group, there were no statistically significant differences in age, noise-exposured working years, intensity of noise exposure, CNE, gender, drinking, hypertension prevalence and noise exposure level in the hearing loss group (P>0.05) , while there were statistically difference in smoking, binaural high-frequency average hearing threshold and binaural speech frequency (P<0.05) . After adjusting for smoking, drinking, hypertension and other factors, in the co-dominant model, compared with GGgenotype, the risk of NIHL was higher in rs1002149 GT genotype and rs2251780 GA genotype (OR=1.558, 95%CI: 1.028-2.361; OR=1.550, 95%CI: 1.020-2.355, P<0.05) ; compared with TT/GT genotype, the rs1002149 TT genotype has a higher risk of developing NIHL (OR=1.494, 95%CI: 1.002-2.228, P<0.05) , while rs3779647 genotype had no relationship with the risk of NIHL (P>0.05) . In the equivalent sound level (L(Aeq)) of noise >85 dB (A) stratification, compared with GG genotype, carrying rs1002149 GT genotype and rs2251780 GT genotype has higher risk of nihl (OR=1.801, 95%CI: 1.093-2.967; OR=1.720, 95%CI: 1.050-2.817, P<0.05) . Haplotype analysis of two sites, rs1002149 and rs2251780, was not found to be related to NIIHL susceptibility. Conclusion: The allele G of rs1695 and rs6591256 may be risk factors of NIHL.

DOI: 10.3760/cma.j.issn.1001-9391.2020.02.005
PubMed: 32306671


Affiliations:


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Le document en format XML

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<term>Case-Control Studies (MeSH)</term>
<term>China (MeSH)</term>
<term>Genetic Predisposition to Disease (MeSH)</term>
<term>Genotype (MeSH)</term>
<term>Glutathione S-Transferase pi (genetics)</term>
<term>Hearing Loss, Noise-Induced (genetics)</term>
<term>Humans (MeSH)</term>
<term>Noise, Occupational (MeSH)</term>
<term>Polymorphism, Single Nucleotide (MeSH)</term>
</keywords>
<keywords scheme="KwdFr" xml:lang="fr">
<term>Bruit au travail (MeSH)</term>
<term>Chine (MeSH)</term>
<term>Glutathione S-transferase pi (génétique)</term>
<term>Génotype (MeSH)</term>
<term>Humains (MeSH)</term>
<term>Polymorphisme de nucléotide simple (MeSH)</term>
<term>Prédisposition génétique à une maladie (MeSH)</term>
<term>Surdité due au bruit (génétique)</term>
<term>Études cas-témoins (MeSH)</term>
</keywords>
<keywords scheme="MESH" type="chemical" qualifier="genetics" xml:lang="en">
<term>Glutathione S-Transferase pi</term>
</keywords>
<keywords scheme="MESH" type="geographic" xml:lang="en">
<term>China</term>
</keywords>
<keywords scheme="MESH" qualifier="genetics" xml:lang="en">
<term>Hearing Loss, Noise-Induced</term>
</keywords>
<keywords scheme="MESH" qualifier="génétique" xml:lang="fr">
<term>Glutathione S-transferase pi</term>
<term>Surdité due au bruit</term>
</keywords>
<keywords scheme="MESH" xml:lang="en">
<term>Case-Control Studies</term>
<term>Genetic Predisposition to Disease</term>
<term>Genotype</term>
<term>Humans</term>
<term>Noise, Occupational</term>
<term>Polymorphism, Single Nucleotide</term>
</keywords>
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<term>Bruit au travail</term>
<term>Chine</term>
<term>Génotype</term>
<term>Humains</term>
<term>Polymorphisme de nucléotide simple</term>
<term>Prédisposition génétique à une maladie</term>
<term>Études cas-témoins</term>
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<front>
<div type="abstract" xml:lang="en">
<b>Objective:</b>
To investigate the association between the single nucleotide polymorphisms (SNPS) at rs1695 and rs6591256 in glutathione S-transferase P1 (GSTP1) gene and susceptibility to noise-induced hearing loss in Chinese Han workers exposed to noise.
<b>Methods:</b>
Using the 1: 1 nested case-control study and taking 6297 workers exposed to noise in a steel plant in Henan province as the cohort study population in July 2019, we screened those who have been exposed to noise for ≥3 years and whose binaural high frequency (3000, 4000, 6000 Hz) average hearing threshold is ≥40 dB (A) into the case group. The control group was selected according to the matching criteria of the same sex, same type of work, and the age difference was not more than 5 years old, and the working age difference was not more than 2 years. 276 subjects were selected into the case group and the control group respectively. The medium and high throughout single nucleotide polymorphism typing technology (SNPscanTM technology) was used to detect the polymorphism of three nucleotide sites of GSR gene, and conditional logistic regression was used to analyze the relationship between single nucleotide polymorphism (SNP) and NIHL, and the relationship between different polymorphic sites and the risk of NIHL after adjusting covariates. After stratification with different cumulative noise exposure (CNE) , Conditional logistic regression analysis was used to analysis the risk of NIHL at different loci.
<b>Results:</b>
The mean and standard deviation of age of the selected subjects was (40.28±8.00) , the mean and standard deviation of noise-exposed working years was (18.7±8.92) years. The range of noise exposure levels and comulative noise exposure were 80.05-93.35dB (A) and 86.83-107.92 dB (A) ·year, respectively. Compared with the control group, there were no statistically significant differences in age, noise-exposured working years, intensity of noise exposure, CNE, gender, drinking, hypertension prevalence and noise exposure level in the hearing loss group (
<i>P</i>
>0.05) , while there were statistically difference in smoking, binaural high-frequency average hearing threshold and binaural speech frequency (
<i>P</i>
<0.05) . After adjusting for smoking, drinking, hypertension and other factors, in the co-dominant model, compared with GGgenotype, the risk of NIHL was higher in rs1002149 GT genotype and rs2251780 GA genotype (
<i>OR</i>
=1.558, 95%
<i>CI</i>
: 1.028-2.361;
<i>OR</i>
=1.550, 95%
<i>CI</i>
: 1.020-2.355,
<i>P</i>
<0.05) ; compared with TT/GT genotype, the rs1002149 TT genotype has a higher risk of developing NIHL (
<i>OR</i>
=1.494, 95%
<i>CI</i>
: 1.002-2.228,
<i>P</i>
<0.05) , while rs3779647 genotype had no relationship with the risk of NIHL (
<i>P</i>
>0.05) . In the equivalent sound level (L(Aeq)) of noise >85 dB (A) stratification, compared with GG genotype, carrying rs1002149 GT genotype and rs2251780 GT genotype has higher risk of nihl (
<i>OR</i>
=1.801, 95%
<i>CI</i>
: 1.093-2.967;
<i>OR</i>
=1.720, 95%
<i>CI</i>
: 1.050-2.817,
<i>P</i>
<0.05) . Haplotype analysis of two sites, rs1002149 and rs2251780, was not found to be related to NIIHL susceptibility.
<b>Conclusion:</b>
The allele G of rs1695 and rs6591256 may be risk factors of NIHL.</div>
</front>
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<Abstract>
<AbstractText>
<b>Objective:</b>
To investigate the association between the single nucleotide polymorphisms (SNPS) at rs1695 and rs6591256 in glutathione S-transferase P1 (GSTP1) gene and susceptibility to noise-induced hearing loss in Chinese Han workers exposed to noise.
<b>Methods:</b>
Using the 1: 1 nested case-control study and taking 6297 workers exposed to noise in a steel plant in Henan province as the cohort study population in July 2019, we screened those who have been exposed to noise for ≥3 years and whose binaural high frequency (3000, 4000, 6000 Hz) average hearing threshold is ≥40 dB (A) into the case group. The control group was selected according to the matching criteria of the same sex, same type of work, and the age difference was not more than 5 years old, and the working age difference was not more than 2 years. 276 subjects were selected into the case group and the control group respectively. The medium and high throughout single nucleotide polymorphism typing technology (SNPscanTM technology) was used to detect the polymorphism of three nucleotide sites of GSR gene, and conditional logistic regression was used to analyze the relationship between single nucleotide polymorphism (SNP) and NIHL, and the relationship between different polymorphic sites and the risk of NIHL after adjusting covariates. After stratification with different cumulative noise exposure (CNE) , Conditional logistic regression analysis was used to analysis the risk of NIHL at different loci.
<b>Results:</b>
The mean and standard deviation of age of the selected subjects was (40.28±8.00) , the mean and standard deviation of noise-exposed working years was (18.7±8.92) years. The range of noise exposure levels and comulative noise exposure were 80.05-93.35dB (A) and 86.83-107.92 dB (A) ·year, respectively. Compared with the control group, there were no statistically significant differences in age, noise-exposured working years, intensity of noise exposure, CNE, gender, drinking, hypertension prevalence and noise exposure level in the hearing loss group (
<i>P</i>
>0.05) , while there were statistically difference in smoking, binaural high-frequency average hearing threshold and binaural speech frequency (
<i>P</i>
<0.05) . After adjusting for smoking, drinking, hypertension and other factors, in the co-dominant model, compared with GGgenotype, the risk of NIHL was higher in rs1002149 GT genotype and rs2251780 GA genotype (
<i>OR</i>
=1.558, 95%
<i>CI</i>
: 1.028-2.361;
<i>OR</i>
=1.550, 95%
<i>CI</i>
: 1.020-2.355,
<i>P</i>
<0.05) ; compared with TT/GT genotype, the rs1002149 TT genotype has a higher risk of developing NIHL (
<i>OR</i>
=1.494, 95%
<i>CI</i>
: 1.002-2.228,
<i>P</i>
<0.05) , while rs3779647 genotype had no relationship with the risk of NIHL (
<i>P</i>
>0.05) . In the equivalent sound level (L(Aeq)) of noise >85 dB (A) stratification, compared with GG genotype, carrying rs1002149 GT genotype and rs2251780 GT genotype has higher risk of nihl (
<i>OR</i>
=1.801, 95%
<i>CI</i>
: 1.093-2.967;
<i>OR</i>
=1.720, 95%
<i>CI</i>
: 1.050-2.817,
<i>P</i>
<0.05) . Haplotype analysis of two sites, rs1002149 and rs2251780, was not found to be related to NIIHL susceptibility.
<b>Conclusion:</b>
The allele G of rs1695 and rs6591256 may be risk factors of NIHL.</AbstractText>
</Abstract>
<AuthorList CompleteYN="Y">
<Author ValidYN="Y">
<LastName>Yuan</LastName>
<ForeName>L L</ForeName>
<Initials>LL</Initials>
<AffiliationInfo>
<Affiliation>Department of Labor and Environment Health, College of Public Health, Zhengzhou University, Zhengzhou 450041, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Chen</LastName>
<ForeName>G S</ForeName>
<Initials>GS</Initials>
<AffiliationInfo>
<Affiliation>Wugang Institute for Occupational Health, Wugang 462599, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Jiao</LastName>
<ForeName>J</ForeName>
<Initials>J</Initials>
<AffiliationInfo>
<Affiliation>Henan Provincial Institute for Occupational Health, Zhengzhou 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zhou</LastName>
<ForeName>W H</ForeName>
<Initials>WH</Initials>
<AffiliationInfo>
<Affiliation>Henan Provincial Institute for Occupational Health, Zhengzhou 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Wu</LastName>
<ForeName>H</ForeName>
<Initials>H</Initials>
<AffiliationInfo>
<Affiliation>Henan Provincial Institute for Occupational Health, Zhengzhou 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Gu</LastName>
<ForeName>G Z</ForeName>
<Initials>GZ</Initials>
<AffiliationInfo>
<Affiliation>Henan Provincial Institute for Occupational Health, Zhengzhou 450052, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zhang</LastName>
<ForeName>H L</ForeName>
<Initials>HL</Initials>
<AffiliationInfo>
<Affiliation>Wugang Institute for Occupational Health, Wugang 462599, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Zheng</LastName>
<ForeName>Y X</ForeName>
<Initials>YX</Initials>
<AffiliationInfo>
<Affiliation>College of Public Health, Qingdao University, Qingdao 266021, China.</Affiliation>
</AffiliationInfo>
</Author>
<Author ValidYN="Y">
<LastName>Yu</LastName>
<ForeName>S F</ForeName>
<Initials>SF</Initials>
<AffiliationInfo>
<Affiliation>Department of Labor and Environment Health, College of Public Health, Zhengzhou University, Zhengzhou 450041, China; Henan Medical College, Zhengzhou 451191, China.</Affiliation>
</AffiliationInfo>
</Author>
</AuthorList>
<Language>chi</Language>
<GrantList CompleteYN="Y">
<Grant>
<GrantID>81372940, 81872574</GrantID>
<Agency>National Natural Science Foundation of China</Agency>
<Country></Country>
</Grant>
<Grant>
<GrantID>2014BAI12B03</GrantID>
<Agency>National Science and Technology Infrastructure Program of China</Agency>
<Country></Country>
</Grant>
</GrantList>
<PublicationTypeList>
<PublicationType UI="D016428">Journal Article</PublicationType>
</PublicationTypeList>
</Article>
<MedlineJournalInfo>
<Country>China</Country>
<MedlineTA>Zhonghua Lao Dong Wei Sheng Zhi Ye Bing Za Zhi</MedlineTA>
<NlmUniqueID>8410840</NlmUniqueID>
<ISSNLinking>1001-9391</ISSNLinking>
</MedlineJournalInfo>
<ChemicalList>
<Chemical>
<RegistryNumber>EC 2.5.1.18</RegistryNumber>
<NameOfSubstance UI="C496556">GSTP1 protein, human</NameOfSubstance>
</Chemical>
<Chemical>
<RegistryNumber>EC 2.5.1.18</RegistryNumber>
<NameOfSubstance UI="D051549">Glutathione S-Transferase pi</NameOfSubstance>
</Chemical>
</ChemicalList>
<CitationSubset>IM</CitationSubset>
<MeshHeadingList>
<MeshHeading>
<DescriptorName UI="D016022" MajorTopicYN="N">Case-Control Studies</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D002681" MajorTopicYN="N" Type="Geographic">China</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D020022" MajorTopicYN="N">Genetic Predisposition to Disease</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D005838" MajorTopicYN="N">Genotype</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D051549" MajorTopicYN="N">Glutathione S-Transferase pi</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006317" MajorTopicYN="N">Hearing Loss, Noise-Induced</DescriptorName>
<QualifierName UI="Q000235" MajorTopicYN="Y">genetics</QualifierName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D006801" MajorTopicYN="N">Humans</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D009623" MajorTopicYN="Y">Noise, Occupational</DescriptorName>
</MeshHeading>
<MeshHeading>
<DescriptorName UI="D020641" MajorTopicYN="N">Polymorphism, Single Nucleotide</DescriptorName>
</MeshHeading>
</MeshHeadingList>
<OtherAbstract Type="Publisher" Language="chi">
<AbstractText>
<b>目的:</b>
探讨谷胱甘肽还原酶(glutathione reductase,GSR)基因多态性与噪声性听力损失(noise-induced hearing loss,NIHL)易感性之间的关系。
<b>方法:</b>
2019年7月采用1∶1巢式病例对照研究方法,以河南省某钢铁厂的6 297名接触噪声作业工人为队列研究人群中,筛选接触噪声工龄≥3年、双耳高频(3 000、4 000、6 000 Hz)平均听阈≥40 dB的研究对象选择为听力损失组;并按照同性别、同工种、年龄相差≤5岁,接触噪声工龄相差≤2年,听力测试中任一耳语频(500、1 000、2 000 Hz)的任一频段听阈≤25 dB的匹配标准选择为对照组,筛选出听力损失组和对照组各276人。对调查对象进行一般体格检查和问卷调查,进行纯音听力测试和作业场所噪声测量。采用中高通量单核苷酸多态性分型检测技术(SNPscan(TM)法)对研究对象的GSR基因的3个核苷酸位点的多态性进行检测,并采用条件logistic回归分析不同单核苷酸多态性(single nucleotide polymorphism,SNP)与NIHL的关系,及调整协变量后不同多态位点与NIHL发生风险的关系;以不同累积噪声暴露量(cumulative noise exposure,CNE)分层后,采用条件logistic回归分析不同位点与NIHL发生风险的关系。
<b>结果:</b>
研究对象的年龄为(40.28±8.00)岁,接噪工龄为(18.71±8.92)年,研究对象接触噪声水平为80.05~93.35 dB(A),CNE为86.83~107.92 dB(A)·年。与对照组比较,听力损失组、CNE、饮酒和噪声接触水平差异均无统计学意义(
<i>P</i>
>0.05);而年龄、接噪工龄、吸烟、双耳高频平均听阈和双耳语频平均听阈水平有差异,差异有统计学意义(
<i>P</i>
<0.05)。在调整吸烟、饮酒、高血压等因素后,在共显性模型下,与携带GG基因型比较,携带rs1002149 GT、rs2251780 GA基因型患NIHL的风险更高(
<i>OR</i>
=1.558,95%
<i>CI</i>
:1.028~2.361;
<i>OR</i>
=1.550,95%
<i>CI</i>
:1.020~2.355,
<i>P</i>
<0.05);与携带TT/GT基因型比较,携带rs1002149TT基因型患NIHL的风险更高(
<i>OR</i>
=1.494,95%
<i>CI</i>
:1.002~2.228,
<i>P</i>
<0.05);rs3779647位点基因型与患NIHL风险无关(
<i>P</i>
>0.05)。在L(A)eq,8 (h)>85 dB(A)分层下,与携带GG基因型相比,携带rs1002149 GT基因型、rs2251780 GT基因型发生NIHL风险更高(
<i>OR</i>
=1.801,95%
<i>CI</i>
:1.093~2.967;
<i>OR</i>
=1.720,95%
<i>CI</i>
:1.050~2.817,
<i>P</i>
<0.05)。对rs1002149和rs2251780两个位点进行单体型分析,未发现与NIHL的易感性有关(
<i>P</i>
>0.05)。
<b>结论:</b>
GSR基因多态性可能与NIHL发生的易感性有关。.</AbstractText>
</OtherAbstract>
<KeywordList Owner="NOTNLM">
<Keyword MajorTopicYN="N">Glutathione S-transferase P1 gene</Keyword>
<Keyword MajorTopicYN="N">Hearing loss, Noise</Keyword>
<Keyword MajorTopicYN="N">Nested case-control study</Keyword>
<Keyword MajorTopicYN="N">Single nucleotide polymorphism, SNP</Keyword>
<Keyword MajorTopicYN="N">Susceptibility</Keyword>
</KeywordList>
</MedlineCitation>
<PubmedData>
<History>
<PubMedPubDate PubStatus="entrez">
<Year>2020</Year>
<Month>4</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="pubmed">
<Year>2020</Year>
<Month>4</Month>
<Day>21</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
<PubMedPubDate PubStatus="medline">
<Year>2020</Year>
<Month>7</Month>
<Day>11</Day>
<Hour>6</Hour>
<Minute>0</Minute>
</PubMedPubDate>
</History>
<PublicationStatus>ppublish</PublicationStatus>
<ArticleIdList>
<ArticleId IdType="pubmed">32306671</ArticleId>
<ArticleId IdType="doi">10.3760/cma.j.issn.1001-9391.2020.02.005</ArticleId>
</ArticleIdList>
</PubmedData>
</pubmed>
<affiliations>
<list>
<country>
<li>République populaire de Chine</li>
</country>
</list>
<tree>
<country name="République populaire de Chine">
<noRegion>
<name sortKey="Yuan, L L" sort="Yuan, L L" uniqKey="Yuan L" first="L L" last="Yuan">L L Yuan</name>
</noRegion>
<name sortKey="Chen, G S" sort="Chen, G S" uniqKey="Chen G" first="G S" last="Chen">G S Chen</name>
<name sortKey="Gu, G Z" sort="Gu, G Z" uniqKey="Gu G" first="G Z" last="Gu">G Z Gu</name>
<name sortKey="Jiao, J" sort="Jiao, J" uniqKey="Jiao J" first="J" last="Jiao">J. Jiao</name>
<name sortKey="Wu, H" sort="Wu, H" uniqKey="Wu H" first="H" last="Wu">H. Wu</name>
<name sortKey="Yu, S F" sort="Yu, S F" uniqKey="Yu S" first="S F" last="Yu">S F Yu</name>
<name sortKey="Zhang, H L" sort="Zhang, H L" uniqKey="Zhang H" first="H L" last="Zhang">H L Zhang</name>
<name sortKey="Zheng, Y X" sort="Zheng, Y X" uniqKey="Zheng Y" first="Y X" last="Zheng">Y X Zheng</name>
<name sortKey="Zhou, W H" sort="Zhou, W H" uniqKey="Zhou W" first="W H" last="Zhou">W H Zhou</name>
</country>
</tree>
</affiliations>
</record>

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