Rapamycin and MCC950 modified gut microbiota in experimental autoimmune encephalomyelitis mouse by brain gut axis.
Identifieur interne : 000063 ( Main/Exploration ); précédent : 000062; suivant : 000064Rapamycin and MCC950 modified gut microbiota in experimental autoimmune encephalomyelitis mouse by brain gut axis.
Auteurs : Ling Xu [République populaire de Chine] ; Cuili Zhang [République populaire de Chine] ; Dan He [République populaire de Chine] ; Nan Jiang [République populaire de Chine] ; Ying Bai [République populaire de Chine] ; Yi Xin [République populaire de Chine]Source :
- Life sciences [ 1879-0631 ] ; 2020.
Descripteurs français
- KwdFr :
- ARN ribosomique 16S (MeSH), Animaux (MeSH), Encéphale (immunologie), Encéphale (physiopathologie), Encéphalomyélite auto-immune expérimentale (immunologie), Encéphalomyélite auto-immune expérimentale (microbiologie), Encéphalomyélite auto-immune expérimentale (traitement médicamenteux), Femelle (MeSH), Furanes (administration et posologie), Furanes (pharmacologie), Gros intestin (anatomopathologie), Gros intestin (immunologie), Inflammation (anatomopathologie), Inflammation (immunologie), Microbiome gastro-intestinal (immunologie), Modèles animaux de maladie humaine (MeSH), Rate (anatomopathologie), Rate (immunologie), Sclérose en plaques (immunologie), Sclérose en plaques (microbiologie), Sclérose en plaques (traitement médicamenteux), Sirolimus (administration et posologie), Sirolimus (pharmacologie), Souris (MeSH), Souris de lignée C57BL (MeSH), Sulfonamides (administration et posologie), Sulfonamides (pharmacologie), Évolution de la maladie (MeSH).
- MESH :
- administration et posologie : Furanes, Sirolimus, Sulfonamides.
- anatomopathologie : Gros intestin, Inflammation, Rate.
- immunologie : Encéphale, Encéphalomyélite auto-immune expérimentale, Gros intestin, Inflammation, Microbiome gastro-intestinal, Rate, Sclérose en plaques.
- microbiologie : Encéphalomyélite auto-immune expérimentale, Sclérose en plaques.
- pharmacologie : Furanes, Sirolimus, Sulfonamides.
- physiopathologie : Encéphale.
- traitement médicamenteux : Encéphalomyélite auto-immune expérimentale, Sclérose en plaques.
- ARN ribosomique 16S, Animaux, Femelle, Modèles animaux de maladie humaine, Souris, Souris de lignée C57BL, Évolution de la maladie.
English descriptors
- KwdEn :
- Animals (MeSH), Brain (immunology), Brain (physiopathology), Disease Models, Animal (MeSH), Disease Progression (MeSH), Encephalomyelitis, Autoimmune, Experimental (drug therapy), Encephalomyelitis, Autoimmune, Experimental (immunology), Encephalomyelitis, Autoimmune, Experimental (microbiology), Female (MeSH), Furans (administration & dosage), Furans (pharmacology), Gastrointestinal Microbiome (immunology), Inflammation (immunology), Inflammation (pathology), Intestine, Large (immunology), Intestine, Large (pathology), Mice (MeSH), Mice, Inbred C57BL (MeSH), Multiple Sclerosis (drug therapy), Multiple Sclerosis (immunology), Multiple Sclerosis (microbiology), RNA, Ribosomal, 16S (MeSH), Sirolimus (administration & dosage), Sirolimus (pharmacology), Spleen (immunology), Spleen (pathology), Sulfonamides (administration & dosage), Sulfonamides (pharmacology).
- MESH :
- chemical , administration & dosage : Furans, Sirolimus, Sulfonamides.
- drug therapy : Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis.
- immunology : Brain, Encephalomyelitis, Autoimmune, Experimental, Gastrointestinal Microbiome, Inflammation, Intestine, Large, Multiple Sclerosis, Spleen.
- microbiology : Encephalomyelitis, Autoimmune, Experimental, Multiple Sclerosis.
- pathology : Inflammation, Intestine, Large, Spleen.
- chemical , pharmacology : Furans, Sirolimus, Sulfonamides.
- physiopathology : Brain.
- Animals, Disease Models, Animal, Disease Progression, Female, Mice, Mice, Inbred C57BL, RNA, Ribosomal, 16S.
Abstract
AIMS
Multiple sclerosis (MS) whose pathogenesis is still unclear is a chronic progressive disease in the central nervous system. Gut microbiota can directly or indirectly affect the immune system through the brain gut axis to engage in the occurrence and development of the disease.
MATERIALS AND METHODS
C57BL/6 mice which were immunized by MOG
KEY FINDINGS
The results showed that rapamycin and MCC950 could alleviate the progression of the disease by inducing autophagy and inhibiting the immune response. The Alpha diversity of EAE model group was no significant difference compering to control group while the number of OTUs was decreased. After the treatment by rapamycin and MCC950, the abundance and composition of gut microbiota was relatively recovered, which was close to that of normal mice.
SIGNIFICANCE
Inhibiting immune cell-mediated inflammation and restoring the composition of gut microbiota may help to alleviate the clinical symptoms of multiple sclerosis. Furthermore, to research the regulatory effect between immune response and gut microbiota may be a new strategy for the prevention and treatment of multiple sclerosis.
DOI: 10.1016/j.lfs.2020.117747
PubMed: 32376270
Affiliations:
Links toward previous steps (curation, corpus...)
Le document en format XML
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& dosage)</term><term>Furans (pharmacology)</term><term>Gastrointestinal Microbiome (immunology)</term><term>Inflammation (immunology)</term><term>Inflammation (pathology)</term><term>Intestine, Large (immunology)</term><term>Intestine, Large (pathology)</term><term>Mice (MeSH)</term><term>Mice, Inbred C57BL (MeSH)</term><term>Multiple Sclerosis (drug therapy)</term><term>Multiple Sclerosis (immunology)</term><term>Multiple Sclerosis (microbiology)</term><term>RNA, Ribosomal, 16S (MeSH)</term><term>Sirolimus (administration & dosage)</term><term>Sirolimus (pharmacology)</term><term>Spleen (immunology)</term><term>Spleen (pathology)</term><term>Sulfonamides (administration & dosage)</term><term>Sulfonamides (pharmacology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>ARN ribosomique 16S (MeSH)</term><term>Animaux (MeSH)</term><term>Encéphale (immunologie)</term><term>Encéphale (physiopathologie)</term><term>Encéphalomyélite auto-immune expérimentale (immunologie)</term><term>Encéphalomyélite auto-immune expérimentale (microbiologie)</term><term>Encéphalomyélite auto-immune expérimentale (traitement médicamenteux)</term><term>Femelle (MeSH)</term><term>Furanes (administration et posologie)</term><term>Furanes (pharmacologie)</term><term>Gros intestin (anatomopathologie)</term><term>Gros intestin (immunologie)</term><term>Inflammation (anatomopathologie)</term><term>Inflammation (immunologie)</term><term>Microbiome gastro-intestinal (immunologie)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Rate (anatomopathologie)</term><term>Rate (immunologie)</term><term>Sclérose en plaques (immunologie)</term><term>Sclérose en plaques (microbiologie)</term><term>Sclérose en plaques (traitement médicamenteux)</term><term>Sirolimus (administration et posologie)</term><term>Sirolimus (pharmacologie)</term><term>Souris (MeSH)</term><term>Souris de lignée C57BL (MeSH)</term><term>Sulfonamides (administration et posologie)</term><term>Sulfonamides (pharmacologie)</term><term>Évolution de la maladie (MeSH)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="administration & dosage" xml:lang="en"><term>Furans</term><term>Sirolimus</term><term>Sulfonamides</term></keywords><keywords scheme="MESH" qualifier="administration et posologie" xml:lang="fr"><term>Furanes</term><term>Sirolimus</term><term>Sulfonamides</term></keywords><keywords scheme="MESH" qualifier="anatomopathologie" xml:lang="fr"><term>Gros intestin</term><term>Inflammation</term><term>Rate</term></keywords><keywords scheme="MESH" qualifier="drug therapy" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term><term>Multiple Sclerosis</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Encéphale</term><term>Encéphalomyélite auto-immune expérimentale</term><term>Gros intestin</term><term>Inflammation</term><term>Microbiome gastro-intestinal</term><term>Rate</term><term>Sclérose en plaques</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Brain</term><term>Encephalomyelitis, Autoimmune, Experimental</term><term>Gastrointestinal Microbiome</term><term>Inflammation</term><term>Intestine, Large</term><term>Multiple Sclerosis</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="microbiologie" xml:lang="fr"><term>Encéphalomyélite auto-immune expérimentale</term><term>Sclérose en plaques</term></keywords><keywords scheme="MESH" qualifier="microbiology" xml:lang="en"><term>Encephalomyelitis, Autoimmune, Experimental</term><term>Multiple Sclerosis</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Inflammation</term><term>Intestine, Large</term><term>Spleen</term></keywords><keywords scheme="MESH" qualifier="pharmacologie" xml:lang="fr"><term>Furanes</term><term>Sirolimus</term><term>Sulfonamides</term></keywords><keywords scheme="MESH" type="chemical" qualifier="pharmacology" xml:lang="en"><term>Furans</term><term>Sirolimus</term><term>Sulfonamides</term></keywords><keywords scheme="MESH" qualifier="physiopathologie" xml:lang="fr"><term>Encéphale</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term></keywords><keywords scheme="MESH" qualifier="traitement médicamenteux" xml:lang="fr"><term>Encéphalomyélite auto-immune expérimentale</term><term>Sclérose en plaques</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Disease Progression</term><term>Female</term><term>Mice</term><term>Mice, Inbred C57BL</term><term>RNA, Ribosomal, 16S</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>ARN ribosomique 16S</term><term>Animaux</term><term>Femelle</term><term>Modèles animaux de maladie humaine</term><term>Souris</term><term>Souris de lignée C57BL</term><term>Évolution de la maladie</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><p><b>AIMS</b></p><p>Multiple sclerosis (MS) whose pathogenesis is still unclear is a chronic progressive disease in the central nervous system. Gut microbiota can directly or indirectly affect the immune system through the brain gut axis to engage in the occurrence and development of the disease.</p></div><div type="abstract" xml:lang="en"><p><b>MATERIALS AND METHODS</b></p><p>C57BL/6 mice which were immunized by MOG</p></div><div type="abstract" xml:lang="en"><p><b>KEY FINDINGS</b></p><p>The results showed that rapamycin and MCC950 could alleviate the progression of the disease by inducing autophagy and inhibiting the immune response. The Alpha diversity of EAE model group was no significant difference compering to control group while the number of OTUs was decreased. After the treatment by rapamycin and MCC950, the abundance and composition of gut microbiota was relatively recovered, which was close to that of normal mice.</p></div><div type="abstract" xml:lang="en"><p><b>SIGNIFICANCE</b></p><p>Inhibiting immune cell-mediated inflammation and restoring the composition of gut microbiota may help to alleviate the clinical symptoms of multiple sclerosis. Furthermore, to research the regulatory effect between immune response and gut microbiota may be a new strategy for the prevention and treatment of multiple sclerosis.</p></div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32376270</PMID><DateCompleted><Year>2020</Year><Month>06</Month><Day>10</Day></DateCompleted><DateRevised><Year>2020</Year><Month>07</Month><Day>20</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1879-0631</ISSN><JournalIssue CitedMedium="Internet"><Volume>253</Volume><PubDate><Year>2020</Year><Month>Jul</Month><Day>15</Day></PubDate></JournalIssue><Title>Life sciences</Title><ISOAbbreviation>Life Sci</ISOAbbreviation></Journal><ArticleTitle>Rapamycin and MCC950 modified gut microbiota in experimental autoimmune encephalomyelitis mouse by brain gut axis.</ArticleTitle><Pagination><MedlinePgn>117747</MedlinePgn></Pagination><ELocationID EIdType="pii" ValidYN="Y">S0024-3205(20)30495-1</ELocationID><ELocationID EIdType="doi" ValidYN="Y">10.1016/j.lfs.2020.117747</ELocationID><Abstract><AbstractText Label="AIMS" NlmCategory="OBJECTIVE">Multiple sclerosis (MS) whose pathogenesis is still unclear is a chronic progressive disease in the central nervous system. Gut microbiota can directly or indirectly affect the immune system through the brain gut axis to engage in the occurrence and development of the disease.</AbstractText><AbstractText Label="MATERIALS AND METHODS" NlmCategory="METHODS">C57BL/6 mice which were immunized by MOG<sub>35</sub><sub>-</sub><sub>55</sub> to prepare experimental autoimmune encephalomyelitis (EAE) animal models were treated with rapamycin and MCC950 (CP-456773) in combination or separately. After sequencing the 16S rRNA V4 region of gut microbiota, the species, abundance and composition of gut microbiota were analyzed by Alpha diversity, Bata diversity and LEfSe analysis. The pathological changes and the expression of CD4 and CD8 of brain, large intestine and spleen were detected.</AbstractText><AbstractText Label="KEY FINDINGS" NlmCategory="RESULTS">The results showed that rapamycin and MCC950 could alleviate the progression of the disease by inducing autophagy and inhibiting the immune response. The Alpha diversity of EAE model group was no significant difference compering to control group while the number of OTUs was decreased. After the treatment by rapamycin and MCC950, the abundance and composition of gut microbiota was relatively recovered, which was close to that of normal mice.</AbstractText><AbstractText Label="SIGNIFICANCE" NlmCategory="CONCLUSIONS">Inhibiting immune cell-mediated inflammation and restoring the composition of gut microbiota may help to alleviate the clinical symptoms of multiple sclerosis. Furthermore, to research the regulatory effect between immune response and gut microbiota may be a new strategy for the prevention and treatment of multiple sclerosis.</AbstractText><CopyrightInformation>Copyright © 2020 Elsevier Inc. All rights reserved.</CopyrightInformation></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Xu</LastName><ForeName>Ling</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Department of Biotechnology, Dalian Medical University, Dalian 116644, China; Department of Clinical Laboratory, Xinhua Hospital Affiliated to Dalian University, Dalian 116021, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Zhang</LastName><ForeName>Cuili</ForeName><Initials>C</Initials><AffiliationInfo><Affiliation>Department of Biotechnology, Dalian Medical University, Dalian 116644, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>He</LastName><ForeName>Dan</ForeName><Initials>D</Initials><AffiliationInfo><Affiliation>Department of Physiology and Pathophysiology, School of Basic Medical Sciences, Peking University, Beijing 100191, China; Key Laboratory of Molecular Cardiovascular Science, Ministry of Education, Beijing 100191, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Jiang</LastName><ForeName>Nan</ForeName><Initials>N</Initials><AffiliationInfo><Affiliation>Department of Pathology, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bai</LastName><ForeName>Ying</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Clinical Laboratory, Xinhua Hospital Affiliated to Dalian University, Dalian 116021, China.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Xin</LastName><ForeName>Yi</ForeName><Initials>Y</Initials><AffiliationInfo><Affiliation>Department of Biotechnology, Dalian Medical University, Dalian 116644, China. Electronic address: jimxin@hotmail.com.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>05</Month><Day>03</Day></ArticleDate></Article><MedlineJournalInfo><Country>Netherlands</Country><MedlineTA>Life Sci</MedlineTA><NlmUniqueID>0375521</NlmUniqueID><ISSNLinking>0024-3205</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D005663">Furans</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="C000597426">MCC-950</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D012336">RNA, Ribosomal, 16S</NameOfSubstance></Chemical><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D013449">Sulfonamides</NameOfSubstance></Chemical><Chemical><RegistryNumber>W36ZG6FT64</RegistryNumber><NameOfSubstance UI="D020123">Sirolimus</NameOfSubstance></Chemical></ChemicalList><CitationSubset>IM</CitationSubset><MeshHeadingList><MeshHeading><DescriptorName UI="D000818" MajorTopicYN="N">Animals</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D001921" MajorTopicYN="N">Brain</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000503" MajorTopicYN="N">physiopathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D004195" MajorTopicYN="N">Disease Models, Animal</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D018450" MajorTopicYN="N">Disease Progression</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D004681" MajorTopicYN="N">Encephalomyelitis, Autoimmune, Experimental</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D005260" MajorTopicYN="N">Female</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D005663" MajorTopicYN="N">Furans</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D000069196" MajorTopicYN="N">Gastrointestinal Microbiome</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="Y">immunology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007249" MajorTopicYN="N">Inflammation</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D007420" MajorTopicYN="N">Intestine, Large</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D051379" MajorTopicYN="N">Mice</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D008810" MajorTopicYN="N">Mice, Inbred C57BL</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D009103" MajorTopicYN="N">Multiple Sclerosis</DescriptorName><QualifierName UI="Q000188" MajorTopicYN="Y">drug therapy</QualifierName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000382" MajorTopicYN="N">microbiology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D012336" MajorTopicYN="N">RNA, Ribosomal, 16S</DescriptorName></MeshHeading><MeshHeading><DescriptorName UI="D020123" MajorTopicYN="N">Sirolimus</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013154" MajorTopicYN="N">Spleen</DescriptorName><QualifierName UI="Q000276" MajorTopicYN="N">immunology</QualifierName><QualifierName UI="Q000473" MajorTopicYN="N">pathology</QualifierName></MeshHeading><MeshHeading><DescriptorName UI="D013449" MajorTopicYN="N">Sulfonamides</DescriptorName><QualifierName UI="Q000008" MajorTopicYN="N">administration & dosage</QualifierName><QualifierName UI="Q000494" MajorTopicYN="Y">pharmacology</QualifierName></MeshHeading></MeshHeadingList><KeywordList Owner="NOTNLM"><Keyword MajorTopicYN="N">16S rRNA sequencing</Keyword><Keyword MajorTopicYN="N">Brain gut axis</Keyword><Keyword MajorTopicYN="N">Gut microbiota</Keyword><Keyword MajorTopicYN="N">MCC950</Keyword><Keyword MajorTopicYN="N">Multiple sclerosis</Keyword><Keyword MajorTopicYN="N">Rapamycin</Keyword></KeywordList><CoiStatement>Declaration of competing interest The authors declare no financial or commercial conflict of interest.</CoiStatement></MedlineCitation><PubmedData><History><PubMedPubDate PubStatus="received"><Year>2020</Year><Month>04</Month><Day>16</Day></PubMedPubDate><PubMedPubDate PubStatus="revised"><Year>2020</Year><Month>04</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="accepted"><Year>2020</Year><Month>04</Month><Day>30</Day></PubMedPubDate><PubMedPubDate PubStatus="pubmed"><Year>2020</Year><Month>5</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="medline"><Year>2020</Year><Month>6</Month><Day>11</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate><PubMedPubDate PubStatus="entrez"><Year>2020</Year><Month>5</Month><Day>8</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32376270</ArticleId><ArticleId IdType="pii">S0024-3205(20)30495-1</ArticleId><ArticleId IdType="doi">10.1016/j.lfs.2020.117747</ArticleId></ArticleIdList></PubmedData></pubmed><affiliations><list><country><li>République populaire de Chine</li></country><region><li>Pékin</li></region><settlement><li>Pékin</li></settlement><orgName><li>Université de Pékin</li></orgName></list><tree><country name="République populaire de Chine"><noRegion><name sortKey="Xu, Ling" sort="Xu, Ling" uniqKey="Xu L" first="Ling" last="Xu">Ling Xu</name></noRegion><name sortKey="Bai, Ying" sort="Bai, Ying" uniqKey="Bai Y" first="Ying" last="Bai">Ying Bai</name><name sortKey="He, Dan" sort="He, Dan" uniqKey="He D" first="Dan" last="He">Dan He</name><name sortKey="Jiang, Nan" sort="Jiang, Nan" uniqKey="Jiang N" first="Nan" last="Jiang">Nan Jiang</name><name sortKey="Xin, Yi" sort="Xin, Yi" uniqKey="Xin Y" first="Yi" last="Xin">Yi Xin</name><name sortKey="Zhang, Cuili" sort="Zhang, Cuili" uniqKey="Zhang C" first="Cuili" last="Zhang">Cuili Zhang</name></country></tree></affiliations></record>Pour 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