Atorvastatin treatment of rats with ischemia-reperfusion injury improves adipose-derived mesenchymal stem cell migration and survival via the SDF-1α/CXCR-4 axis
Adipose-derived mesenchymal stem cells (ASCs) transplantation is a promising approach for myocardium repair. Promotion of ASCs migration and survival is the key for improving ASCs efficiency. SDF-1α is a critical factor responsible for ASCs migration and survival. Atorvastatin (Ator) is capable of u...
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| Veröffentlicht in: | PloS one 2013-12, Vol.8 (12), p.e79100-e79100 |
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| creator | Cai, Anping Qiu, Ruofeng Li, Liwen Zheng, Dongdan Dong, Yugang Yu, Danqing Huang, Yuli Rao, Shaoqi Zhou, Yingling Mai, Weiyi |
| description | Adipose-derived mesenchymal stem cells (ASCs) transplantation is a promising approach for myocardium repair. Promotion of ASCs migration and survival is the key for improving ASCs efficiency. SDF-1α is a critical factor responsible for ASCs migration and survival. Atorvastatin (Ator) is capable of up-regulating SDF-1α. Therefore, we're going to investigate whether ASCs migration and survival could be improved with atorvastatin.
In vitro study, cardiomyocytes were subjected to anoxia-reoxygenation injury and subsequently divided into different groups: group blank control, Ator, Ator plus L-NAME (A+L-NAME) and Ator plus AMD3100 (A+AMD3100).When migration analysis completed, cardiomyocytes were used for subsequent analyses. In vivo study, rats underwent ischemia-reperfusion injury were assigned into different groups corresponding to in vitro protocols. ASCs were transplanted on the seventh day of atorvastatin therapy. Seven days later, the rates of migration, differentiation and apoptosis were evaluated.
Compared with other groups, ASCs migration in vitro was significantly improved in group Ator, which was dependent on SDF-1α/CXCR-4 coupling. Results of in vivo study were consistent with that of in vitro study, further supporting the notion that the efficacy of atorvastatin on ASCs migration improvement was related to SDF-1α/CXCR-4 axis. Higher vessel density in group Ator might be another mechanism responsible for migration improvement. Concomitantly, apoptosis was significantly reduced in group Ator, whereas no significant difference of differentiation was found.
Migration and survival of ASCs could be improved by atorvastatin under ischemia-reperfusion injury, which were ascribed to SDF-1α/CXCR-4 axis. |
| doi_str_mv | 10.1371/journal.pone.0079100 |
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In vitro study, cardiomyocytes were subjected to anoxia-reoxygenation injury and subsequently divided into different groups: group blank control, Ator, Ator plus L-NAME (A+L-NAME) and Ator plus AMD3100 (A+AMD3100).When migration analysis completed, cardiomyocytes were used for subsequent analyses. In vivo study, rats underwent ischemia-reperfusion injury were assigned into different groups corresponding to in vitro protocols. ASCs were transplanted on the seventh day of atorvastatin therapy. Seven days later, the rates of migration, differentiation and apoptosis were evaluated.
Compared with other groups, ASCs migration in vitro was significantly improved in group Ator, which was dependent on SDF-1α/CXCR-4 coupling. Results of in vivo study were consistent with that of in vitro study, further supporting the notion that the efficacy of atorvastatin on ASCs migration improvement was related to SDF-1α/CXCR-4 axis. Higher vessel density in group Ator might be another mechanism responsible for migration improvement. Concomitantly, apoptosis was significantly reduced in group Ator, whereas no significant difference of differentiation was found.
Migration and survival of ASCs could be improved by atorvastatin under ischemia-reperfusion injury, which were ascribed to SDF-1α/CXCR-4 axis.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0079100</identifier><identifier>PMID: 24312447</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Allografts ; Animals ; Anoxia ; Apoptosis ; Atorvastatin ; Atorvastatin Calcium ; Bone marrow ; Cardiology ; Cardiomyocytes ; Cardiovascular disease ; Cell migration ; Cell Movement - drug effects ; Cell survival ; Cell Survival - drug effects ; Chemokine CXCL12 - metabolism ; Differentiation ; Heart attacks ; Heptanoic Acids - pharmacology ; Hospitals ; Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology ; In vitro methods and tests ; In vivo methods and tests ; Injuries ; Injury analysis ; Ischemia ; Male ; Medical research ; Mesenchymal Stem Cell Transplantation ; Mesenchymal stem cells ; Mesenchymal Stromal Cells - metabolism ; Mesenchymal Stromal Cells - pathology ; Mesenchyme ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - therapy ; Myocardium ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; NG-Nitroarginine methyl ester ; Nitric oxide ; Pyrroles - pharmacology ; Rats ; Rats, Sprague-Dawley ; Receptors, CXCR4 - metabolism ; Reperfusion ; Rodents ; Stem cells ; Survival ; Transplantation</subject><ispartof>PloS one, 2013-12, Vol.8 (12), p.e79100-e79100</ispartof><rights>2013 Cai et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/3.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2013 Cai et al 2013 Cai et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-6d93f55e916ddfabb3ac27da15e3b8cd45b3193259b8780eaef490ca8b46757d3</citedby><cites>FETCH-LOGICAL-c526t-6d93f55e916ddfabb3ac27da15e3b8cd45b3193259b8780eaef490ca8b46757d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846471/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3846471/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2095,2914,23846,27903,27904,53770,53772,79347,79348</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24312447$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Katare, Rajesh Gopalrao</contributor><creatorcontrib>Cai, Anping</creatorcontrib><creatorcontrib>Qiu, Ruofeng</creatorcontrib><creatorcontrib>Li, Liwen</creatorcontrib><creatorcontrib>Zheng, Dongdan</creatorcontrib><creatorcontrib>Dong, Yugang</creatorcontrib><creatorcontrib>Yu, Danqing</creatorcontrib><creatorcontrib>Huang, Yuli</creatorcontrib><creatorcontrib>Rao, Shaoqi</creatorcontrib><creatorcontrib>Zhou, Yingling</creatorcontrib><creatorcontrib>Mai, Weiyi</creatorcontrib><title>Atorvastatin treatment of rats with ischemia-reperfusion injury improves adipose-derived mesenchymal stem cell migration and survival via the SDF-1α/CXCR-4 axis</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Adipose-derived mesenchymal stem cells (ASCs) transplantation is a promising approach for myocardium repair. Promotion of ASCs migration and survival is the key for improving ASCs efficiency. SDF-1α is a critical factor responsible for ASCs migration and survival. Atorvastatin (Ator) is capable of up-regulating SDF-1α. Therefore, we're going to investigate whether ASCs migration and survival could be improved with atorvastatin.
In vitro study, cardiomyocytes were subjected to anoxia-reoxygenation injury and subsequently divided into different groups: group blank control, Ator, Ator plus L-NAME (A+L-NAME) and Ator plus AMD3100 (A+AMD3100).When migration analysis completed, cardiomyocytes were used for subsequent analyses. In vivo study, rats underwent ischemia-reperfusion injury were assigned into different groups corresponding to in vitro protocols. ASCs were transplanted on the seventh day of atorvastatin therapy. Seven days later, the rates of migration, differentiation and apoptosis were evaluated.
Compared with other groups, ASCs migration in vitro was significantly improved in group Ator, which was dependent on SDF-1α/CXCR-4 coupling. Results of in vivo study were consistent with that of in vitro study, further supporting the notion that the efficacy of atorvastatin on ASCs migration improvement was related to SDF-1α/CXCR-4 axis. Higher vessel density in group Ator might be another mechanism responsible for migration improvement. Concomitantly, apoptosis was significantly reduced in group Ator, whereas no significant difference of differentiation was found.
Migration and survival of ASCs could be improved by atorvastatin under ischemia-reperfusion injury, which were ascribed to SDF-1α/CXCR-4 axis.</description><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Allografts</subject><subject>Animals</subject><subject>Anoxia</subject><subject>Apoptosis</subject><subject>Atorvastatin</subject><subject>Atorvastatin Calcium</subject><subject>Bone marrow</subject><subject>Cardiology</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cell migration</subject><subject>Cell Movement - drug effects</subject><subject>Cell survival</subject><subject>Cell Survival - drug effects</subject><subject>Chemokine CXCL12 - metabolism</subject><subject>Differentiation</subject><subject>Heart attacks</subject><subject>Heptanoic Acids - pharmacology</subject><subject>Hospitals</subject><subject>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</subject><subject>In vitro methods and tests</subject><subject>In vivo methods and tests</subject><subject>Injuries</subject><subject>Injury analysis</subject><subject>Ischemia</subject><subject>Male</subject><subject>Medical research</subject><subject>Mesenchymal Stem Cell Transplantation</subject><subject>Mesenchymal stem cells</subject><subject>Mesenchymal Stromal Cells - metabolism</subject><subject>Mesenchymal Stromal Cells - pathology</subject><subject>Mesenchyme</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - therapy</subject><subject>Myocardium</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>NG-Nitroarginine methyl ester</subject><subject>Nitric oxide</subject><subject>Pyrroles - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptors, CXCR4 - metabolism</subject><subject>Reperfusion</subject><subject>Rodents</subject><subject>Stem cells</subject><subject>Survival</subject><subject>Transplantation</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptUttu1DAQjRCIlsIfILDECy_Z2rEdxy9I1UKhUiUkLhJv1iSedL1K4sV2Avs5fAI_wjeR7W6rFvFka3zOmZnjk2XPGV0wrtjp2o9hgG6x8QMuKFWaUfogO2aaF3lZUP7wzv0oexLjmlLJq7J8nB0VgrNCCHWc_TpLPkwQEyQ3kBQQUo9DIr4lAVIkP1xaERebFfYO8oAbDO0YnR-IG9Zj2BLXb4KfMBKwbuMj5haDm9CSHiMOzWrbQ0diwp402HWkd1ez7o4PgyVxDJObZsDkgKQVks9vz3P25_fp8tvyUy4I_HTxafaohS7is8N5kn09f_dl-SG__Pj-Ynl2mTeyKFNeWs1bKVGz0toW6ppDUygLTCKvq8YKWfOdH1LXlaooArZC0waqWpRKKstPspd73U3nozm4Gw0TJadaKaFnxMUeYT2szSa4HsLWeHDmuuDDlYGQXNOhKamWVcFaqkGIhtYVEyjnklKlFpXGWevNodtY92ib2fMA3T3R-y-DW5krPxleiVIoNgu8PggE_33EmEw_f9NsMQzox-u5ZVVKpsQMffUP9P_biT2qCT7GgO3tMIyaXeJuWGaXOHNI3Ex7cXeRW9JNxPhf8U3X-w</recordid><startdate>20131202</startdate><enddate>20131202</enddate><creator>Cai, Anping</creator><creator>Qiu, Ruofeng</creator><creator>Li, Liwen</creator><creator>Zheng, Dongdan</creator><creator>Dong, Yugang</creator><creator>Yu, Danqing</creator><creator>Huang, Yuli</creator><creator>Rao, Shaoqi</creator><creator>Zhou, Yingling</creator><creator>Mai, Weiyi</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20131202</creationdate><title>Atorvastatin treatment of rats with ischemia-reperfusion injury improves adipose-derived mesenchymal stem cell migration and survival via the SDF-1α/CXCR-4 axis</title><author>Cai, Anping ; Qiu, Ruofeng ; Li, Liwen ; Zheng, Dongdan ; Dong, Yugang ; Yu, Danqing ; Huang, Yuli ; Rao, Shaoqi ; Zhou, Yingling ; Mai, Weiyi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-6d93f55e916ddfabb3ac27da15e3b8cd45b3193259b8780eaef490ca8b46757d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2013</creationdate><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - pathology</topic><topic>Allografts</topic><topic>Animals</topic><topic>Anoxia</topic><topic>Apoptosis</topic><topic>Atorvastatin</topic><topic>Atorvastatin Calcium</topic><topic>Bone marrow</topic><topic>Cardiology</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cell migration</topic><topic>Cell Movement - drug effects</topic><topic>Cell survival</topic><topic>Cell Survival - drug effects</topic><topic>Chemokine CXCL12 - metabolism</topic><topic>Differentiation</topic><topic>Heart attacks</topic><topic>Heptanoic Acids - pharmacology</topic><topic>Hospitals</topic><topic>Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology</topic><topic>In vitro methods and tests</topic><topic>In vivo methods and tests</topic><topic>Injuries</topic><topic>Injury analysis</topic><topic>Ischemia</topic><topic>Male</topic><topic>Medical research</topic><topic>Mesenchymal Stem Cell Transplantation</topic><topic>Mesenchymal stem cells</topic><topic>Mesenchymal Stromal Cells - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cai, Anping</au><au>Qiu, Ruofeng</au><au>Li, Liwen</au><au>Zheng, Dongdan</au><au>Dong, Yugang</au><au>Yu, Danqing</au><au>Huang, Yuli</au><au>Rao, Shaoqi</au><au>Zhou, Yingling</au><au>Mai, Weiyi</au><au>Katare, Rajesh Gopalrao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Atorvastatin treatment of rats with ischemia-reperfusion injury improves adipose-derived mesenchymal stem cell migration and survival via the SDF-1α/CXCR-4 axis</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2013-12-02</date><risdate>2013</risdate><volume>8</volume><issue>12</issue><spage>e79100</spage><epage>e79100</epage><pages>e79100-e79100</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Adipose-derived mesenchymal stem cells (ASCs) transplantation is a promising approach for myocardium repair. Promotion of ASCs migration and survival is the key for improving ASCs efficiency. SDF-1α is a critical factor responsible for ASCs migration and survival. Atorvastatin (Ator) is capable of up-regulating SDF-1α. Therefore, we're going to investigate whether ASCs migration and survival could be improved with atorvastatin.
In vitro study, cardiomyocytes were subjected to anoxia-reoxygenation injury and subsequently divided into different groups: group blank control, Ator, Ator plus L-NAME (A+L-NAME) and Ator plus AMD3100 (A+AMD3100).When migration analysis completed, cardiomyocytes were used for subsequent analyses. In vivo study, rats underwent ischemia-reperfusion injury were assigned into different groups corresponding to in vitro protocols. ASCs were transplanted on the seventh day of atorvastatin therapy. Seven days later, the rates of migration, differentiation and apoptosis were evaluated.
Compared with other groups, ASCs migration in vitro was significantly improved in group Ator, which was dependent on SDF-1α/CXCR-4 coupling. Results of in vivo study were consistent with that of in vitro study, further supporting the notion that the efficacy of atorvastatin on ASCs migration improvement was related to SDF-1α/CXCR-4 axis. Higher vessel density in group Ator might be another mechanism responsible for migration improvement. Concomitantly, apoptosis was significantly reduced in group Ator, whereas no significant difference of differentiation was found.
Migration and survival of ASCs could be improved by atorvastatin under ischemia-reperfusion injury, which were ascribed to SDF-1α/CXCR-4 axis.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>24312447</pmid><doi>10.1371/journal.pone.0079100</doi><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2013-12, Vol.8 (12), p.e79100-e79100 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1463097749 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS) Journals Open Access; EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adipose Tissue - metabolism Adipose Tissue - pathology Allografts Animals Anoxia Apoptosis Atorvastatin Atorvastatin Calcium Bone marrow Cardiology Cardiomyocytes Cardiovascular disease Cell migration Cell Movement - drug effects Cell survival Cell Survival - drug effects Chemokine CXCL12 - metabolism Differentiation Heart attacks Heptanoic Acids - pharmacology Hospitals Hydroxymethylglutaryl-CoA Reductase Inhibitors - pharmacology In vitro methods and tests In vivo methods and tests Injuries Injury analysis Ischemia Male Medical research Mesenchymal Stem Cell Transplantation Mesenchymal stem cells Mesenchymal Stromal Cells - metabolism Mesenchymal Stromal Cells - pathology Mesenchyme Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - therapy Myocardium Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology NG-Nitroarginine methyl ester Nitric oxide Pyrroles - pharmacology Rats Rats, Sprague-Dawley Receptors, CXCR4 - metabolism Reperfusion Rodents Stem cells Survival Transplantation |
| title | Atorvastatin treatment of rats with ischemia-reperfusion injury improves adipose-derived mesenchymal stem cell migration and survival via the SDF-1α/CXCR-4 axis |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T01%3A09%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Atorvastatin%20treatment%20of%20rats%20with%20ischemia-reperfusion%20injury%20improves%20adipose-derived%20mesenchymal%20stem%20cell%20migration%20and%20survival%20via%20the%20SDF-1%CE%B1/CXCR-4%20axis&rft.jtitle=PloS%20one&rft.au=Cai,%20Anping&rft.date=2013-12-02&rft.volume=8&rft.issue=12&rft.spage=e79100&rft.epage=e79100&rft.pages=e79100-e79100&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0079100&rft_dat=%3Cproquest_plos_%3E3143501791%3C/proquest_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1463097749&rft_id=info:pmid/24312447&rft_doaj_id=oai_doaj_org_article_6095821f09a44c0b814e59587769489e&rfr_iscdi=true |