Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells
Hydrogen sulfide (H(2)S), the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2)S donor) on tumor necrosis factor (TNF)-α-...
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| description | Hydrogen sulfide (H(2)S), the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2)S donor) on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVEC) dysfunction.
Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS.
H(2)S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1. |
| doi_str_mv | 10.1371/journal.pone.0019766 |
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Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS.
H(2)S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0019766</identifier><identifier>PMID: 21572963</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adhesion ; Biology ; Cell adhesion ; Cell adhesion & migration ; Cell Adhesion - drug effects ; Cell adhesion molecules ; Cell Nucleus - drug effects ; Cell Nucleus - metabolism ; Cytokines ; E-selectin ; Endothelial cells ; Endothelial Cells - drug effects ; Endothelial Cells - enzymology ; Endothelial Cells - pathology ; Endothelium ; Enzyme Activation - drug effects ; Gene expression ; Heme ; Heme oxygenase (decyclizing) ; Heme Oxygenase-1 - genetics ; Heme Oxygenase-1 - metabolism ; Humans ; Hydrogen ; Hydrogen ion concentration ; Hydrogen sulfide ; I-kappa B Proteins - metabolism ; Inflammation ; Inflammation - metabolism ; Inflammation - pathology ; Intercellular adhesion molecule 1 ; Intercellular Adhesion Molecule-1 - genetics ; Intercellular Adhesion Molecule-1 - metabolism ; Intracellular Space - drug effects ; Intracellular Space - metabolism ; Kinases ; Medicine ; Monocytes ; Necrosis ; NF-KappaB Inhibitor alpha ; NF-κB protein ; Nuclear transport ; Oxidative stress ; Oxygenase ; P-selectin ; p38 Mitogen-Activated Protein Kinases - metabolism ; Pharmacology ; Pharmacy ; Phosphorylation ; Phosphorylation - drug effects ; Protein Processing, Post-Translational - drug effects ; Protein Transport - drug effects ; Proteins ; Reactive Oxygen Species - metabolism ; RNA, Messenger - genetics ; RNA, Messenger - metabolism ; Rodents ; Signal transduction ; Signal Transduction - drug effects ; Signaling ; Sodium ; Studies ; Sulfide ; Sulfides - pharmacology ; Transcription Factor RelA - metabolism ; Translocation ; Tumor Necrosis Factor-alpha - pharmacology ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α ; U937 Cells ; Umbilical vein ; Up-Regulation - drug effects ; Vascular cell adhesion molecule 1 ; Vascular Cell Adhesion Molecule-1 - genetics ; Vascular Cell Adhesion Molecule-1 - metabolism</subject><ispartof>PloS one, 2011-05, Vol.6 (5), p.e19766</ispartof><rights>2011 Pan et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License: https://creativecommons.org/licenses/by/4.0/ (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>Pan et al. 2011</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c525t-4345a8e15b784cfa14ecba1005bbc33d5314f203516bd9cf2be3f3d46abcd8c53</citedby><cites>FETCH-LOGICAL-c525t-4345a8e15b784cfa14ecba1005bbc33d5314f203516bd9cf2be3f3d46abcd8c53</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/PMC3091882/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3091882/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79342,79343</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/21572963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pan, Li-Long</creatorcontrib><creatorcontrib>Liu, Xin-Hua</creatorcontrib><creatorcontrib>Gong, Qi-Hai</creatorcontrib><creatorcontrib>Wu, Dan</creatorcontrib><creatorcontrib>Zhu, Yi-Zhun</creatorcontrib><title>Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Hydrogen sulfide (H(2)S), the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2)S donor) on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVEC) dysfunction.
Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS.
H(2)S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1.</description><subject>Adhesion</subject><subject>Biology</subject><subject>Cell adhesion</subject><subject>Cell adhesion & migration</subject><subject>Cell Adhesion - drug effects</subject><subject>Cell adhesion molecules</subject><subject>Cell Nucleus - drug effects</subject><subject>Cell Nucleus - metabolism</subject><subject>Cytokines</subject><subject>E-selectin</subject><subject>Endothelial cells</subject><subject>Endothelial Cells - drug effects</subject><subject>Endothelial Cells - enzymology</subject><subject>Endothelial Cells - pathology</subject><subject>Endothelium</subject><subject>Enzyme Activation - drug effects</subject><subject>Gene expression</subject><subject>Heme</subject><subject>Heme oxygenase (decyclizing)</subject><subject>Heme Oxygenase-1 - genetics</subject><subject>Heme Oxygenase-1 - metabolism</subject><subject>Humans</subject><subject>Hydrogen</subject><subject>Hydrogen ion concentration</subject><subject>Hydrogen sulfide</subject><subject>I-kappa B Proteins - metabolism</subject><subject>Inflammation</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Intercellular adhesion molecule 1</subject><subject>Intercellular Adhesion Molecule-1 - genetics</subject><subject>Intercellular Adhesion Molecule-1 - metabolism</subject><subject>Intracellular Space - drug effects</subject><subject>Intracellular Space - metabolism</subject><subject>Kinases</subject><subject>Medicine</subject><subject>Monocytes</subject><subject>Necrosis</subject><subject>NF-KappaB Inhibitor alpha</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Oxidative stress</subject><subject>Oxygenase</subject><subject>P-selectin</subject><subject>p38 Mitogen-Activated Protein Kinases - metabolism</subject><subject>Pharmacology</subject><subject>Pharmacy</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Protein Processing, Post-Translational - drug effects</subject><subject>Protein Transport - drug effects</subject><subject>Proteins</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA, Messenger - genetics</subject><subject>RNA, Messenger - metabolism</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Signal Transduction - drug effects</subject><subject>Signaling</subject><subject>Sodium</subject><subject>Studies</subject><subject>Sulfide</subject><subject>Sulfides - pharmacology</subject><subject>Transcription Factor RelA - metabolism</subject><subject>Translocation</subject><subject>Tumor Necrosis Factor-alpha - pharmacology</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><subject>U937 Cells</subject><subject>Umbilical vein</subject><subject>Up-Regulation - drug effects</subject><subject>Vascular cell adhesion molecule 1</subject><subject>Vascular Cell Adhesion Molecule-1 - genetics</subject><subject>Vascular Cell Adhesion Molecule-1 - metabolism</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2011</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNptks1u1DAUhSMEoqXwBggssWCVIf5NskGqKqCVKrGBtXXjn6lHjj3YTqVZ8ki8CM-Eh5lWLWJly_7u8T3Xp2le426FaY8_bOKSAvjVNgaz6jo89kI8aU7xSEkrSEefPtifNC9y3nQdp4MQz5sTgnlPRkFPm5-XO53i2gSUF2-dNghKMWGBYjQqyxwTCkalmF1GFlSJqf39q3VBL6oCLlgP8wz1eIeyW9d-XFgjCBrpXbZLUMXFUDF0C1ktHhIyQcdyY7wDj5TxPr9snlnw2bw6rmfN98-fvl1cttdfv1xdnF-3ihNeWkYZh8FgPvUDUxYwM2oCXD1Nk6JUc4qZrVY5FpMelSWToZZqJmBSelCcnjVvD7pbH7M8Ti9LTEbe9VVzrMTVgdARNnKb3AxpJyM4-fcgprWEVJzyRmpiSa8mao2ljKkRRqbowLEdsLAaWNX6eHxtmWajlQklgX8k-vgmuBu5jreSdiMeBlIF3h8FUvyxmFzk7PJ-YBBMXLIcRE8Jo72o5Lt_yP-bYwdq_5k5GXvfC-7kPlB3VXIfKHkMVC1789DHfdFdgugfdXvO8Q</recordid><startdate>20110510</startdate><enddate>20110510</enddate><creator>Pan, Li-Long</creator><creator>Liu, Xin-Hua</creator><creator>Gong, Qi-Hai</creator><creator>Wu, Dan</creator><creator>Zhu, Yi-Zhun</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>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20110510</creationdate><title>Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells</title><author>Pan, Li-Long ; Liu, Xin-Hua ; Gong, Qi-Hai ; Wu, Dan ; Zhu, Yi-Zhun</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c525t-4345a8e15b784cfa14ecba1005bbc33d5314f203516bd9cf2be3f3d46abcd8c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2011</creationdate><topic>Adhesion</topic><topic>Biology</topic><topic>Cell adhesion</topic><topic>Cell adhesion & migration</topic><topic>Cell Adhesion - drug effects</topic><topic>Cell adhesion molecules</topic><topic>Cell Nucleus - drug effects</topic><topic>Cell Nucleus - metabolism</topic><topic>Cytokines</topic><topic>E-selectin</topic><topic>Endothelial cells</topic><topic>Endothelial Cells - drug effects</topic><topic>Endothelial Cells - enzymology</topic><topic>Endothelial Cells - pathology</topic><topic>Endothelium</topic><topic>Enzyme Activation - drug effects</topic><topic>Gene expression</topic><topic>Heme</topic><topic>Heme oxygenase (decyclizing)</topic><topic>Heme Oxygenase-1 - genetics</topic><topic>Heme Oxygenase-1 - metabolism</topic><topic>Humans</topic><topic>Hydrogen</topic><topic>Hydrogen ion concentration</topic><topic>Hydrogen sulfide</topic><topic>I-kappa B Proteins - metabolism</topic><topic>Inflammation</topic><topic>Inflammation - metabolism</topic><topic>Inflammation - pathology</topic><topic>Intercellular adhesion molecule 1</topic><topic>Intercellular Adhesion Molecule-1 - genetics</topic><topic>Intercellular Adhesion Molecule-1 - metabolism</topic><topic>Intracellular Space - drug effects</topic><topic>Intracellular Space - metabolism</topic><topic>Kinases</topic><topic>Medicine</topic><topic>Monocytes</topic><topic>Necrosis</topic><topic>NF-KappaB Inhibitor alpha</topic><topic>NF-κB protein</topic><topic>Nuclear transport</topic><topic>Oxidative stress</topic><topic>Oxygenase</topic><topic>P-selectin</topic><topic>p38 Mitogen-Activated Protein Kinases - metabolism</topic><topic>Pharmacology</topic><topic>Pharmacy</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Protein Processing, Post-Translational - drug effects</topic><topic>Protein Transport - drug effects</topic><topic>Proteins</topic><topic>Reactive Oxygen Species - metabolism</topic><topic>RNA, Messenger - genetics</topic><topic>RNA, Messenger - metabolism</topic><topic>Rodents</topic><topic>Signal transduction</topic><topic>Signal Transduction - drug effects</topic><topic>Signaling</topic><topic>Sodium</topic><topic>Studies</topic><topic>Sulfide</topic><topic>Sulfides - 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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>Pan, Li-Long</au><au>Liu, Xin-Hua</au><au>Gong, Qi-Hai</au><au>Wu, Dan</au><au>Zhu, Yi-Zhun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2011-05-10</date><risdate>2011</risdate><volume>6</volume><issue>5</issue><spage>e19766</spage><pages>e19766-</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Hydrogen sulfide (H(2)S), the third physiologically relevant gaseous molecule, is recognized increasingly as an anti-inflammatory mediator in various inflammatory conditions. Herein, we explored the effects and mechanisms of sodium hydrosulfide (NaHS, a H(2)S donor) on tumor necrosis factor (TNF)-α-induced human umbilical vein endothelial cells (HUVEC) dysfunction.
Application of NaHS concentration-dependently suppressed TNF-α-induced mRNA and proteins expressions of intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1), mRNA expression of P-selectin and E-selectin as well as U937 monocytes adhesion to HUVEC. Western blot analysis revealed that the expression of the cytoprotective enzyme, heme oxygenase-1 (HO-1), was induced and coincident with the anti-inflammatory action of NaHS. Furthermore, TNF-α-induced NF-κB activation assessed by IκBα degradation and p65 phosphorylation and nuclear translocation and ROS production were diminished in cells subjected to treatment with NaHS.
H(2)S can exert an anti-inflammatory effect in endothelial cells through a mechanism that involves the up-regulation of HO-1.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>21572963</pmid><doi>10.1371/journal.pone.0019766</doi><oa>free_for_read</oa></addata></record> |
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| ispartof | PloS one, 2011-05, Vol.6 (5), p.e19766 |
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| recordid | cdi_plos_journals_1295077849 |
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| subjects | Adhesion Biology Cell adhesion Cell adhesion & migration Cell Adhesion - drug effects Cell adhesion molecules Cell Nucleus - drug effects Cell Nucleus - metabolism Cytokines E-selectin Endothelial cells Endothelial Cells - drug effects Endothelial Cells - enzymology Endothelial Cells - pathology Endothelium Enzyme Activation - drug effects Gene expression Heme Heme oxygenase (decyclizing) Heme Oxygenase-1 - genetics Heme Oxygenase-1 - metabolism Humans Hydrogen Hydrogen ion concentration Hydrogen sulfide I-kappa B Proteins - metabolism Inflammation Inflammation - metabolism Inflammation - pathology Intercellular adhesion molecule 1 Intercellular Adhesion Molecule-1 - genetics Intercellular Adhesion Molecule-1 - metabolism Intracellular Space - drug effects Intracellular Space - metabolism Kinases Medicine Monocytes Necrosis NF-KappaB Inhibitor alpha NF-κB protein Nuclear transport Oxidative stress Oxygenase P-selectin p38 Mitogen-Activated Protein Kinases - metabolism Pharmacology Pharmacy Phosphorylation Phosphorylation - drug effects Protein Processing, Post-Translational - drug effects Protein Transport - drug effects Proteins Reactive Oxygen Species - metabolism RNA, Messenger - genetics RNA, Messenger - metabolism Rodents Signal transduction Signal Transduction - drug effects Signaling Sodium Studies Sulfide Sulfides - pharmacology Transcription Factor RelA - metabolism Translocation Tumor Necrosis Factor-alpha - pharmacology Tumor necrosis factor-TNF Tumor necrosis factor-α U937 Cells Umbilical vein Up-Regulation - drug effects Vascular cell adhesion molecule 1 Vascular Cell Adhesion Molecule-1 - genetics Vascular Cell Adhesion Molecule-1 - metabolism |
| title | Hydrogen sulfide attenuated tumor necrosis factor-α-induced inflammatory signaling and dysfunction in vascular endothelial cells |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-05T04%3A46%3A56IST&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=Hydrogen%20sulfide%20attenuated%20tumor%20necrosis%20factor-%CE%B1-induced%20inflammatory%20signaling%20and%20dysfunction%20in%20vascular%20endothelial%20cells&rft.jtitle=PloS%20one&rft.au=Pan,%20Li-Long&rft.date=2011-05-10&rft.volume=6&rft.issue=5&rft.spage=e19766&rft.pages=e19766-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0019766&rft_dat=%3Cproquest_plos_%3E867324376%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=1295077849&rft_id=info:pmid/21572963&rft_doaj_id=oai_doaj_org_article_d2f27cb3fef344c9a94c3851f816fda4&rfr_iscdi=true |