Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and upregulation of IL-1Ra in melanoma model
To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5(-/-)) mice and wild type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR...
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| description | To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5(-/-)) mice and wild type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5(+/+) mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5(-/-) mice compared to melanoma tissues of CCR5(+/+) mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5(-/-) mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5(-/-) mice compared to the level in CCR5(+/+) mice. Moreover, infiltration of CD8(+) cytotoxic T cell and CD57(+) natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5(-/-) mice compared to that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra. |
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CCR5(-/-) mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5(+/+) mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5(-/-) mice compared to melanoma tissues of CCR5(+/+) mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5(-/-) mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5(-/-) mice compared to the level in CCR5(+/+) mice. Moreover, infiltration of CD8(+) cytotoxic T cell and CD57(+) natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5(-/-) mice compared to that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0033747</identifier><identifier>PMID: 22567084</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adenoviruses ; Animal models ; Animal tissues ; Animals ; Apoptosis ; Apoptosis - genetics ; Apoptosis - physiology ; BAX protein ; Bcl-2 protein ; Binding sites ; Biology ; Blotting, Western ; Breast cancer ; Caspase ; Caspase-3 ; CC chemokine receptors ; CCR5 protein ; CD57 antigen ; CD8 antigen ; Cell death ; Cell growth ; Cell Line, Tumor ; Chemokines ; Chemotherapy ; Cytokines ; Cytotoxicity ; Deactivation ; Deoxyribonucleic acid ; DNA ; Gene expression ; Gene regulation ; Immunohistochemistry ; Inactivation ; Infiltration ; Inhibition ; Interleukin 1 receptor antagonist ; Interleukin 1 Receptor Antagonist Protein - genetics ; Interleukin 1 Receptor Antagonist Protein - metabolism ; Interleukin 1 receptors ; Kinases ; Ligands ; Lymphocytes T ; Lymphoma ; Medical research ; Medicine ; Melanoma ; Melanoma - genetics ; Melanoma - metabolism ; Melanoma - pathology ; Metastases ; Metastasis ; Mice ; Mice, Knockout ; Natural killer cells ; NF- Kappa B protein ; NF-kappa B - genetics ; NF-kappa B - metabolism ; NF-κB protein ; Nuclear transport ; Pharmacy ; Phosphorylation ; Poly(ADP-ribose) polymerase ; Prostate cancer ; Receptors, CCR5 - deficiency ; Receptors, CCR5 - genetics ; Rodents ; Signal transduction ; Skin cancer ; Spleen ; Studies ; Survival ; Tissues ; Transcription ; Transcription factors ; Translocation ; Tumors ; Up-regulation ; Weight reduction</subject><ispartof>PloS one, 2012-05, Vol.7 (5), p.e33747-e33747</ispartof><rights>2012 Song 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>Song et al. 2012</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c559t-7926019e2edddeda9da7b1b450c57d07aafa4a8bccd95022e9ecf0735ed1407a3</citedby><cites>FETCH-LOGICAL-c559t-7926019e2edddeda9da7b1b450c57d07aafa4a8bccd95022e9ecf0735ed1407a3</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/PMC3342329/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3342329/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79343,79344</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22567084$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Li, Jun</contributor><creatorcontrib>Song, Ju Kyoung</creatorcontrib><creatorcontrib>Park, Mi Hee</creatorcontrib><creatorcontrib>Choi, Dong-Young</creatorcontrib><creatorcontrib>Yoo, Hwan Soo</creatorcontrib><creatorcontrib>Han, Sang Bae</creatorcontrib><creatorcontrib>Yoon, Do Young</creatorcontrib><creatorcontrib>Hong, Jin Tae</creatorcontrib><title>Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and upregulation of IL-1Ra in melanoma model</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5(-/-)) mice and wild type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5(+/+) mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5(-/-) mice compared to melanoma tissues of CCR5(+/+) mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5(-/-) mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5(-/-) mice compared to the level in CCR5(+/+) mice. Moreover, infiltration of CD8(+) cytotoxic T cell and CD57(+) natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5(-/-) mice compared to that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra.</description><subject>Adenoviruses</subject><subject>Animal models</subject><subject>Animal tissues</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Apoptosis - physiology</subject><subject>BAX protein</subject><subject>Bcl-2 protein</subject><subject>Binding sites</subject><subject>Biology</subject><subject>Blotting, Western</subject><subject>Breast cancer</subject><subject>Caspase</subject><subject>Caspase-3</subject><subject>CC chemokine receptors</subject><subject>CCR5 protein</subject><subject>CD57 antigen</subject><subject>CD8 antigen</subject><subject>Cell death</subject><subject>Cell growth</subject><subject>Cell Line, Tumor</subject><subject>Chemokines</subject><subject>Chemotherapy</subject><subject>Cytokines</subject><subject>Cytotoxicity</subject><subject>Deactivation</subject><subject>Deoxyribonucleic acid</subject><subject>DNA</subject><subject>Gene expression</subject><subject>Gene regulation</subject><subject>Immunohistochemistry</subject><subject>Inactivation</subject><subject>Infiltration</subject><subject>Inhibition</subject><subject>Interleukin 1 receptor antagonist</subject><subject>Interleukin 1 Receptor Antagonist Protein - genetics</subject><subject>Interleukin 1 Receptor Antagonist Protein - metabolism</subject><subject>Interleukin 1 receptors</subject><subject>Kinases</subject><subject>Ligands</subject><subject>Lymphocytes T</subject><subject>Lymphoma</subject><subject>Medical research</subject><subject>Medicine</subject><subject>Melanoma</subject><subject>Melanoma - genetics</subject><subject>Melanoma - metabolism</subject><subject>Melanoma - pathology</subject><subject>Metastases</subject><subject>Metastasis</subject><subject>Mice</subject><subject>Mice, Knockout</subject><subject>Natural killer cells</subject><subject>NF- Kappa B protein</subject><subject>NF-kappa B - genetics</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Pharmacy</subject><subject>Phosphorylation</subject><subject>Poly(ADP-ribose) polymerase</subject><subject>Prostate cancer</subject><subject>Receptors, CCR5 - deficiency</subject><subject>Receptors, CCR5 - genetics</subject><subject>Rodents</subject><subject>Signal transduction</subject><subject>Skin cancer</subject><subject>Spleen</subject><subject>Studies</subject><subject>Survival</subject><subject>Tissues</subject><subject>Transcription</subject><subject>Transcription factors</subject><subject>Translocation</subject><subject>Tumors</subject><subject>Up-regulation</subject><subject>Weight reduction</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNUstu1DAUjRCIlsIfILDEhk0GP-N4gwQDhZEqkBCsLY99M_WQxKmdjNRv4I_4CL4Jh5mOWsSCla17zzn3-vgUxVOCF4RJ8mobptibdjGEHhYYMya5vFecEsVoWVHM7t-6nxSPUtpiLFhdVQ-LE0pFJXHNT4sf76Dx1kNvr1Fo0LJcInsJXfjue0ARLAxjiEigNA1DhJQgoXHqcsnBDtowdNCPaOcN8r2xo9-Z0Yd-Vvp0Xv76-RaZ3qEpMzdTe2ytLkryZWagDlrTh86gLjhoHxcPGtMmeHI4z4pv5--_Lj-WF58_rJZvLkorhBpLqWiFiQIKzjlwRjkj12TNBbZCOiyNaQw39dpapwSmFBTYBksmwBGe2-yseL7XHdqQ9MHHpAmjvMICE5wRqz3CBbPVQ_Sdidc6GK__FELcaBNHb1vQFbfECYbXggre1MYoYRx2sq4Z46qZtV4fpk3rDpzNhkXT3hG92-n9pd6Enc58yqjKAi8PAjFcTZBG3flkoc3WQZjy3pjmr8wJkP8BJaTmTNXzWi_-gv7bCL5H2RhSitAc9yZYzzG8Yek5hvoQw0x7dvvNR9JN7thvIKHc3w</recordid><startdate>20120502</startdate><enddate>20120502</enddate><creator>Song, Ju Kyoung</creator><creator>Park, Mi Hee</creator><creator>Choi, Dong-Young</creator><creator>Yoo, Hwan Soo</creator><creator>Han, Sang Bae</creator><creator>Yoon, Do Young</creator><creator>Hong, Jin Tae</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>20120502</creationdate><title>Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and upregulation of IL-1Ra in melanoma model</title><author>Song, Ju Kyoung ; Park, Mi Hee ; Choi, Dong-Young ; Yoo, Hwan Soo ; Han, Sang Bae ; Yoon, Do Young ; Hong, Jin Tae</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c559t-7926019e2edddeda9da7b1b450c57d07aafa4a8bccd95022e9ecf0735ed1407a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Adenoviruses</topic><topic>Animal models</topic><topic>Animal tissues</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Apoptosis - physiology</topic><topic>BAX protein</topic><topic>Bcl-2 protein</topic><topic>Binding sites</topic><topic>Biology</topic><topic>Blotting, Western</topic><topic>Breast cancer</topic><topic>Caspase</topic><topic>Caspase-3</topic><topic>CC chemokine receptors</topic><topic>CCR5 protein</topic><topic>CD57 antigen</topic><topic>CD8 antigen</topic><topic>Cell death</topic><topic>Cell growth</topic><topic>Cell Line, Tumor</topic><topic>Chemokines</topic><topic>Chemotherapy</topic><topic>Cytokines</topic><topic>Cytotoxicity</topic><topic>Deactivation</topic><topic>Deoxyribonucleic acid</topic><topic>DNA</topic><topic>Gene expression</topic><topic>Gene regulation</topic><topic>Immunohistochemistry</topic><topic>Inactivation</topic><topic>Infiltration</topic><topic>Inhibition</topic><topic>Interleukin 1 receptor antagonist</topic><topic>Interleukin 1 Receptor Antagonist Protein - genetics</topic><topic>Interleukin 1 Receptor Antagonist Protein - metabolism</topic><topic>Interleukin 1 receptors</topic><topic>Kinases</topic><topic>Ligands</topic><topic>Lymphocytes T</topic><topic>Lymphoma</topic><topic>Medical research</topic><topic>Medicine</topic><topic>Melanoma</topic><topic>Melanoma - 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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>Song, Ju Kyoung</au><au>Park, Mi Hee</au><au>Choi, Dong-Young</au><au>Yoo, Hwan Soo</au><au>Han, Sang Bae</au><au>Yoon, Do Young</au><au>Hong, Jin Tae</au><au>Li, Jun</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and upregulation of IL-1Ra in melanoma model</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2012-05-02</date><risdate>2012</risdate><volume>7</volume><issue>5</issue><spage>e33747</spage><epage>e33747</epage><pages>e33747-e33747</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>To evaluate the relevance of C-C chemokine receptor type 5 (CCR5) expression and tumor development, we compared melanoma growth in CCR5 knockout (CCR5(-/-)) mice and wild type (CCR5(+/+)) mice. CCR5(-/-) mice showed reduced tumor volume, tumor weight, and increased survival rate when compared to CCR5(+/+) mice. We investigated the activation of NF-κB since it is an implicated transcription factor in the regulation of genes involving cell growth, apoptosis, and tumor growth. Significant inhibition of DNA binding activity of NF-κB, and translocation of p50 and p65 into the nucleus through the inhibition of phosphorylation of IκB was found in the melanoma tissues of CCR5(-/-) mice compared to melanoma tissues of CCR5(+/+) mice. NF-κB target apoptotic protein expression, such as cleaved caspase-3, cleaved PARP, and Bax, was elevated, whereas the survival protein expression levels, such as Bcl-2, C-IAP1, was decreased in the melanoma tissues of CCR5(-/-) mice. Interestingly, we found that the level of IL-1Ra, a tumor growth suppressive cytokine, was significantly elevated in tumor tissue and spleen of CCR5(-/-) mice compared to the level in CCR5(+/+) mice. Moreover, infiltration of CD8(+) cytotoxic T cell and CD57(+) natural killer cells was significantly increased in melanoma tumor and spleen tissue of CCR5(-/-) mice compared to that of CCR5(+/+) mice. Therefore, these results showed that CCR5 deficiency caused apoptotic cell death of melanoma through inhibition of NF-κB and upregulation of IL-1Ra.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>22567084</pmid><doi>10.1371/journal.pone.0033747</doi><oa>free_for_read</oa></addata></record> |
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| recordid | cdi_plos_journals_1324605010 |
| source | Public Library of Science (PLoS) Journals Open Access; MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adenoviruses Animal models Animal tissues Animals Apoptosis Apoptosis - genetics Apoptosis - physiology BAX protein Bcl-2 protein Binding sites Biology Blotting, Western Breast cancer Caspase Caspase-3 CC chemokine receptors CCR5 protein CD57 antigen CD8 antigen Cell death Cell growth Cell Line, Tumor Chemokines Chemotherapy Cytokines Cytotoxicity Deactivation Deoxyribonucleic acid DNA Gene expression Gene regulation Immunohistochemistry Inactivation Infiltration Inhibition Interleukin 1 receptor antagonist Interleukin 1 Receptor Antagonist Protein - genetics Interleukin 1 Receptor Antagonist Protein - metabolism Interleukin 1 receptors Kinases Ligands Lymphocytes T Lymphoma Medical research Medicine Melanoma Melanoma - genetics Melanoma - metabolism Melanoma - pathology Metastases Metastasis Mice Mice, Knockout Natural killer cells NF- Kappa B protein NF-kappa B - genetics NF-kappa B - metabolism NF-κB protein Nuclear transport Pharmacy Phosphorylation Poly(ADP-ribose) polymerase Prostate cancer Receptors, CCR5 - deficiency Receptors, CCR5 - genetics Rodents Signal transduction Skin cancer Spleen Studies Survival Tissues Transcription Transcription factors Translocation Tumors Up-regulation Weight reduction |
| title | Deficiency of C-C chemokine receptor 5 suppresses tumor development via inactivation of NF-κB and upregulation of IL-1Ra in melanoma model |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-30T16%3A00%3A40IST&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=Deficiency%20of%20C-C%20chemokine%20receptor%205%20suppresses%20tumor%20development%20via%20inactivation%20of%20NF-%CE%BAB%20and%20upregulation%20of%20IL-1Ra%20in%20melanoma%20model&rft.jtitle=PloS%20one&rft.au=Song,%20Ju%20Kyoung&rft.date=2012-05-02&rft.volume=7&rft.issue=5&rft.spage=e33747&rft.epage=e33747&rft.pages=e33747-e33747&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0033747&rft_dat=%3Cproquest_plos_%3E1011843980%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=1324605010&rft_id=info:pmid/22567084&rft_doaj_id=oai_doaj_org_article_64c1d530b5254f8aa95ad0d7883349f0&rfr_iscdi=true |