Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia
Objective: Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibitin...
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| Veröffentlicht in: | Diabetes & vascular disease research 2020-03, Vol.17 (3), p.1479164120907971-1479164120907971 |
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| container_issue | 3 |
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| container_title | Diabetes & vascular disease research |
| container_volume | 17 |
| creator | Weihrauch, Dorothee Martin, Dustin P Jones, Deron Krolikowski, John Struve, Janine Naylor, Stephen Pritchard, Kirkwood A |
| description | Objective:
Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibiting myeloperoxidase reduces oxidative stress and neutrophil infiltration, increases vascularization, and improves blood flow in a diabetic murine model of hindlimb ischaemia.
Methods:
Leptin receptor–deficient (db/db) mice were subjected to hindlimb ischaemia. Ischaemic mice were treated with N-acetyl-lysyltyrosylcysteine-amide (KYC) to inhibit myeloperoxidase. After ligating the femoral artery, effects of treatments were determined with respect to hindlimb blood flow, neutrophil infiltration, oxidative damage, and the capability of hindlimb extracellular matrix to support human endothelial cell proliferation and migration.
Results:
KYC treatment improved hindlimb blood flow at 7 and 14 days in db/db mice; decreased the formation of advanced glycation end products, 4-hydroxynonenal, and 3-chlorotyrosine; reduced neutrophil infiltration into the hindlimbs; and improved the ability of hindlimb extracellular matrix from db/db mice to support endothelial cell proliferation and migration.
Conclusion:
These results demonstrate that inhibiting myeloperoxidase reduces oxidative stress in ischaemic hindlimbs of db/db mice, which improves blood flow and reduces neutrophil infiltration such that hindlimb extracellular matrix from db/db mice supports endothelial cell proliferation and migration. |
| doi_str_mv | 10.1177/1479164120907971 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_7510377</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sage_id>10.1177_1479164120907971</sage_id><sourcerecordid>2384819671</sourcerecordid><originalsourceid>FETCH-LOGICAL-c434t-921d29524e7ac1e5a0bc0f98cee2efe0e6622c12bda19148d585460c8f4ebf23</originalsourceid><addsrcrecordid>eNp1UUtrFTEUDqLY2nbvSrJ0M5pkMpNkI0jxUSh0033IJGd6U_K4JjNX253_3NzeWlRwdQ58j_P4EHpNyTtKhXhPuVB05JQRRYQS9Bk6pmJgnVSSP299g7s9foRe1XpLyDCKQb5ERz1jrO-pOkY_L9LGT37xOeE843gHIW-h5B_emQrYJ1ugNRUX2Jlq12CKvzcPdJMc9nFb8q7BU8jZ4Tnk702DDXbeTLB4i2Nem0_MDsJ-wMYnF3ycsK92YyB6c4pezCZUOHusJ-j686fr86_d5dWXi_OPl53lPV86xahjamAchLEUBkMmS2YlLQCDGQiMI2OWsskZqiiXbpADH4mVM4dpZv0J-nCw3a5TBGchLcUEvS0-mnKns_H6byT5jb7JOy0GSnohmsHbR4OSv61QFx3bDRCCSdBu1KyXXFI1Ctqo5EC1JddaYH4aQ4neB6f_Da5J3vy53pPgd1KN0B0I1dyAvs1rSe1b_zf8BVRtpMU</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>2384819671</pqid></control><display><type>article</type><title>Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia</title><source>MEDLINE</source><source>DOAJ Directory of Open Access Journals</source><source>Sage Journals GOLD Open Access 2024</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>PubMed Central Open Access</source><source>PubMed Central</source><creator>Weihrauch, Dorothee ; Martin, Dustin P ; Jones, Deron ; Krolikowski, John ; Struve, Janine ; Naylor, Stephen ; Pritchard, Kirkwood A</creator><creatorcontrib>Weihrauch, Dorothee ; Martin, Dustin P ; Jones, Deron ; Krolikowski, John ; Struve, Janine ; Naylor, Stephen ; Pritchard, Kirkwood A</creatorcontrib><description>Objective:
Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibiting myeloperoxidase reduces oxidative stress and neutrophil infiltration, increases vascularization, and improves blood flow in a diabetic murine model of hindlimb ischaemia.
Methods:
Leptin receptor–deficient (db/db) mice were subjected to hindlimb ischaemia. Ischaemic mice were treated with N-acetyl-lysyltyrosylcysteine-amide (KYC) to inhibit myeloperoxidase. After ligating the femoral artery, effects of treatments were determined with respect to hindlimb blood flow, neutrophil infiltration, oxidative damage, and the capability of hindlimb extracellular matrix to support human endothelial cell proliferation and migration.
Results:
KYC treatment improved hindlimb blood flow at 7 and 14 days in db/db mice; decreased the formation of advanced glycation end products, 4-hydroxynonenal, and 3-chlorotyrosine; reduced neutrophil infiltration into the hindlimbs; and improved the ability of hindlimb extracellular matrix from db/db mice to support endothelial cell proliferation and migration.
Conclusion:
These results demonstrate that inhibiting myeloperoxidase reduces oxidative stress in ischaemic hindlimbs of db/db mice, which improves blood flow and reduces neutrophil infiltration such that hindlimb extracellular matrix from db/db mice supports endothelial cell proliferation and migration.</description><identifier>ISSN: 1479-1641</identifier><identifier>EISSN: 1752-8984</identifier><identifier>DOI: 10.1177/1479164120907971</identifier><identifier>PMID: 32223319</identifier><language>eng</language><publisher>London, England: SAGE Publications</publisher><subject>Angiogenesis Inducing Agents - pharmacology ; Animals ; Brief Report ; Cell Movement - drug effects ; Cell Proliferation - drug effects ; Cells, Cultured ; Diabetes Mellitus - genetics ; Diabetes Mellitus - metabolism ; Diabetes Mellitus - physiopathology ; Disease Models, Animal ; Enzyme Inhibitors - pharmacology ; Extracellular Matrix - metabolism ; Hindlimb ; Human Umbilical Vein Endothelial Cells - drug effects ; Human Umbilical Vein Endothelial Cells - metabolism ; Humans ; Ischemia - drug therapy ; Ischemia - enzymology ; Ischemia - physiopathology ; Male ; Mice, Inbred C57BL ; Mice, Knockout ; Muscle, Skeletal - blood supply ; Neovascularization, Physiologic - drug effects ; Neutrophil Infiltration - drug effects ; Neutrophils - drug effects ; Neutrophils - enzymology ; Oligopeptides - pharmacology ; Oxidative Stress - drug effects ; Peroxidase - antagonists & inhibitors ; Peroxidase - metabolism ; Receptors, Leptin - deficiency ; Receptors, Leptin - genetics ; Regional Blood Flow ; Signal Transduction</subject><ispartof>Diabetes & vascular disease research, 2020-03, Vol.17 (3), p.1479164120907971-1479164120907971</ispartof><rights>The Author(s) 2020</rights><rights>The Author(s) 2020 2020 SAGE Publications Ltd unless otherwise noted. Manuscript content on this site is licensed under Creative Commons Licenses</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c434t-921d29524e7ac1e5a0bc0f98cee2efe0e6622c12bda19148d585460c8f4ebf23</citedby><cites>FETCH-LOGICAL-c434t-921d29524e7ac1e5a0bc0f98cee2efe0e6622c12bda19148d585460c8f4ebf23</cites><orcidid>0000-0003-3681-2580</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7510377/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC7510377/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,21965,27852,27923,27924,44944,45332,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/32223319$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Weihrauch, Dorothee</creatorcontrib><creatorcontrib>Martin, Dustin P</creatorcontrib><creatorcontrib>Jones, Deron</creatorcontrib><creatorcontrib>Krolikowski, John</creatorcontrib><creatorcontrib>Struve, Janine</creatorcontrib><creatorcontrib>Naylor, Stephen</creatorcontrib><creatorcontrib>Pritchard, Kirkwood A</creatorcontrib><title>Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia</title><title>Diabetes & vascular disease research</title><addtitle>Diab Vasc Dis Res</addtitle><description>Objective:
Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibiting myeloperoxidase reduces oxidative stress and neutrophil infiltration, increases vascularization, and improves blood flow in a diabetic murine model of hindlimb ischaemia.
Methods:
Leptin receptor–deficient (db/db) mice were subjected to hindlimb ischaemia. Ischaemic mice were treated with N-acetyl-lysyltyrosylcysteine-amide (KYC) to inhibit myeloperoxidase. After ligating the femoral artery, effects of treatments were determined with respect to hindlimb blood flow, neutrophil infiltration, oxidative damage, and the capability of hindlimb extracellular matrix to support human endothelial cell proliferation and migration.
Results:
KYC treatment improved hindlimb blood flow at 7 and 14 days in db/db mice; decreased the formation of advanced glycation end products, 4-hydroxynonenal, and 3-chlorotyrosine; reduced neutrophil infiltration into the hindlimbs; and improved the ability of hindlimb extracellular matrix from db/db mice to support endothelial cell proliferation and migration.
Conclusion:
These results demonstrate that inhibiting myeloperoxidase reduces oxidative stress in ischaemic hindlimbs of db/db mice, which improves blood flow and reduces neutrophil infiltration such that hindlimb extracellular matrix from db/db mice supports endothelial cell proliferation and migration.</description><subject>Angiogenesis Inducing Agents - pharmacology</subject><subject>Animals</subject><subject>Brief Report</subject><subject>Cell Movement - drug effects</subject><subject>Cell Proliferation - drug effects</subject><subject>Cells, Cultured</subject><subject>Diabetes Mellitus - genetics</subject><subject>Diabetes Mellitus - metabolism</subject><subject>Diabetes Mellitus - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Extracellular Matrix - metabolism</subject><subject>Hindlimb</subject><subject>Human Umbilical Vein Endothelial Cells - drug effects</subject><subject>Human Umbilical Vein Endothelial Cells - metabolism</subject><subject>Humans</subject><subject>Ischemia - drug therapy</subject><subject>Ischemia - enzymology</subject><subject>Ischemia - physiopathology</subject><subject>Male</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Muscle, Skeletal - blood supply</subject><subject>Neovascularization, Physiologic - drug effects</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>Neutrophils - drug effects</subject><subject>Neutrophils - enzymology</subject><subject>Oligopeptides - pharmacology</subject><subject>Oxidative Stress - drug effects</subject><subject>Peroxidase - antagonists & inhibitors</subject><subject>Peroxidase - metabolism</subject><subject>Receptors, Leptin - deficiency</subject><subject>Receptors, Leptin - genetics</subject><subject>Regional Blood Flow</subject><subject>Signal Transduction</subject><issn>1479-1641</issn><issn>1752-8984</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AFRWT</sourceid><sourceid>EIF</sourceid><recordid>eNp1UUtrFTEUDqLY2nbvSrJ0M5pkMpNkI0jxUSh0033IJGd6U_K4JjNX253_3NzeWlRwdQ58j_P4EHpNyTtKhXhPuVB05JQRRYQS9Bk6pmJgnVSSP299g7s9foRe1XpLyDCKQb5ERz1jrO-pOkY_L9LGT37xOeE843gHIW-h5B_emQrYJ1ugNRUX2Jlq12CKvzcPdJMc9nFb8q7BU8jZ4Tnk702DDXbeTLB4i2Nem0_MDsJ-wMYnF3ycsK92YyB6c4pezCZUOHusJ-j686fr86_d5dWXi_OPl53lPV86xahjamAchLEUBkMmS2YlLQCDGQiMI2OWsskZqiiXbpADH4mVM4dpZv0J-nCw3a5TBGchLcUEvS0-mnKns_H6byT5jb7JOy0GSnohmsHbR4OSv61QFx3bDRCCSdBu1KyXXFI1Ctqo5EC1JddaYH4aQ4neB6f_Da5J3vy53pPgd1KN0B0I1dyAvs1rSe1b_zf8BVRtpMU</recordid><startdate>20200301</startdate><enddate>20200301</enddate><creator>Weihrauch, Dorothee</creator><creator>Martin, Dustin P</creator><creator>Jones, Deron</creator><creator>Krolikowski, John</creator><creator>Struve, Janine</creator><creator>Naylor, Stephen</creator><creator>Pritchard, Kirkwood A</creator><general>SAGE Publications</general><scope>AFRWT</scope><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>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-3681-2580</orcidid></search><sort><creationdate>20200301</creationdate><title>Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia</title><author>Weihrauch, Dorothee ; Martin, Dustin P ; Jones, Deron ; Krolikowski, John ; Struve, Janine ; Naylor, Stephen ; Pritchard, Kirkwood A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c434t-921d29524e7ac1e5a0bc0f98cee2efe0e6622c12bda19148d585460c8f4ebf23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Angiogenesis Inducing Agents - pharmacology</topic><topic>Animals</topic><topic>Brief Report</topic><topic>Cell Movement - drug effects</topic><topic>Cell Proliferation - drug effects</topic><topic>Cells, Cultured</topic><topic>Diabetes Mellitus - genetics</topic><topic>Diabetes Mellitus - metabolism</topic><topic>Diabetes Mellitus - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Extracellular Matrix - metabolism</topic><topic>Hindlimb</topic><topic>Human Umbilical Vein Endothelial Cells - drug effects</topic><topic>Human Umbilical Vein Endothelial Cells - metabolism</topic><topic>Humans</topic><topic>Ischemia - drug therapy</topic><topic>Ischemia - enzymology</topic><topic>Ischemia - physiopathology</topic><topic>Male</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Knockout</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Neovascularization, Physiologic - drug effects</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>Neutrophils - drug effects</topic><topic>Neutrophils - enzymology</topic><topic>Oligopeptides - pharmacology</topic><topic>Oxidative Stress - drug effects</topic><topic>Peroxidase - antagonists & inhibitors</topic><topic>Peroxidase - metabolism</topic><topic>Receptors, Leptin - deficiency</topic><topic>Receptors, Leptin - genetics</topic><topic>Regional Blood Flow</topic><topic>Signal Transduction</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Weihrauch, Dorothee</creatorcontrib><creatorcontrib>Martin, Dustin P</creatorcontrib><creatorcontrib>Jones, Deron</creatorcontrib><creatorcontrib>Krolikowski, John</creatorcontrib><creatorcontrib>Struve, Janine</creatorcontrib><creatorcontrib>Naylor, Stephen</creatorcontrib><creatorcontrib>Pritchard, Kirkwood A</creatorcontrib><collection>Sage Journals GOLD Open Access 2024</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Diabetes & vascular disease research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Weihrauch, Dorothee</au><au>Martin, Dustin P</au><au>Jones, Deron</au><au>Krolikowski, John</au><au>Struve, Janine</au><au>Naylor, Stephen</au><au>Pritchard, Kirkwood A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia</atitle><jtitle>Diabetes & vascular disease research</jtitle><addtitle>Diab Vasc Dis Res</addtitle><date>2020-03-01</date><risdate>2020</risdate><volume>17</volume><issue>3</issue><spage>1479164120907971</spage><epage>1479164120907971</epage><pages>1479164120907971-1479164120907971</pages><issn>1479-1641</issn><eissn>1752-8984</eissn><abstract>Objective:
Diabetes mellitus is a significant risk factor for peripheral artery disease. Diabetes mellitus induces chronic states of oxidative stress and vascular inflammation that increase neutrophil activation and release of myeloperoxidase. The goal of this study is to determine whether inhibiting myeloperoxidase reduces oxidative stress and neutrophil infiltration, increases vascularization, and improves blood flow in a diabetic murine model of hindlimb ischaemia.
Methods:
Leptin receptor–deficient (db/db) mice were subjected to hindlimb ischaemia. Ischaemic mice were treated with N-acetyl-lysyltyrosylcysteine-amide (KYC) to inhibit myeloperoxidase. After ligating the femoral artery, effects of treatments were determined with respect to hindlimb blood flow, neutrophil infiltration, oxidative damage, and the capability of hindlimb extracellular matrix to support human endothelial cell proliferation and migration.
Results:
KYC treatment improved hindlimb blood flow at 7 and 14 days in db/db mice; decreased the formation of advanced glycation end products, 4-hydroxynonenal, and 3-chlorotyrosine; reduced neutrophil infiltration into the hindlimbs; and improved the ability of hindlimb extracellular matrix from db/db mice to support endothelial cell proliferation and migration.
Conclusion:
These results demonstrate that inhibiting myeloperoxidase reduces oxidative stress in ischaemic hindlimbs of db/db mice, which improves blood flow and reduces neutrophil infiltration such that hindlimb extracellular matrix from db/db mice supports endothelial cell proliferation and migration.</abstract><cop>London, England</cop><pub>SAGE Publications</pub><pmid>32223319</pmid><doi>10.1177/1479164120907971</doi><orcidid>https://orcid.org/0000-0003-3681-2580</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Sage Journals GOLD Open Access 2024; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; PubMed Central |
| subjects | Angiogenesis Inducing Agents - pharmacology Animals Brief Report Cell Movement - drug effects Cell Proliferation - drug effects Cells, Cultured Diabetes Mellitus - genetics Diabetes Mellitus - metabolism Diabetes Mellitus - physiopathology Disease Models, Animal Enzyme Inhibitors - pharmacology Extracellular Matrix - metabolism Hindlimb Human Umbilical Vein Endothelial Cells - drug effects Human Umbilical Vein Endothelial Cells - metabolism Humans Ischemia - drug therapy Ischemia - enzymology Ischemia - physiopathology Male Mice, Inbred C57BL Mice, Knockout Muscle, Skeletal - blood supply Neovascularization, Physiologic - drug effects Neutrophil Infiltration - drug effects Neutrophils - drug effects Neutrophils - enzymology Oligopeptides - pharmacology Oxidative Stress - drug effects Peroxidase - antagonists & inhibitors Peroxidase - metabolism Receptors, Leptin - deficiency Receptors, Leptin - genetics Regional Blood Flow Signal Transduction |
| title | Inhibition of myeloperoxidase increases revascularization and improves blood flow in a diabetic mouse model of hindlimb ischaemia |
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