Iron elevation and adipose tissue remodeling in the epididymal depot of a mouse model of polygenic obesity
Iron dysregulation is a potential contributor to the pathology of obesity-related metabolic complications. KK/HIJ (KK) mice, a polygenic obese mouse model, have elevated serum iron levels. A subset of KK male mice display a bronzing of epididymal adipose tissue (eAT) associated with >100-fold (p0...
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| description | Iron dysregulation is a potential contributor to the pathology of obesity-related metabolic complications. KK/HIJ (KK) mice, a polygenic obese mouse model, have elevated serum iron levels. A subset of KK male mice display a bronzing of epididymal adipose tissue (eAT) associated with >100-fold (p0.05). The eAT histology revealed iron retention, macrophage clustering, tissue fibrosis, cell death as well as accumulation of HIF-2α in the high iron eAT. qPCR showed significantly decreased Lep (leptin) and AdipoQ (adiponectin), whereas Tnfα (tumor necrosis factor α), and Slc40a1 (ferroportin) were up-regulated in HI (p |
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To further phenotype and characterize the adipose tissue iron overload, 27 male KK mice were evaluated. 14 had bronzing eAT and 13 had normal appearing eAT. Fasting serum and tissues were collected for iron content, qPCR, histology and western blot.
High iron levels were confirmed in bronzing eAT (High Iron group, HI) versus normal iron level (NI) in normal appearing eAT. Surprisingly, iron levels in subcutaneous and brown adipose depots were not different between the groups (p>0.05). The eAT histology revealed iron retention, macrophage clustering, tissue fibrosis, cell death as well as accumulation of HIF-2α in the high iron eAT. qPCR showed significantly decreased Lep (leptin) and AdipoQ (adiponectin), whereas Tnfα (tumor necrosis factor α), and Slc40a1 (ferroportin) were up-regulated in HI (p<0.05). Elevated HIF-2α, oxidative stress and local insulin signaling loss was also observed.
Our data suggest that deposition of iron in adipose tissue is limited to the epididymal depot in male KK mice. A robust adipose tissue remodeling is concomitant with the high iron concentration, which causes local adipose tissue insulin resistance.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0179889</identifier><identifier>PMID: 28651003</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adiponectin ; Adiponectin - genetics ; Adipose tissue ; Adipose Tissue - metabolism ; Adipose Tissue - pathology ; Adiposity ; Alpha iron ; Analysis ; Animals ; Biology and Life Sciences ; Blood Glucose - metabolism ; Body fat ; Cell death ; Clustering ; Complications ; Cytokines ; Deposition ; Diabetes ; Diet ; Disease Models, Animal ; Endocrinology ; Epididymis - metabolism ; Epididymis - pathology ; Fasting ; Females ; Fibrosis ; Gene expression ; Genotype & phenotype ; Health aspects ; Histology ; Homeostasis ; Hypoxia ; Insulin ; Insulin Resistance ; Internal medicine ; Iron ; Iron - metabolism ; Iron content ; Iron Overload - genetics ; Iron Overload - metabolism ; Iron Overload - pathology ; Kinesiology ; Leptin ; Leptin - genetics ; Macrophages ; Male ; Males ; Medicine and Health Sciences ; Metabolism ; Mice ; Mice, Mutant Strains ; Nickel ; Nutrition research ; Obesity ; Obesity - genetics ; Obesity - metabolism ; Obesity - pathology ; Oxidative stress ; Pathology ; Physiology ; Remodeling ; Research and Analysis Methods ; Risk factors ; Rodents ; Stress concentration ; Studies ; Tissue Distribution ; Tissues ; Tumor necrosis factor ; Type 2 diabetes</subject><ispartof>PloS one, 2017-06, Vol.12 (6), p.e0179889</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Ma et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://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>2017 Ma et al 2017 Ma et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-e42ee4f6b3a65cebd5eccfaabd82a403a94287f70d749504449c54db29874c653</citedby><cites>FETCH-LOGICAL-c692t-e42ee4f6b3a65cebd5eccfaabd82a403a94287f70d749504449c54db29874c653</cites><orcidid>0000-0001-8249-0178</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/PMC5484604/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5484604/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28651003$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Aalto-Setala, Katriina</contributor><creatorcontrib>Ma, Xiaoya</creatorcontrib><creatorcontrib>Pham, Vinh T</creatorcontrib><creatorcontrib>Mori, Hiroyuki</creatorcontrib><creatorcontrib>MacDougald, Ormond A</creatorcontrib><creatorcontrib>Shah, Yatrik M</creatorcontrib><creatorcontrib>Bodary, Peter F</creatorcontrib><title>Iron elevation and adipose tissue remodeling in the epididymal depot of a mouse model of polygenic obesity</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Iron dysregulation is a potential contributor to the pathology of obesity-related metabolic complications. KK/HIJ (KK) mice, a polygenic obese mouse model, have elevated serum iron levels. A subset of KK male mice display a bronzing of epididymal adipose tissue (eAT) associated with >100-fold (p<0.001) higher iron concentration.
To further phenotype and characterize the adipose tissue iron overload, 27 male KK mice were evaluated. 14 had bronzing eAT and 13 had normal appearing eAT. Fasting serum and tissues were collected for iron content, qPCR, histology and western blot.
High iron levels were confirmed in bronzing eAT (High Iron group, HI) versus normal iron level (NI) in normal appearing eAT. Surprisingly, iron levels in subcutaneous and brown adipose depots were not different between the groups (p>0.05). The eAT histology revealed iron retention, macrophage clustering, tissue fibrosis, cell death as well as accumulation of HIF-2α in the high iron eAT. qPCR showed significantly decreased Lep (leptin) and AdipoQ (adiponectin), whereas Tnfα (tumor necrosis factor α), and Slc40a1 (ferroportin) were up-regulated in HI (p<0.05). Elevated HIF-2α, oxidative stress and local insulin signaling loss was also observed.
Our data suggest that deposition of iron in adipose tissue is limited to the epididymal depot in male KK mice. A robust adipose tissue remodeling is concomitant with the high iron concentration, which causes local adipose tissue insulin resistance.</description><subject>Adiponectin</subject><subject>Adiponectin - genetics</subject><subject>Adipose tissue</subject><subject>Adipose Tissue - metabolism</subject><subject>Adipose Tissue - pathology</subject><subject>Adiposity</subject><subject>Alpha iron</subject><subject>Analysis</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Blood Glucose - metabolism</subject><subject>Body fat</subject><subject>Cell death</subject><subject>Clustering</subject><subject>Complications</subject><subject>Cytokines</subject><subject>Deposition</subject><subject>Diabetes</subject><subject>Diet</subject><subject>Disease Models, Animal</subject><subject>Endocrinology</subject><subject>Epididymis - metabolism</subject><subject>Epididymis - pathology</subject><subject>Fasting</subject><subject>Females</subject><subject>Fibrosis</subject><subject>Gene expression</subject><subject>Genotype & phenotype</subject><subject>Health aspects</subject><subject>Histology</subject><subject>Homeostasis</subject><subject>Hypoxia</subject><subject>Insulin</subject><subject>Insulin Resistance</subject><subject>Internal medicine</subject><subject>Iron</subject><subject>Iron - metabolism</subject><subject>Iron content</subject><subject>Iron Overload - genetics</subject><subject>Iron Overload - metabolism</subject><subject>Iron Overload - pathology</subject><subject>Kinesiology</subject><subject>Leptin</subject><subject>Leptin - genetics</subject><subject>Macrophages</subject><subject>Male</subject><subject>Males</subject><subject>Medicine and Health Sciences</subject><subject>Metabolism</subject><subject>Mice</subject><subject>Mice, Mutant Strains</subject><subject>Nickel</subject><subject>Nutrition research</subject><subject>Obesity</subject><subject>Obesity - genetics</subject><subject>Obesity - metabolism</subject><subject>Obesity - pathology</subject><subject>Oxidative stress</subject><subject>Pathology</subject><subject>Physiology</subject><subject>Remodeling</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Stress concentration</subject><subject>Studies</subject><subject>Tissue Distribution</subject><subject>Tissues</subject><subject>Tumor necrosis factor</subject><subject>Type 2 diabetes</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</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>eNqNkl2L1DAYhYso7jr6D0QDguDFjGmTpu2NsCx-DCws-HUb3iZvOxnSpjbp4vx7MzvdZQsKkouEN885CYeTJC9TuklZkb7fu2nswW4G1-OGpkVVltWj5DytWLYWGWWPH5zPkmfe7ynNWSnE0-QsK0WeUsrOk_12dD1BizcQTDxBrwloMziPJBjvJyQjdk6jNX1LTE_CDgkORht96MASjYMLxDUESOemKLplj4PB2UOLvVHE1ehNODxPnjRgPb6Y91Xy49PH75df1lfXn7eXF1drJaosrJFniLwRNQORK6x1jko1ALUuM-CUQcWzsmgKqgte5ZRzXqmc6zqryoIrkbNV8vrkO1jn5RyTl2kVYysZixarZHsitIO9HEbTwXiQDoy8HbixlTAGoyxKXqpUCMq4QOAKsG4yoBnkRV1rWgCLXh_m16a6Q62wDyPYhenypjc72bobmfOSC8qjwZvZYHS_JvThH1-eqRbir0zfuGimOuOVvOBVQWlasixSm79QcWnsjIpFaUycLwTvFoLIBPwdWpi8l9tvX_-fvf65ZN8-YHcINuy8s9OxY34J8hOoRuf9iM19cimVx57fpSGPPZdzz6Ps1cPU70V3xWZ_APpk-ZA</recordid><startdate>20170626</startdate><enddate>20170626</enddate><creator>Ma, Xiaoya</creator><creator>Pham, Vinh T</creator><creator>Mori, Hiroyuki</creator><creator>MacDougald, Ormond A</creator><creator>Shah, Yatrik M</creator><creator>Bodary, Peter F</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>IOV</scope><scope>ISR</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>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>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-8249-0178</orcidid></search><sort><creationdate>20170626</creationdate><title>Iron elevation and adipose tissue remodeling in the epididymal depot of a mouse model of polygenic obesity</title><author>Ma, Xiaoya ; Pham, Vinh T ; Mori, Hiroyuki ; MacDougald, Ormond A ; Shah, Yatrik M ; Bodary, Peter F</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-e42ee4f6b3a65cebd5eccfaabd82a403a94287f70d749504449c54db29874c653</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adiponectin</topic><topic>Adiponectin - genetics</topic><topic>Adipose tissue</topic><topic>Adipose Tissue - metabolism</topic><topic>Adipose Tissue - pathology</topic><topic>Adiposity</topic><topic>Alpha iron</topic><topic>Analysis</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Blood Glucose - metabolism</topic><topic>Body fat</topic><topic>Cell death</topic><topic>Clustering</topic><topic>Complications</topic><topic>Cytokines</topic><topic>Deposition</topic><topic>Diabetes</topic><topic>Diet</topic><topic>Disease Models, Animal</topic><topic>Endocrinology</topic><topic>Epididymis - metabolism</topic><topic>Epididymis - pathology</topic><topic>Fasting</topic><topic>Females</topic><topic>Fibrosis</topic><topic>Gene expression</topic><topic>Genotype & phenotype</topic><topic>Health aspects</topic><topic>Histology</topic><topic>Homeostasis</topic><topic>Hypoxia</topic><topic>Insulin</topic><topic>Insulin Resistance</topic><topic>Internal medicine</topic><topic>Iron</topic><topic>Iron - metabolism</topic><topic>Iron content</topic><topic>Iron Overload - genetics</topic><topic>Iron Overload - metabolism</topic><topic>Iron Overload - pathology</topic><topic>Kinesiology</topic><topic>Leptin</topic><topic>Leptin - genetics</topic><topic>Macrophages</topic><topic>Male</topic><topic>Males</topic><topic>Medicine and Health Sciences</topic><topic>Metabolism</topic><topic>Mice</topic><topic>Mice, Mutant Strains</topic><topic>Nickel</topic><topic>Nutrition research</topic><topic>Obesity</topic><topic>Obesity - genetics</topic><topic>Obesity - metabolism</topic><topic>Obesity - pathology</topic><topic>Oxidative stress</topic><topic>Pathology</topic><topic>Physiology</topic><topic>Remodeling</topic><topic>Research and Analysis Methods</topic><topic>Risk factors</topic><topic>Rodents</topic><topic>Stress concentration</topic><topic>Studies</topic><topic>Tissue Distribution</topic><topic>Tissues</topic><topic>Tumor necrosis factor</topic><topic>Type 2 diabetes</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ma, Xiaoya</creatorcontrib><creatorcontrib>Pham, Vinh T</creatorcontrib><creatorcontrib>Mori, Hiroyuki</creatorcontrib><creatorcontrib>MacDougald, Ormond A</creatorcontrib><creatorcontrib>Shah, Yatrik M</creatorcontrib><creatorcontrib>Bodary, Peter F</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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KK/HIJ (KK) mice, a polygenic obese mouse model, have elevated serum iron levels. A subset of KK male mice display a bronzing of epididymal adipose tissue (eAT) associated with >100-fold (p<0.001) higher iron concentration.
To further phenotype and characterize the adipose tissue iron overload, 27 male KK mice were evaluated. 14 had bronzing eAT and 13 had normal appearing eAT. Fasting serum and tissues were collected for iron content, qPCR, histology and western blot.
High iron levels were confirmed in bronzing eAT (High Iron group, HI) versus normal iron level (NI) in normal appearing eAT. Surprisingly, iron levels in subcutaneous and brown adipose depots were not different between the groups (p>0.05). The eAT histology revealed iron retention, macrophage clustering, tissue fibrosis, cell death as well as accumulation of HIF-2α in the high iron eAT. qPCR showed significantly decreased Lep (leptin) and AdipoQ (adiponectin), whereas Tnfα (tumor necrosis factor α), and Slc40a1 (ferroportin) were up-regulated in HI (p<0.05). Elevated HIF-2α, oxidative stress and local insulin signaling loss was also observed.
Our data suggest that deposition of iron in adipose tissue is limited to the epididymal depot in male KK mice. A robust adipose tissue remodeling is concomitant with the high iron concentration, which causes local adipose tissue insulin resistance.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28651003</pmid><doi>10.1371/journal.pone.0179889</doi><tpages>e0179889</tpages><orcidid>https://orcid.org/0000-0001-8249-0178</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2017-06, Vol.12 (6), p.e0179889 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1913783340 |
| 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 | Adiponectin Adiponectin - genetics Adipose tissue Adipose Tissue - metabolism Adipose Tissue - pathology Adiposity Alpha iron Analysis Animals Biology and Life Sciences Blood Glucose - metabolism Body fat Cell death Clustering Complications Cytokines Deposition Diabetes Diet Disease Models, Animal Endocrinology Epididymis - metabolism Epididymis - pathology Fasting Females Fibrosis Gene expression Genotype & phenotype Health aspects Histology Homeostasis Hypoxia Insulin Insulin Resistance Internal medicine Iron Iron - metabolism Iron content Iron Overload - genetics Iron Overload - metabolism Iron Overload - pathology Kinesiology Leptin Leptin - genetics Macrophages Male Males Medicine and Health Sciences Metabolism Mice Mice, Mutant Strains Nickel Nutrition research Obesity Obesity - genetics Obesity - metabolism Obesity - pathology Oxidative stress Pathology Physiology Remodeling Research and Analysis Methods Risk factors Rodents Stress concentration Studies Tissue Distribution Tissues Tumor necrosis factor Type 2 diabetes |
| title | Iron elevation and adipose tissue remodeling in the epididymal depot of a mouse model of polygenic obesity |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-23T04%3A56%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Iron%20elevation%20and%20adipose%20tissue%20remodeling%20in%20the%20epididymal%20depot%20of%20a%20mouse%20model%20of%20polygenic%20obesity&rft.jtitle=PloS%20one&rft.au=Ma,%20Xiaoya&rft.date=2017-06-26&rft.volume=12&rft.issue=6&rft.spage=e0179889&rft.pages=e0179889-&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0179889&rft_dat=%3Cgale_plos_%3EA497001832%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1913783340&rft_id=info:pmid/28651003&rft_galeid=A497001832&rft_doaj_id=oai_doaj_org_article_48c1660346ea4caebf2a02a57bbd07a3&rfr_iscdi=true |