Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production
The toxicity of gadolinium-based contrast agents (GBCAs) has drawn a lot of attention. Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonanc...
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| description | The toxicity of gadolinium-based contrast agents (GBCAs) has drawn a lot of attention. Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonance imaging (MRI). However, most of the works investigating the toxicity of GBCAs are focusing on its high-concentration (0.5–10 mM) part, which is not reflective of the physiological conditions in human beings. Macrophages play a regulatory role in immune responses and are responsible for the fibrosis process. Their role in gadolinium retention and the pathogenesis of NSF, however, has seldom been investigated. This study aimed to evaluate the immune response generated by macrophages (RAW 264.7) exposing to low levels of GBCAs. The incubation concentration of GBCAs, including Omniscan®, Primovist®, Magnevist®, and Gadovist®, is proportional to the level of gadolinium uptake when detected via inductively coupled plasma mass spectrometry (ICP-MS) and imaged by MRI, whereas Primovist® treatment groups have highest gadolinium uptake among all of the tested concentrations. Low-concentration (2.5 μmol/L) Gd chloride or GBCAs exposure promoted the reactive production of oxygen species (ROS), nitrate/nitrite, prostaglandin E2 (PGE2), and suppressed the potential of mitochondrial membrane. There was higher ROS, nitrate/nitrite, and PGE2 production in the Primovist®, Omniscan®, and Magnevist® groups compared to the Gadovist® group. In face of lipopolysaccharide (LPS) stimulation, Primovist®, Omniscan®, and Magnevist® groups exhibited elevated nitrite/nitrate and suppressed IL-1β secretion and IL-6 and IL-10 secretion. Moreover, upon LPS stimulation, there is decreased TNF-α secretion 4 hours after Primovist® or Omiscan® exposure but the TNF-α secretion increased at 24 hours. Our data suggest that there is upregulated inflammation even in the presence of low levels of GBCAs, even similar to the physiological condition in murine macrophage. Further investigation of GBCAs on the human macrophage or in vivo animal study may clarify the role of macrophage on the pathogenesis of NSF and other GBCAs-related disease. |
| doi_str_mv | 10.1155/2018/3535769 |
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Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonance imaging (MRI). However, most of the works investigating the toxicity of GBCAs are focusing on its high-concentration (0.5–10 mM) part, which is not reflective of the physiological conditions in human beings. Macrophages play a regulatory role in immune responses and are responsible for the fibrosis process. Their role in gadolinium retention and the pathogenesis of NSF, however, has seldom been investigated. This study aimed to evaluate the immune response generated by macrophages (RAW 264.7) exposing to low levels of GBCAs. The incubation concentration of GBCAs, including Omniscan®, Primovist®, Magnevist®, and Gadovist®, is proportional to the level of gadolinium uptake when detected via inductively coupled plasma mass spectrometry (ICP-MS) and imaged by MRI, whereas Primovist® treatment groups have highest gadolinium uptake among all of the tested concentrations. Low-concentration (2.5 μmol/L) Gd chloride or GBCAs exposure promoted the reactive production of oxygen species (ROS), nitrate/nitrite, prostaglandin E2 (PGE2), and suppressed the potential of mitochondrial membrane. There was higher ROS, nitrate/nitrite, and PGE2 production in the Primovist®, Omniscan®, and Magnevist® groups compared to the Gadovist® group. In face of lipopolysaccharide (LPS) stimulation, Primovist®, Omniscan®, and Magnevist® groups exhibited elevated nitrite/nitrate and suppressed IL-1β secretion and IL-6 and IL-10 secretion. Moreover, upon LPS stimulation, there is decreased TNF-α secretion 4 hours after Primovist® or Omiscan® exposure but the TNF-α secretion increased at 24 hours. Our data suggest that there is upregulated inflammation even in the presence of low levels of GBCAs, even similar to the physiological condition in murine macrophage. Further investigation of GBCAs on the human macrophage or in vivo animal study may clarify the role of macrophage on the pathogenesis of NSF and other GBCAs-related disease.</description><identifier>ISSN: 1555-4309</identifier><identifier>EISSN: 1555-4317</identifier><identifier>DOI: 10.1155/2018/3535769</identifier><identifier>PMID: 30627059</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Apoptosis ; Biocompatibility ; Brain ; Contrast agents ; Contrast media ; Contrast Media - chemistry ; Contrast Media - pharmacology ; Contrast Media - toxicity ; Cytokines ; Cytokines - biosynthesis ; Cytokines - drug effects ; Cytotoxicity ; Dinoprostone ; Drug dosages ; Exposure ; Fibrosis ; Gadolinium ; Gadolinium - pharmacokinetics ; Gadopentetate dimeglumine ; Humans ; IL-1β ; Immune response ; Immune system ; Immunology ; In vivo methods and tests ; Inductively coupled plasma mass spectrometry ; Interleukin 10 ; Interleukin 6 ; Lipopolysaccharides ; Macrophages ; Macrophages - drug effects ; Magnetic resonance imaging ; Magnetic Resonance Imaging - methods ; Mass spectrometry ; Mass spectroscopy ; Membrane Potential, Mitochondrial ; Mice ; Mitochondria ; Nephrogenic Fibrosing Dermopathy - chemically induced ; Neuroimaging ; Nitrates ; Nitric oxide ; Nitrites ; NMR ; Nuclear magnetic resonance ; Oxidative stress ; Oxidative Stress - drug effects ; Pathogenesis ; Physiology ; Prostaglandin E2 ; RAW 264.7 Cells ; Reactive Oxygen Species ; Retention ; Stimulation ; Toxicity ; Toxicology ; Tumor necrosis factor-α ; Work stations</subject><ispartof>Contrast media and molecular imaging, 2018-01, Vol.2018 (2018), p.1-10</ispartof><rights>Copyright © 2018 Te-I Weng et al.</rights><rights>Copyright © 2018 Te-I Weng et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. http://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Te-I Weng et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c471t-64d2be1a96a201a0f627157015cc7698c7e8d530dba59e4cf4296c23e671ea023</citedby><cites>FETCH-LOGICAL-c471t-64d2be1a96a201a0f627157015cc7698c7e8d530dba59e4cf4296c23e671ea023</cites><orcidid>0000-0002-5249-1679</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/PMC6305030/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6305030/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27901,27902,53766,53768</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30627059$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Wang, Changning</contributor><contributor>Changning Wang</contributor><creatorcontrib>Hsiao, Jong-Kai</creatorcontrib><creatorcontrib>Wu, Jia-Lun</creatorcontrib><creatorcontrib>Ho, Yu-Chin</creatorcontrib><creatorcontrib>Lu, Chen-Wen</creatorcontrib><creatorcontrib>Chen, Huang Jen</creatorcontrib><creatorcontrib>Weng, Te-I</creatorcontrib><creatorcontrib>Liu, Shing-Hwa</creatorcontrib><title>Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production</title><title>Contrast media and molecular imaging</title><addtitle>Contrast Media Mol Imaging</addtitle><description>The toxicity of gadolinium-based contrast agents (GBCAs) has drawn a lot of attention. Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonance imaging (MRI). However, most of the works investigating the toxicity of GBCAs are focusing on its high-concentration (0.5–10 mM) part, which is not reflective of the physiological conditions in human beings. Macrophages play a regulatory role in immune responses and are responsible for the fibrosis process. Their role in gadolinium retention and the pathogenesis of NSF, however, has seldom been investigated. This study aimed to evaluate the immune response generated by macrophages (RAW 264.7) exposing to low levels of GBCAs. The incubation concentration of GBCAs, including Omniscan®, Primovist®, Magnevist®, and Gadovist®, is proportional to the level of gadolinium uptake when detected via inductively coupled plasma mass spectrometry (ICP-MS) and imaged by MRI, whereas Primovist® treatment groups have highest gadolinium uptake among all of the tested concentrations. Low-concentration (2.5 μmol/L) Gd chloride or GBCAs exposure promoted the reactive production of oxygen species (ROS), nitrate/nitrite, prostaglandin E2 (PGE2), and suppressed the potential of mitochondrial membrane. There was higher ROS, nitrate/nitrite, and PGE2 production in the Primovist®, Omniscan®, and Magnevist® groups compared to the Gadovist® group. In face of lipopolysaccharide (LPS) stimulation, Primovist®, Omniscan®, and Magnevist® groups exhibited elevated nitrite/nitrate and suppressed IL-1β secretion and IL-6 and IL-10 secretion. Moreover, upon LPS stimulation, there is decreased TNF-α secretion 4 hours after Primovist® or Omiscan® exposure but the TNF-α secretion increased at 24 hours. Our data suggest that there is upregulated inflammation even in the presence of low levels of GBCAs, even similar to the physiological condition in murine macrophage. Further investigation of GBCAs on the human macrophage or in vivo animal study may clarify the role of macrophage on the pathogenesis of NSF and other GBCAs-related disease.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biocompatibility</subject><subject>Brain</subject><subject>Contrast agents</subject><subject>Contrast media</subject><subject>Contrast Media - chemistry</subject><subject>Contrast Media - pharmacology</subject><subject>Contrast Media - toxicity</subject><subject>Cytokines</subject><subject>Cytokines - biosynthesis</subject><subject>Cytokines - drug effects</subject><subject>Cytotoxicity</subject><subject>Dinoprostone</subject><subject>Drug dosages</subject><subject>Exposure</subject><subject>Fibrosis</subject><subject>Gadolinium</subject><subject>Gadolinium - pharmacokinetics</subject><subject>Gadopentetate dimeglumine</subject><subject>Humans</subject><subject>IL-1β</subject><subject>Immune response</subject><subject>Immune system</subject><subject>Immunology</subject><subject>In vivo methods and tests</subject><subject>Inductively coupled plasma mass spectrometry</subject><subject>Interleukin 10</subject><subject>Interleukin 6</subject><subject>Lipopolysaccharides</subject><subject>Macrophages</subject><subject>Macrophages - drug effects</subject><subject>Magnetic resonance imaging</subject><subject>Magnetic Resonance Imaging - methods</subject><subject>Mass spectrometry</subject><subject>Mass spectroscopy</subject><subject>Membrane Potential, Mitochondrial</subject><subject>Mice</subject><subject>Mitochondria</subject><subject>Nephrogenic Fibrosing Dermopathy - chemically induced</subject><subject>Neuroimaging</subject><subject>Nitrates</subject><subject>Nitric oxide</subject><subject>Nitrites</subject><subject>NMR</subject><subject>Nuclear magnetic resonance</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Pathogenesis</subject><subject>Physiology</subject><subject>Prostaglandin E2</subject><subject>RAW 264.7 Cells</subject><subject>Reactive Oxygen Species</subject><subject>Retention</subject><subject>Stimulation</subject><subject>Toxicity</subject><subject>Toxicology</subject><subject>Tumor necrosis factor-α</subject><subject>Work stations</subject><issn>1555-4309</issn><issn>1555-4317</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNqNkc1v1DAQxSMEoh9w44wscUEqoXYcJ2sOSLCUUmmrIgFna9aedF0SO9hO2_3v8WqX5ePEydbMT0_vzSuKZ4y-ZkyI04qy2SkXXLSNfFAc5pEoa87ah_s_lQfFUYw3lNY1l_xxccBpU7VUyMNifXY_-jgFJL4jl6CDH1dwjZEkTxb-rvzgI5JzML63zk5D-R4iGjL3LgWIiVyiydM35GIYQSfiHbm6twaSvUXyJQWMkYDL_Dr579Zl2c_Bm0kn692T4lEHfcSnu_e4-Pbx7Ov8U7m4Or-Yv1uUum5ZKpvaVEtkIBvISYF22TkTLWVC65x4plucGcGpWYKQWOuurmSjK45NyxBoxY-Lt1vdcVoOaDRurPdqDHaAsFYerPp74-xKXftb1XAqKKdZ4OVOIPgfE8akBhs19j049FNUFWsl5_mcPKMv_kFv_BRcjpcpSRmrZFVn6tWWyteOMWC3N8Oo2nSqNp2qXacZf_5ngD38q8QMnGyBlXUG7ux_ymFmsIPfNOOMN5z_BF0Ns-Y</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Hsiao, Jong-Kai</creator><creator>Wu, Jia-Lun</creator><creator>Ho, Yu-Chin</creator><creator>Lu, Chen-Wen</creator><creator>Chen, Huang Jen</creator><creator>Weng, Te-I</creator><creator>Liu, Shing-Hwa</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>3V.</scope><scope>7QO</scope><scope>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>BYOGL</scope><scope>CCPQU</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5249-1679</orcidid></search><sort><creationdate>20180101</creationdate><title>Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production</title><author>Hsiao, Jong-Kai ; Wu, Jia-Lun ; Ho, Yu-Chin ; Lu, Chen-Wen ; Chen, Huang Jen ; Weng, Te-I ; Liu, Shing-Hwa</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c471t-64d2be1a96a201a0f627157015cc7698c7e8d530dba59e4cf4296c23e671ea023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biocompatibility</topic><topic>Brain</topic><topic>Contrast agents</topic><topic>Contrast media</topic><topic>Contrast Media - chemistry</topic><topic>Contrast Media - pharmacology</topic><topic>Contrast Media - toxicity</topic><topic>Cytokines</topic><topic>Cytokines - biosynthesis</topic><topic>Cytokines - drug effects</topic><topic>Cytotoxicity</topic><topic>Dinoprostone</topic><topic>Drug dosages</topic><topic>Exposure</topic><topic>Fibrosis</topic><topic>Gadolinium</topic><topic>Gadolinium - pharmacokinetics</topic><topic>Gadopentetate dimeglumine</topic><topic>Humans</topic><topic>IL-1β</topic><topic>Immune response</topic><topic>Immune system</topic><topic>Immunology</topic><topic>In vivo methods and tests</topic><topic>Inductively coupled plasma mass spectrometry</topic><topic>Interleukin 10</topic><topic>Interleukin 6</topic><topic>Lipopolysaccharides</topic><topic>Macrophages</topic><topic>Macrophages - drug effects</topic><topic>Magnetic resonance imaging</topic><topic>Magnetic Resonance Imaging - methods</topic><topic>Mass spectrometry</topic><topic>Mass spectroscopy</topic><topic>Membrane Potential, Mitochondrial</topic><topic>Mice</topic><topic>Mitochondria</topic><topic>Nephrogenic Fibrosing Dermopathy - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Contrast media and molecular imaging</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hsiao, Jong-Kai</au><au>Wu, Jia-Lun</au><au>Ho, Yu-Chin</au><au>Lu, Chen-Wen</au><au>Chen, Huang Jen</au><au>Weng, Te-I</au><au>Liu, Shing-Hwa</au><au>Wang, Changning</au><au>Changning Wang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production</atitle><jtitle>Contrast media and molecular imaging</jtitle><addtitle>Contrast Media Mol Imaging</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1555-4309</issn><eissn>1555-4317</eissn><abstract>The toxicity of gadolinium-based contrast agents (GBCAs) has drawn a lot of attention. Nephrogenic systemic fibrosis (NSF), a lethal disease related to the use of GBCAs, is still not understood. Recently, gadolinium retention is found in brain tissues after repeated use of GBCAs in magnetic resonance imaging (MRI). However, most of the works investigating the toxicity of GBCAs are focusing on its high-concentration (0.5–10 mM) part, which is not reflective of the physiological conditions in human beings. Macrophages play a regulatory role in immune responses and are responsible for the fibrosis process. Their role in gadolinium retention and the pathogenesis of NSF, however, has seldom been investigated. This study aimed to evaluate the immune response generated by macrophages (RAW 264.7) exposing to low levels of GBCAs. The incubation concentration of GBCAs, including Omniscan®, Primovist®, Magnevist®, and Gadovist®, is proportional to the level of gadolinium uptake when detected via inductively coupled plasma mass spectrometry (ICP-MS) and imaged by MRI, whereas Primovist® treatment groups have highest gadolinium uptake among all of the tested concentrations. Low-concentration (2.5 μmol/L) Gd chloride or GBCAs exposure promoted the reactive production of oxygen species (ROS), nitrate/nitrite, prostaglandin E2 (PGE2), and suppressed the potential of mitochondrial membrane. There was higher ROS, nitrate/nitrite, and PGE2 production in the Primovist®, Omniscan®, and Magnevist® groups compared to the Gadovist® group. In face of lipopolysaccharide (LPS) stimulation, Primovist®, Omniscan®, and Magnevist® groups exhibited elevated nitrite/nitrate and suppressed IL-1β secretion and IL-6 and IL-10 secretion. Moreover, upon LPS stimulation, there is decreased TNF-α secretion 4 hours after Primovist® or Omiscan® exposure but the TNF-α secretion increased at 24 hours. Our data suggest that there is upregulated inflammation even in the presence of low levels of GBCAs, even similar to the physiological condition in murine macrophage. Further investigation of GBCAs on the human macrophage or in vivo animal study may clarify the role of macrophage on the pathogenesis of NSF and other GBCAs-related disease.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30627059</pmid><doi>10.1155/2018/3535769</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-5249-1679</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Alma/SFX Local Collection; PubMed Central Open Access |
| subjects | Animals Apoptosis Biocompatibility Brain Contrast agents Contrast media Contrast Media - chemistry Contrast Media - pharmacology Contrast Media - toxicity Cytokines Cytokines - biosynthesis Cytokines - drug effects Cytotoxicity Dinoprostone Drug dosages Exposure Fibrosis Gadolinium Gadolinium - pharmacokinetics Gadopentetate dimeglumine Humans IL-1β Immune response Immune system Immunology In vivo methods and tests Inductively coupled plasma mass spectrometry Interleukin 10 Interleukin 6 Lipopolysaccharides Macrophages Macrophages - drug effects Magnetic resonance imaging Magnetic Resonance Imaging - methods Mass spectrometry Mass spectroscopy Membrane Potential, Mitochondrial Mice Mitochondria Nephrogenic Fibrosing Dermopathy - chemically induced Neuroimaging Nitrates Nitric oxide Nitrites NMR Nuclear magnetic resonance Oxidative stress Oxidative Stress - drug effects Pathogenesis Physiology Prostaglandin E2 RAW 264.7 Cells Reactive Oxygen Species Retention Stimulation Toxicity Toxicology Tumor necrosis factor-α Work stations |
| title | Exposure of Macrophages to Low-Dose Gadolinium-Based Contrast Medium: Impact on Oxidative Stress and Cytokines Production |
| 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%3A41%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Exposure%20of%20Macrophages%20to%20Low-Dose%20Gadolinium-Based%20Contrast%20Medium:%20Impact%20on%20Oxidative%20Stress%20and%20Cytokines%20Production&rft.jtitle=Contrast%20media%20and%20molecular%20imaging&rft.au=Hsiao,%20Jong-Kai&rft.date=2018-01-01&rft.volume=2018&rft.issue=2018&rft.spage=1&rft.epage=10&rft.pages=1-10&rft.issn=1555-4309&rft.eissn=1555-4317&rft_id=info:doi/10.1155/2018/3535769&rft_dat=%3Cproquest_pubme%3E2179337053%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2190112924&rft_id=info:pmid/30627059&rfr_iscdi=true |