Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway
Abstract Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontit...
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Veröffentlicht in: | Cellular physiology and biochemistry 2018-01, Vol.49 (3), p.884-898 |
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description | Abstract
Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells. Results: OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus. Conclusion: This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway. |
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Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells. Results: OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus. Conclusion: This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway.</description><identifier>ISSN: 1015-8987</identifier><identifier>EISSN: 1421-9778</identifier><identifier>DOI: 10.1159/000493219</identifier><identifier>PMID: 30184545</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Animal control ; Animals ; Bone absorption ; Cathepsin K - genetics ; Cathepsin K - metabolism ; Cell Differentiation - drug effects ; Cytokines ; Disease Models, Animal ; Gum disease ; Humans ; Interleukin-6 - genetics ; Interleukin-6 - metabolism ; Laboratories ; Lipopolysaccharides - pharmacology ; Male ; Mandible - diagnostic imaging ; Membranes ; Mice ; Mice, Inbred C57BL ; NF-kappa B - metabolism ; NF-κB ; Original Paper ; Osteopontin ; Osteopontin - antagonists & inhibitors ; Osteopontin - genetics ; Osteopontin - metabolism ; Pathogenesis ; Patients ; Periapical periodontitis ; Periapical Periodontitis - diagnostic imaging ; Periapical Periodontitis - metabolism ; Periapical Periodontitis - pathology ; Periapical Tissue - diagnostic imaging ; Periapical Tissue - metabolism ; Periodontal Ligament - metabolism ; Proteins ; RAW 264.7 Cells ; RNA Interference ; RNA, Small Interfering - metabolism ; Signal Transduction ; Stem cells ; Teeth</subject><ispartof>Cellular physiology and biochemistry, 2018-01, Vol.49 (3), p.884-898</ispartof><rights>2018 The Author(s). Published by S. Karger AG, Basel</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel.</rights><rights>2018 The Author(s). Published by S. Karger AG, Basel . Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the associated terms available at: https://uk.sagepub.com/en-gb/eur/reusing-open-access-and-sage-choice-content</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c435t-97797251d319d72e1fbc8878525ab0350e863300c6e84411e93daef7f38eb0f63</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,860,2095,27614,27903,27904</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30184545$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dong, Ming</creatorcontrib><creatorcontrib>Yu, Xinxin</creatorcontrib><creatorcontrib>Chen, Wanfang</creatorcontrib><creatorcontrib>Guo, Zhenzhen</creatorcontrib><creatorcontrib>Sui, Linlin</creatorcontrib><creatorcontrib>Xu, Yuefei</creatorcontrib><creatorcontrib>Shang, Yuhong</creatorcontrib><creatorcontrib>Niu, Weidong</creatorcontrib><creatorcontrib>Kong, Ying</creatorcontrib><title>Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway</title><title>Cellular physiology and biochemistry</title><addtitle>Cell Physiol Biochem</addtitle><description>Abstract
Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells. Results: OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus. Conclusion: This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway.</description><subject>Animal control</subject><subject>Animals</subject><subject>Bone absorption</subject><subject>Cathepsin K - genetics</subject><subject>Cathepsin K - metabolism</subject><subject>Cell Differentiation - drug effects</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Gum disease</subject><subject>Humans</subject><subject>Interleukin-6 - genetics</subject><subject>Interleukin-6 - metabolism</subject><subject>Laboratories</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Mandible - diagnostic imaging</subject><subject>Membranes</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>NF-kappa B - metabolism</subject><subject>NF-κB</subject><subject>Original Paper</subject><subject>Osteopontin</subject><subject>Osteopontin - antagonists & inhibitors</subject><subject>Osteopontin - genetics</subject><subject>Osteopontin - metabolism</subject><subject>Pathogenesis</subject><subject>Patients</subject><subject>Periapical periodontitis</subject><subject>Periapical Periodontitis - diagnostic imaging</subject><subject>Periapical Periodontitis - metabolism</subject><subject>Periapical Periodontitis - pathology</subject><subject>Periapical Tissue - diagnostic imaging</subject><subject>Periapical Tissue - metabolism</subject><subject>Periodontal Ligament - metabolism</subject><subject>Proteins</subject><subject>RAW 264.7 Cells</subject><subject>RNA Interference</subject><subject>RNA, Small Interfering - metabolism</subject><subject>Signal Transduction</subject><subject>Stem cells</subject><subject>Teeth</subject><issn>1015-8987</issn><issn>1421-9778</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>M--</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DOA</sourceid><recordid>eNpdkUFvFCEUx4nR2Fo9eDdmEi_2MAoDDHBsq61NGtuDngkwb7ass8MWGM1-tX6IfiaZ7nYPPfF4_N4_j_8fofcEfyGEq68YY6ZoQ9QLdEhYQ2olhHxZakx4LZUUB-hNSktcrkI1r9EBxUQyzvghstcpQ1iHMfuxuolhFTKk6jSMUH2DlOPksg9jNT9C9GbtnRkey9DNM9mnym6qk0L9NUViUeVbqH6e1w_3p9WNybf_zOYtetWbIcG73XmEfp9__3X2o766vrg8O7mqHaM8zzsr0XDSUaI60QDprZNSSN5wYzHlGGRLKcauBckYIaBoZ6AXPZVgcd_SI3S51e2CWep19CsTNzoYrx8bIS60idm7AbRo21Yqxq3sMWMASnS9Y6Z4aaWzMGt93mqtY7ibihF65ZODYTAjhCnphmBMi-NiRj89Q5dhimP5aaGIIMV-0hTqeEu5GFKK0O8XJFjPIep9iIX9uFOc7Aq6PfmUWgE-bIE_Ji4g7oHd_H_Ci56l</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Dong, Ming</creator><creator>Yu, Xinxin</creator><creator>Chen, Wanfang</creator><creator>Guo, Zhenzhen</creator><creator>Sui, Linlin</creator><creator>Xu, Yuefei</creator><creator>Shang, Yuhong</creator><creator>Niu, Weidong</creator><creator>Kong, Ying</creator><general>S. Karger AG</general><general>Cell Physiol Biochem Press GmbH & Co KG</general><scope>M--</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>DOA</scope></search><sort><creationdate>20180101</creationdate><title>Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway</title><author>Dong, Ming ; Yu, Xinxin ; Chen, Wanfang ; Guo, Zhenzhen ; Sui, Linlin ; Xu, Yuefei ; Shang, Yuhong ; Niu, Weidong ; Kong, Ying</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c435t-97797251d319d72e1fbc8878525ab0350e863300c6e84411e93daef7f38eb0f63</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animal control</topic><topic>Animals</topic><topic>Bone absorption</topic><topic>Cathepsin K - genetics</topic><topic>Cathepsin K - metabolism</topic><topic>Cell Differentiation - drug effects</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Gum disease</topic><topic>Humans</topic><topic>Interleukin-6 - genetics</topic><topic>Interleukin-6 - metabolism</topic><topic>Laboratories</topic><topic>Lipopolysaccharides - pharmacology</topic><topic>Male</topic><topic>Mandible - diagnostic imaging</topic><topic>Membranes</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>NF-kappa B - metabolism</topic><topic>NF-κB</topic><topic>Original Paper</topic><topic>Osteopontin</topic><topic>Osteopontin - antagonists & inhibitors</topic><topic>Osteopontin - genetics</topic><topic>Osteopontin - metabolism</topic><topic>Pathogenesis</topic><topic>Patients</topic><topic>Periapical periodontitis</topic><topic>Periapical Periodontitis - diagnostic imaging</topic><topic>Periapical Periodontitis - metabolism</topic><topic>Periapical Periodontitis - pathology</topic><topic>Periapical Tissue - diagnostic imaging</topic><topic>Periapical Tissue - metabolism</topic><topic>Periodontal Ligament - metabolism</topic><topic>Proteins</topic><topic>RAW 264.7 Cells</topic><topic>RNA Interference</topic><topic>RNA, Small Interfering - metabolism</topic><topic>Signal Transduction</topic><topic>Stem cells</topic><topic>Teeth</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dong, Ming</creatorcontrib><creatorcontrib>Yu, Xinxin</creatorcontrib><creatorcontrib>Chen, Wanfang</creatorcontrib><creatorcontrib>Guo, Zhenzhen</creatorcontrib><creatorcontrib>Sui, Linlin</creatorcontrib><creatorcontrib>Xu, Yuefei</creatorcontrib><creatorcontrib>Shang, Yuhong</creatorcontrib><creatorcontrib>Niu, Weidong</creatorcontrib><creatorcontrib>Kong, Ying</creatorcontrib><collection>Karger Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Cellular physiology and biochemistry</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dong, Ming</au><au>Yu, Xinxin</au><au>Chen, Wanfang</au><au>Guo, Zhenzhen</au><au>Sui, Linlin</au><au>Xu, Yuefei</au><au>Shang, Yuhong</au><au>Niu, Weidong</au><au>Kong, Ying</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway</atitle><jtitle>Cellular physiology and biochemistry</jtitle><addtitle>Cell Physiol Biochem</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>49</volume><issue>3</issue><spage>884</spage><epage>898</epage><pages>884-898</pages><issn>1015-8987</issn><eissn>1421-9778</eissn><abstract>Abstract
Background/Aims: Periapical periodontitis is caused by bacterial infection and results in both one destruction and tooth loss. Osteopontin (OPN) is a secreted phosphorylated glycoprotein that participates in bone metabolism. Methods: Thirty-three patients with chronic periapical periodontitis and 10 patients who had undergone the orthodontic removal of healthy tooth tissue (control) at the periodontal ligament were investigated, and an animal model of mouse periapical periodontitis was established for an in vivo analysis. The relationship between OPN and bone destruction during periapical periodontitis was analyzed. Osteoblasts and osteoclasts were cultured in vitro and treated with lipopolysaccharide. An inhibitor of NF-κB was used to pretreat the transfected cells. Results: OPN increased osteoclast proliferation and differentiation, but reduced osteoblasts proliferation and differentiation. OPN activated the NF-κB pathway during periapical periodontitis and accelerated the transfer and phosphorylation of P65 from the cytoplasm to the nucleus. Conclusion: This study demonstrated that OPN played important roles in the progression of periapical periodontitis, and a dual role in bone metabolism during periapical periodontitis, linking osteoclasts and osteoblasts. The underlying mechanism may be related to the NF-κB pathway.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>30184545</pmid><doi>10.1159/000493219</doi><tpages>15</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animal control Animals Bone absorption Cathepsin K - genetics Cathepsin K - metabolism Cell Differentiation - drug effects Cytokines Disease Models, Animal Gum disease Humans Interleukin-6 - genetics Interleukin-6 - metabolism Laboratories Lipopolysaccharides - pharmacology Male Mandible - diagnostic imaging Membranes Mice Mice, Inbred C57BL NF-kappa B - metabolism NF-κB Original Paper Osteopontin Osteopontin - antagonists & inhibitors Osteopontin - genetics Osteopontin - metabolism Pathogenesis Patients Periapical periodontitis Periapical Periodontitis - diagnostic imaging Periapical Periodontitis - metabolism Periapical Periodontitis - pathology Periapical Tissue - diagnostic imaging Periapical Tissue - metabolism Periodontal Ligament - metabolism Proteins RAW 264.7 Cells RNA Interference RNA, Small Interfering - metabolism Signal Transduction Stem cells Teeth |
title | Osteopontin Promotes Bone Destruction in Periapical Periodontitis by Activating the NF-κB Pathway |
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