Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation
Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the under...
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| Veröffentlicht in: | The American journal of emergency medicine 2017-03, Vol.35 (3), p.402-409 |
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| creator | Fangyan, Wang Zengyou, Jin Kaiyi, Shen Tingting, Weng Zhisong, Chen Jiahui, Feng Zhengzheng, Zhang Jiaming, Liu Xiaolong, Zhang Maoping, Chu |
| description | Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Methods Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. Results The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < .01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < .01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < .01 or P < .05). Conclusions In conclusion, pretreatment with butyrate attenuated septic heart depression via anti -inflammation and anti-oxidation. |
| doi_str_mv | 10.1016/j.ajem.2016.11.022 |
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It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Methods Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. Results The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < .01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < .01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < .01 or P < .05). Conclusions In conclusion, pretreatment with butyrate attenuated septic heart depression via anti -inflammation and anti-oxidation.</description><identifier>ISSN: 0735-6757</identifier><identifier>EISSN: 1532-8171</identifier><identifier>DOI: 10.1016/j.ajem.2016.11.022</identifier><identifier>PMID: 27884587</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Butyrate ; Butyrates - administration & dosage ; Chemoprevention - methods ; Cytokines ; Disease Models, Animal ; Emergency ; Emergency medical care ; Endotoxins ; Experiments ; Heart depression ; Heart Injuries - etiology ; Heart Injuries - prevention & control ; Heart rate ; Inflammation ; Laboratory animals ; Lipopolysaccharides ; Male ; Medical research ; Mice ; Multiple organ dysfunction syndrome ; Oxidation ; Oxidative stress ; Oxidative Stress - drug effects ; Physiology ; Rodents ; Sepsis ; Sepsis - complications ; Sepsis - drug therapy ; Studies ; Tumor necrosis factor-TNF</subject><ispartof>The American journal of emergency medicine, 2017-03, Vol.35 (3), p.402-409</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><rights>Copyright Elsevier Limited 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c538t-c6cbbd8c6d49f423731406e1fdc152bad9e7cf5c5ca52bcd15e6fbe1024317313</citedby><cites>FETCH-LOGICAL-c538t-c6cbbd8c6d49f423731406e1fdc152bad9e7cf5c5ca52bcd15e6fbe1024317313</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.proquest.com/docview/1878847719?pq-origsite=primo$$EHTML$$P50$$Gproquest$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995,64385,64387,64389,72469</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27884587$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fangyan, Wang</creatorcontrib><creatorcontrib>Zengyou, Jin</creatorcontrib><creatorcontrib>Kaiyi, Shen</creatorcontrib><creatorcontrib>Tingting, Weng</creatorcontrib><creatorcontrib>Zhisong, Chen</creatorcontrib><creatorcontrib>Jiahui, Feng</creatorcontrib><creatorcontrib>Zhengzheng, Zhang</creatorcontrib><creatorcontrib>Jiaming, Liu</creatorcontrib><creatorcontrib>Xiaolong, Zhang</creatorcontrib><creatorcontrib>Maoping, Chu</creatorcontrib><title>Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation</title><title>The American journal of emergency medicine</title><addtitle>Am J Emerg Med</addtitle><description>Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Methods Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. Results The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < .01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < .01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < .01 or P < .05). Conclusions In conclusion, pretreatment with butyrate attenuated septic heart depression via anti -inflammation and anti-oxidation.</description><subject>Animals</subject><subject>Butyrate</subject><subject>Butyrates - administration & dosage</subject><subject>Chemoprevention - methods</subject><subject>Cytokines</subject><subject>Disease Models, Animal</subject><subject>Emergency</subject><subject>Emergency medical care</subject><subject>Endotoxins</subject><subject>Experiments</subject><subject>Heart depression</subject><subject>Heart Injuries - etiology</subject><subject>Heart Injuries - prevention & control</subject><subject>Heart rate</subject><subject>Inflammation</subject><subject>Laboratory animals</subject><subject>Lipopolysaccharides</subject><subject>Male</subject><subject>Medical research</subject><subject>Mice</subject><subject>Multiple organ dysfunction syndrome</subject><subject>Oxidation</subject><subject>Oxidative stress</subject><subject>Oxidative Stress - drug effects</subject><subject>Physiology</subject><subject>Rodents</subject><subject>Sepsis</subject><subject>Sepsis - complications</subject><subject>Sepsis - drug therapy</subject><subject>Studies</subject><subject>Tumor necrosis factor-TNF</subject><issn>0735-6757</issn><issn>1532-8171</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNks2KFDEUhYMoTs_oC7iQgBs3Vebmp6oaRBiH8QcGXKjrkEpuYdqqVJukBvsNfGxTdqswC3GV5N7vHLj3hJAnwGpg0LzY1WaHU83LvQaoGef3yAaU4FUHLdwnG9YKVTWtas_IeUo7xgCkkg_JGW-7Tqqu3ZAfr5d8iCYj3UfMEU2eMGRqcsawlHKiX9DETB2Wfkp-DtQHaujkLdJpdjjSeaAY3Jzn7z5UPrjFoqMJ98kneusNNSF7WhrDaKbJ5NXCBHcqF5H7VXtEHgxmTPj4dF6Qz2-uP129q24-vH1_dXlTWSW6XNnG9r3rbOPkdpBctAIkaxAGZ0Hx3rgttnZQVllTntaBwmboERiXAgosLsjzo-8-zt8WTFlPPlkcRxNwXpKGrixPblXT_AcqJeONkLKgz-6gu3mJoQxSqHXZbQvbQvEjZeOcUsRB76OfTDxoYHqNVO_0GqleI9UAukRaRE9P1ks_ofsj-Z1hAV4eASxru_UYdbIeQ0nBR7RZu9n_2__VHbkdffDWjF_xgOnvHDpxzfTH9VOtfwoawToBXPwEW-zI_g</recordid><startdate>20170301</startdate><enddate>20170301</enddate><creator>Fangyan, Wang</creator><creator>Zengyou, Jin</creator><creator>Kaiyi, Shen</creator><creator>Tingting, Weng</creator><creator>Zhisong, Chen</creator><creator>Jiahui, Feng</creator><creator>Zhengzheng, Zhang</creator><creator>Jiaming, Liu</creator><creator>Xiaolong, Zhang</creator><creator>Maoping, Chu</creator><general>Elsevier Inc</general><general>Elsevier Limited</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>7RV</scope><scope>7T5</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>H94</scope><scope>K9.</scope><scope>KB0</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>7QL</scope><scope>C1K</scope></search><sort><creationdate>20170301</creationdate><title>Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation</title><author>Fangyan, Wang ; Zengyou, Jin ; Kaiyi, Shen ; Tingting, Weng ; Zhisong, Chen ; Jiahui, Feng ; Zhengzheng, Zhang ; Jiaming, Liu ; Xiaolong, Zhang ; Maoping, Chu</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c538t-c6cbbd8c6d49f423731406e1fdc152bad9e7cf5c5ca52bcd15e6fbe1024317313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Animals</topic><topic>Butyrate</topic><topic>Butyrates - administration & dosage</topic><topic>Chemoprevention - methods</topic><topic>Cytokines</topic><topic>Disease Models, Animal</topic><topic>Emergency</topic><topic>Emergency medical care</topic><topic>Endotoxins</topic><topic>Experiments</topic><topic>Heart depression</topic><topic>Heart Injuries - etiology</topic><topic>Heart Injuries - prevention & control</topic><topic>Heart rate</topic><topic>Inflammation</topic><topic>Laboratory animals</topic><topic>Lipopolysaccharides</topic><topic>Male</topic><topic>Medical research</topic><topic>Mice</topic><topic>Multiple organ dysfunction syndrome</topic><topic>Oxidation</topic><topic>Oxidative stress</topic><topic>Oxidative Stress - drug effects</topic><topic>Physiology</topic><topic>Rodents</topic><topic>Sepsis</topic><topic>Sepsis - complications</topic><topic>Sepsis - drug therapy</topic><topic>Studies</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fangyan, Wang</creatorcontrib><creatorcontrib>Zengyou, Jin</creatorcontrib><creatorcontrib>Kaiyi, Shen</creatorcontrib><creatorcontrib>Tingting, Weng</creatorcontrib><creatorcontrib>Zhisong, Chen</creatorcontrib><creatorcontrib>Jiahui, Feng</creatorcontrib><creatorcontrib>Zhengzheng, Zhang</creatorcontrib><creatorcontrib>Jiaming, Liu</creatorcontrib><creatorcontrib>Xiaolong, Zhang</creatorcontrib><creatorcontrib>Maoping, Chu</creatorcontrib><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>Nursing & Allied Health Database</collection><collection>Immunology Abstracts</collection><collection>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>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>Research Library Prep</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Nursing & Allied Health Premium</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 Basic</collection><collection>MEDLINE - Academic</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Environmental Sciences and Pollution Management</collection><jtitle>The American journal of emergency medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fangyan, Wang</au><au>Zengyou, Jin</au><au>Kaiyi, Shen</au><au>Tingting, Weng</au><au>Zhisong, Chen</au><au>Jiahui, Feng</au><au>Zhengzheng, Zhang</au><au>Jiaming, Liu</au><au>Xiaolong, Zhang</au><au>Maoping, Chu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation</atitle><jtitle>The American journal of emergency medicine</jtitle><addtitle>Am J Emerg Med</addtitle><date>2017-03-01</date><risdate>2017</risdate><volume>35</volume><issue>3</issue><spage>402</spage><epage>409</epage><pages>402-409</pages><issn>0735-6757</issn><eissn>1532-8171</eissn><abstract>Abstract Objectives The depressed heart function is the main complication to cause death of septic patients in clinic. It is urgent to find effective interventions for this intractable disease. In this study, we investigated whether butyrate could be protective for heart against sepsis and the underlying mechanism. Methods Mice were randomly divided into three groups. Model group challenged with LPS (30 mg/kg, i.p.) only. Butyrate group received butyrate (200 mg/kg·d) for 3 days prior to LPS administration (30 mg/kg). Normal group received saline only. 6 h and 12 h after LPS administration were chosen for detection the parameters to estimate the effects or mechanism of butyrate pretreatment on heart of sepsis. Results The data showed that septic heart depression was attenuated by butyrate pretreatment through improvement of heart function depression (P < .01) and reduction of morphological changes of myocardium. The overexpression of proinflammatory factors, TNF-α, IL-6 and LTB4, in heart tissues induced by sepsis was significantly alleviated by butyrate pretreatment (P < .01). As oxidative stress indicators, SOD and CAT activity, and MDA content in heart were deteriorated by LPS challenge, which was noticeably ameliorated by butyrate pretreatment (P < .01 or P < .05). Conclusions In conclusion, pretreatment with butyrate attenuated septic heart depression via anti -inflammation and anti-oxidation.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27884587</pmid><doi>10.1016/j.ajem.2016.11.022</doi><tpages>8</tpages></addata></record> |
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| subjects | Animals Butyrate Butyrates - administration & dosage Chemoprevention - methods Cytokines Disease Models, Animal Emergency Emergency medical care Endotoxins Experiments Heart depression Heart Injuries - etiology Heart Injuries - prevention & control Heart rate Inflammation Laboratory animals Lipopolysaccharides Male Medical research Mice Multiple organ dysfunction syndrome Oxidation Oxidative stress Oxidative Stress - drug effects Physiology Rodents Sepsis Sepsis - complications Sepsis - drug therapy Studies Tumor necrosis factor-TNF |
| title | Butyrate pretreatment attenuates heart depression in a mice model of endotoxin-induced sepsis via anti -inflammation and anti -oxidation |
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