Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice
Ischemic stroke is a devastating complication of bone fracture. Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours...
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description | Ischemic stroke is a devastating complication of bone fracture. Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours before permanent middle cerebral artery occlusion (pMCAO) on C57BL/6J mice or Ccr2RFP/+Cx3cr1GFP/+ mice that have the RFP gene knocked into one allele of Ccr2 gene and GFP gene knocked into one allele of Cx3cr1 gene. Behavior was tested 3 days after pMCAO. Infarct volume, the number of CD68+ cells, apoptotic neurons, bone marrow-derived macrophages (RFP+), and microgila (GFP+) in the peri-infarct region were quantified. Compared to mice subjected to pMCAO only, bone fracture 6 or 24 hours before pMCAO increased behavioral deficits, the infarct volume, and the number of CD68+ cells and apoptotic neurons in the peri-infarct area. Both bone marrow-derived macrophages (CCR2+) and microglia (CX3CR1+) increased in the peri-infarct regions of mice subjected to bone fracture before pMCAO compared to stroke-only mice. The mice subjected to bone fracture 6 hours before pMCAO had more severe injury than mice that had bone fracture 24 hours before pMCAO. Our data showed that bone fracture shortly before stroke also increases neuroinflammation and exacerbates ischemic cerebral injury. Our findings suggest that inhibition of neuroinflammation or management of stroke risk factors before major bone surgery would be beneficial for patients who are likely to suffer from stroke. |
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Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours before permanent middle cerebral artery occlusion (pMCAO) on C57BL/6J mice or Ccr2RFP/+Cx3cr1GFP/+ mice that have the RFP gene knocked into one allele of Ccr2 gene and GFP gene knocked into one allele of Cx3cr1 gene. Behavior was tested 3 days after pMCAO. Infarct volume, the number of CD68+ cells, apoptotic neurons, bone marrow-derived macrophages (RFP+), and microgila (GFP+) in the peri-infarct region were quantified. Compared to mice subjected to pMCAO only, bone fracture 6 or 24 hours before pMCAO increased behavioral deficits, the infarct volume, and the number of CD68+ cells and apoptotic neurons in the peri-infarct area. Both bone marrow-derived macrophages (CCR2+) and microglia (CX3CR1+) increased in the peri-infarct regions of mice subjected to bone fracture before pMCAO compared to stroke-only mice. The mice subjected to bone fracture 6 hours before pMCAO had more severe injury than mice that had bone fracture 24 hours before pMCAO. Our data showed that bone fracture shortly before stroke also increases neuroinflammation and exacerbates ischemic cerebral injury. Our findings suggest that inhibition of neuroinflammation or management of stroke risk factors before major bone surgery would be beneficial for patients who are likely to suffer from stroke.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0153835</identifier><identifier>PMID: 27089041</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Alleles ; Analysis ; Animal cognition ; Animal experimentation ; Animals ; Apoptosis ; Behavior, Animal ; Biology and Life Sciences ; Bone marrow ; Bone surgery ; Brain Injuries - etiology ; Brain Injuries - metabolism ; Brain Injuries - pathology ; Brain Ischemia - etiology ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain research ; CCR2 protein ; Cerebral blood flow ; Cerebral ischemia ; Complications and side effects ; CX3C Chemokine Receptor 1 ; CX3CR1 protein ; Cytokines - metabolism ; Disease Models, Animal ; Enzyme-Linked Immunosorbent Assay ; FDA approval ; Fractures (Injuries) ; Fractures, Bone - complications ; Fractures, Bone - metabolism ; Fractures, Bone - pathology ; Green fluorescent protein ; Health risks ; Hospitals ; House mouse ; Immunoenzyme Techniques ; Infarction, Middle Cerebral Artery - physiopathology ; Inflammation ; Inflammation - etiology ; Inflammation - metabolism ; Inflammation - pathology ; Injuries ; Ischemia ; Macrophages ; Male ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Microglia ; Microglia - immunology ; Microglia - pathology ; Monocyte chemoattractant protein 1 ; Neurons ; Neurosurgery ; Occlusion ; Pain ; Proteins ; Receptors, CCR2 - physiology ; Receptors, Chemokine - physiology ; Risk analysis ; Risk factors ; Risk management ; Rodents ; Stroke ; Stroke - etiology ; Stroke - metabolism ; Stroke - pathology ; Surgery ; Tibia</subject><ispartof>PloS one, 2016-04, Vol.11 (4), p.e0153835-e0153835</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Wang 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>2016 Wang et al 2016 Wang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-69e0afce6c64b1eea434154a96089742ae196abef1d73f3747ee17603572960b3</citedby><cites>FETCH-LOGICAL-c692t-69e0afce6c64b1eea434154a96089742ae196abef1d73f3747ee17603572960b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835054/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4835054/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,860,881,2096,2915,23845,27901,27902,53766,53768,79569,79570</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27089041$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Liang</creatorcontrib><creatorcontrib>Kang, Shuai</creatorcontrib><creatorcontrib>Zou, Dingquan</creatorcontrib><creatorcontrib>Zhan, Lei</creatorcontrib><creatorcontrib>Li, Zhengxi</creatorcontrib><creatorcontrib>Zhu, Wan</creatorcontrib><creatorcontrib>Su, Hua</creatorcontrib><title>Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Ischemic stroke is a devastating complication of bone fracture. Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours before permanent middle cerebral artery occlusion (pMCAO) on C57BL/6J mice or Ccr2RFP/+Cx3cr1GFP/+ mice that have the RFP gene knocked into one allele of Ccr2 gene and GFP gene knocked into one allele of Cx3cr1 gene. Behavior was tested 3 days after pMCAO. Infarct volume, the number of CD68+ cells, apoptotic neurons, bone marrow-derived macrophages (RFP+), and microgila (GFP+) in the peri-infarct region were quantified. Compared to mice subjected to pMCAO only, bone fracture 6 or 24 hours before pMCAO increased behavioral deficits, the infarct volume, and the number of CD68+ cells and apoptotic neurons in the peri-infarct area. Both bone marrow-derived macrophages (CCR2+) and microglia (CX3CR1+) increased in the peri-infarct regions of mice subjected to bone fracture before pMCAO compared to stroke-only mice. The mice subjected to bone fracture 6 hours before pMCAO had more severe injury than mice that had bone fracture 24 hours before pMCAO. Our data showed that bone fracture shortly before stroke also increases neuroinflammation and exacerbates ischemic cerebral injury. Our findings suggest that inhibition of neuroinflammation or management of stroke risk factors before major bone surgery would be beneficial for patients who are likely to suffer from stroke.</description><subject>Alleles</subject><subject>Analysis</subject><subject>Animal cognition</subject><subject>Animal experimentation</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Behavior, Animal</subject><subject>Biology and Life Sciences</subject><subject>Bone marrow</subject><subject>Bone surgery</subject><subject>Brain Injuries - etiology</subject><subject>Brain Injuries - metabolism</subject><subject>Brain Injuries - pathology</subject><subject>Brain Ischemia - etiology</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain research</subject><subject>CCR2 protein</subject><subject>Cerebral blood flow</subject><subject>Cerebral ischemia</subject><subject>Complications and side effects</subject><subject>CX3C Chemokine Receptor 1</subject><subject>CX3CR1 protein</subject><subject>Cytokines - metabolism</subject><subject>Disease Models, Animal</subject><subject>Enzyme-Linked Immunosorbent Assay</subject><subject>FDA approval</subject><subject>Fractures (Injuries)</subject><subject>Fractures, Bone - complications</subject><subject>Fractures, Bone - metabolism</subject><subject>Fractures, Bone - pathology</subject><subject>Green fluorescent protein</subject><subject>Health risks</subject><subject>Hospitals</subject><subject>House mouse</subject><subject>Immunoenzyme Techniques</subject><subject>Infarction, Middle Cerebral Artery - physiopathology</subject><subject>Inflammation</subject><subject>Inflammation - etiology</subject><subject>Inflammation - metabolism</subject><subject>Inflammation - pathology</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Macrophages</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Knockout</subject><subject>Mice, Transgenic</subject><subject>Microglia</subject><subject>Microglia - immunology</subject><subject>Microglia - pathology</subject><subject>Monocyte chemoattractant protein 1</subject><subject>Neurons</subject><subject>Neurosurgery</subject><subject>Occlusion</subject><subject>Pain</subject><subject>Proteins</subject><subject>Receptors, CCR2 - physiology</subject><subject>Receptors, Chemokine - physiology</subject><subject>Risk analysis</subject><subject>Risk factors</subject><subject>Risk management</subject><subject>Rodents</subject><subject>Stroke</subject><subject>Stroke - etiology</subject><subject>Stroke - metabolism</subject><subject>Stroke - pathology</subject><subject>Surgery</subject><subject>Tibia</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><sourceid>DOA</sourceid><recordid>eNqNkk9v0zAYxiMEYmPwDRBEQkJwSLFjx04uSKPaINJgiAFXy3Ffty5pXGwHbd8eZ82qBu2AcnBk_57n_ZskzzGaYcLxu7XtXSfb2dZ2MEO4ICUpHiTHuCJ5xnJEHh78HyVPvF8jFCHGHidHOUdlhSg-Tr58iPL03EkVegfpVwdZ7dUKNkalV8HZX5CeXUsFrpEBfLp_m4ODxsk2rbt1725S06WfjYKnySMtWw_PxvMk-XF-9n3-Kbu4_FjPTy8yxao8ZKwCJLUCphhtMICkhOKCyorFvDjNJeCKyQY0XnCiCaccAHOGSMHzyDTkJHm589221ouxFV5gXuISIY6qSNQ7YmHlWmyd2Uh3I6w04vbCuqWQLhjVgsgLxrTGTZ4rRFFTlQ1hFOOF1kBQDB-93o_R-mYDCwVdiKVPTKcvnVmJpf0jaJwJKmg0eDMaOPu7Bx_ExngFbSs7sP1t3nlJYtZlRF_9g95f3UgtZSzAdNrGuGowFae0IJTyqhrCzu6h4rcYZhgHr028nwjeTgSRCXAdlrL3XtRX3_6fvfw5ZV8fsCuQbVh52_bB2M5PQboDlbPeO9D7JmMkhrW_64YY1l6Max9lLw4HtBfd7Tn5C4W2-t4</recordid><startdate>20160418</startdate><enddate>20160418</enddate><creator>Wang, Liang</creator><creator>Kang, Shuai</creator><creator>Zou, Dingquan</creator><creator>Zhan, Lei</creator><creator>Li, Zhengxi</creator><creator>Zhu, Wan</creator><creator>Su, Hua</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>AEUYN</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>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160418</creationdate><title>Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice</title><author>Wang, Liang ; Kang, Shuai ; Zou, Dingquan ; Zhan, Lei ; Li, Zhengxi ; Zhu, Wan ; Su, Hua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-69e0afce6c64b1eea434154a96089742ae196abef1d73f3747ee17603572960b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Alleles</topic><topic>Analysis</topic><topic>Animal cognition</topic><topic>Animal experimentation</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Behavior, Animal</topic><topic>Biology and Life Sciences</topic><topic>Bone marrow</topic><topic>Bone surgery</topic><topic>Brain Injuries - etiology</topic><topic>Brain Injuries - metabolism</topic><topic>Brain Injuries - pathology</topic><topic>Brain Ischemia - etiology</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain research</topic><topic>CCR2 protein</topic><topic>Cerebral blood flow</topic><topic>Cerebral ischemia</topic><topic>Complications and side effects</topic><topic>CX3C Chemokine Receptor 1</topic><topic>CX3CR1 protein</topic><topic>Cytokines - metabolism</topic><topic>Disease Models, Animal</topic><topic>Enzyme-Linked Immunosorbent Assay</topic><topic>FDA approval</topic><topic>Fractures (Injuries)</topic><topic>Fractures, Bone - complications</topic><topic>Fractures, Bone - metabolism</topic><topic>Fractures, Bone - pathology</topic><topic>Green fluorescent protein</topic><topic>Health risks</topic><topic>Hospitals</topic><topic>House mouse</topic><topic>Immunoenzyme Techniques</topic><topic>Infarction, Middle Cerebral Artery - physiopathology</topic><topic>Inflammation</topic><topic>Inflammation - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Liang</au><au>Kang, Shuai</au><au>Zou, Dingquan</au><au>Zhan, Lei</au><au>Li, Zhengxi</au><au>Zhu, Wan</au><au>Su, Hua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-04-18</date><risdate>2016</risdate><volume>11</volume><issue>4</issue><spage>e0153835</spage><epage>e0153835</epage><pages>e0153835-e0153835</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Ischemic stroke is a devastating complication of bone fracture. Bone fracture shortly after stroke enhances stroke injury by augmenting inflammation. We hypothesize that bone fracture shortly before ischemic stroke also exacerbates ischemic cerebral injury. Tibia fracture was performed 6 or 24 hours before permanent middle cerebral artery occlusion (pMCAO) on C57BL/6J mice or Ccr2RFP/+Cx3cr1GFP/+ mice that have the RFP gene knocked into one allele of Ccr2 gene and GFP gene knocked into one allele of Cx3cr1 gene. Behavior was tested 3 days after pMCAO. Infarct volume, the number of CD68+ cells, apoptotic neurons, bone marrow-derived macrophages (RFP+), and microgila (GFP+) in the peri-infarct region were quantified. Compared to mice subjected to pMCAO only, bone fracture 6 or 24 hours before pMCAO increased behavioral deficits, the infarct volume, and the number of CD68+ cells and apoptotic neurons in the peri-infarct area. Both bone marrow-derived macrophages (CCR2+) and microglia (CX3CR1+) increased in the peri-infarct regions of mice subjected to bone fracture before pMCAO compared to stroke-only mice. The mice subjected to bone fracture 6 hours before pMCAO had more severe injury than mice that had bone fracture 24 hours before pMCAO. Our data showed that bone fracture shortly before stroke also increases neuroinflammation and exacerbates ischemic cerebral injury. Our findings suggest that inhibition of neuroinflammation or management of stroke risk factors before major bone surgery would be beneficial for patients who are likely to suffer from stroke.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>27089041</pmid><doi>10.1371/journal.pone.0153835</doi><oa>free_for_read</oa></addata></record> |
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recordid | cdi_plos_journals_1781800709 |
source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central; Free Full-Text Journals in Chemistry; Public Library of Science (PLoS) |
subjects | Alleles Analysis Animal cognition Animal experimentation Animals Apoptosis Behavior, Animal Biology and Life Sciences Bone marrow Bone surgery Brain Injuries - etiology Brain Injuries - metabolism Brain Injuries - pathology Brain Ischemia - etiology Brain Ischemia - metabolism Brain Ischemia - pathology Brain research CCR2 protein Cerebral blood flow Cerebral ischemia Complications and side effects CX3C Chemokine Receptor 1 CX3CR1 protein Cytokines - metabolism Disease Models, Animal Enzyme-Linked Immunosorbent Assay FDA approval Fractures (Injuries) Fractures, Bone - complications Fractures, Bone - metabolism Fractures, Bone - pathology Green fluorescent protein Health risks Hospitals House mouse Immunoenzyme Techniques Infarction, Middle Cerebral Artery - physiopathology Inflammation Inflammation - etiology Inflammation - metabolism Inflammation - pathology Injuries Ischemia Macrophages Male Medicine and Health Sciences Mice Mice, Inbred C57BL Mice, Knockout Mice, Transgenic Microglia Microglia - immunology Microglia - pathology Monocyte chemoattractant protein 1 Neurons Neurosurgery Occlusion Pain Proteins Receptors, CCR2 - physiology Receptors, Chemokine - physiology Risk analysis Risk factors Risk management Rodents Stroke Stroke - etiology Stroke - metabolism Stroke - pathology Surgery Tibia |
title | Bone Fracture Pre-Ischemic Stroke Exacerbates Ischemic Cerebral Injury in Mice |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-17T21%3A01%3A46IST&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=Bone%20Fracture%20Pre-Ischemic%20Stroke%20Exacerbates%20Ischemic%20Cerebral%20Injury%20in%20Mice&rft.jtitle=PloS%20one&rft.au=Wang,%20Liang&rft.date=2016-04-18&rft.volume=11&rft.issue=4&rft.spage=e0153835&rft.epage=e0153835&rft.pages=e0153835-e0153835&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0153835&rft_dat=%3Cgale_plos_%3EA453447994%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=1781800709&rft_id=info:pmid/27089041&rft_galeid=A453447994&rft_doaj_id=oai_doaj_org_article_2566ff1b22c040b98b36411dffe303f3&rfr_iscdi=true |