Direct evidence for tumor necrosis factor-α signaling in arteriogenesis
Arteriogenesis serves as an efficient mechanism for flow restoration after arterial occlusion. This process is associated with inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), although their role in arteriogenesis remains unclear. We hypothesized that arteriogenesis is reduced...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-04, Vol.105 (14), p.1639-1641 |
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| creator | HOEFER, Imo E VAN ROYEN, Niels RECTENWALD, John E BRAY, Elizabeth J ABOUHAMZE, Zaher MOLDAWER, Lyle L VOSKUIL, Michiel PIEK, Jan J BUSCHMANN, Ivo R OZAKI, C. Keith |
| description | Arteriogenesis serves as an efficient mechanism for flow restoration after arterial occlusion. This process is associated with inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), although their role in arteriogenesis remains unclear. We hypothesized that arteriogenesis is reduced in mice lacking functional TNF-alpha or p55 receptor. To test this hypothesis, we developed a novel microsphere-based murine model of hindlimb perfusion measurement.
Unilateral femoral arteries of nude (n=9), TNF-alpha(-/-) (n=9), TNF-alpha receptor p55(-/-) (n=8), and p75(-/-) (n=8) mice as well as their appropriate genetic background controls were occluded. The nude mice underwent laser Doppler hindlimb flux measurements preoperatively, postoperatively, and after 7 days. Seven days after ligation, all animals underwent tissue perfusion determinations using fluorescent microspheres. Laser Doppler findings confirmed acute decrease in flux with falsely normal values after 1 week. Microsphere results from control mice showed perfusion restoration to values approximately 50% of normal within 7 days. TNF-alpha(-/-) mice demonstrated a significant reduction (45.1%) in collateral artery perfusion compared with controls (TNF-alpha(-/-) 22.4+/-5.1% versus B6x129 49.7+/-9.3%; P |
| doi_str_mv | 10.1161/01.CIR.0000014987.32865.8E |
| format | Article |
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Unilateral femoral arteries of nude (n=9), TNF-alpha(-/-) (n=9), TNF-alpha receptor p55(-/-) (n=8), and p75(-/-) (n=8) mice as well as their appropriate genetic background controls were occluded. The nude mice underwent laser Doppler hindlimb flux measurements preoperatively, postoperatively, and after 7 days. Seven days after ligation, all animals underwent tissue perfusion determinations using fluorescent microspheres. Laser Doppler findings confirmed acute decrease in flux with falsely normal values after 1 week. Microsphere results from control mice showed perfusion restoration to values approximately 50% of normal within 7 days. TNF-alpha(-/-) mice demonstrated a significant reduction (45.1%) in collateral artery perfusion compared with controls (TNF-alpha(-/-) 22.4+/-5.1% versus B6x129 49.7+/-9.3%; P<0.01). p55(-/-) mice exhibited an almost identical 45.8% reduction in collateral artery formation (p55(-/-) 28.3+/-4.3% versus C57BL/6J 61.8+/-9.1%; P<0.01), whereas p75(-/-) mice were equivalent to controls (p75(-/-) 54.5+/-5.5%; P=0.13).
Microsphere techniques in mice offer a tool for the molecular dissection of arteriogenesis mechanisms. These results suggest that TNF-alpha positively modulates arteriogenesis probably via signaling through its p55 receptor.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000014987.32865.8E</identifier><identifier>PMID: 11940540</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Antigens, CD - genetics ; Antigens, CD - metabolism ; Biological and medical sciences ; Blood Flow Velocity ; Blood vessels and receptors ; Femoral Artery - physiology ; Fluorescent Dyes ; Fundamental and applied biological sciences. Psychology ; Hindlimb ; Laser-Doppler Flowmetry ; Ligation ; Mice ; Mice, Inbred Strains ; Mice, Knockout ; Mice, Nude ; Microspheres ; Models, Animal ; Neovascularization, Physiologic - physiology ; Receptors, Tumor Necrosis Factor - deficiency ; Receptors, Tumor Necrosis Factor - genetics ; Receptors, Tumor Necrosis Factor - metabolism ; Receptors, Tumor Necrosis Factor, Type I ; Receptors, Tumor Necrosis Factor, Type II ; Signal Transduction - physiology ; Tumor Necrosis Factor-alpha - deficiency ; Tumor Necrosis Factor-alpha - genetics ; Tumor Necrosis Factor-alpha - metabolism ; Vertebrates: cardiovascular system</subject><ispartof>Circulation (New York, N.Y.), 2002-04, Vol.105 (14), p.1639-1641</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Apr 9, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c481t-2d00bcea57bc8f25ffa0357b45812022486488fdedd455c88d275211ba3df1ec3</citedby><cites>FETCH-LOGICAL-c481t-2d00bcea57bc8f25ffa0357b45812022486488fdedd455c88d275211ba3df1ec3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3687,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13612960$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11940540$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HOEFER, Imo E</creatorcontrib><creatorcontrib>VAN ROYEN, Niels</creatorcontrib><creatorcontrib>RECTENWALD, John E</creatorcontrib><creatorcontrib>BRAY, Elizabeth J</creatorcontrib><creatorcontrib>ABOUHAMZE, Zaher</creatorcontrib><creatorcontrib>MOLDAWER, Lyle L</creatorcontrib><creatorcontrib>VOSKUIL, Michiel</creatorcontrib><creatorcontrib>PIEK, Jan J</creatorcontrib><creatorcontrib>BUSCHMANN, Ivo R</creatorcontrib><creatorcontrib>OZAKI, C. Keith</creatorcontrib><title>Direct evidence for tumor necrosis factor-α signaling in arteriogenesis</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Arteriogenesis serves as an efficient mechanism for flow restoration after arterial occlusion. This process is associated with inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), although their role in arteriogenesis remains unclear. We hypothesized that arteriogenesis is reduced in mice lacking functional TNF-alpha or p55 receptor. To test this hypothesis, we developed a novel microsphere-based murine model of hindlimb perfusion measurement.
Unilateral femoral arteries of nude (n=9), TNF-alpha(-/-) (n=9), TNF-alpha receptor p55(-/-) (n=8), and p75(-/-) (n=8) mice as well as their appropriate genetic background controls were occluded. The nude mice underwent laser Doppler hindlimb flux measurements preoperatively, postoperatively, and after 7 days. Seven days after ligation, all animals underwent tissue perfusion determinations using fluorescent microspheres. Laser Doppler findings confirmed acute decrease in flux with falsely normal values after 1 week. Microsphere results from control mice showed perfusion restoration to values approximately 50% of normal within 7 days. TNF-alpha(-/-) mice demonstrated a significant reduction (45.1%) in collateral artery perfusion compared with controls (TNF-alpha(-/-) 22.4+/-5.1% versus B6x129 49.7+/-9.3%; P<0.01). p55(-/-) mice exhibited an almost identical 45.8% reduction in collateral artery formation (p55(-/-) 28.3+/-4.3% versus C57BL/6J 61.8+/-9.1%; P<0.01), whereas p75(-/-) mice were equivalent to controls (p75(-/-) 54.5+/-5.5%; P=0.13).
Microsphere techniques in mice offer a tool for the molecular dissection of arteriogenesis mechanisms. These results suggest that TNF-alpha positively modulates arteriogenesis probably via signaling through its p55 receptor.</description><subject>Animals</subject><subject>Antigens, CD - genetics</subject><subject>Antigens, CD - metabolism</subject><subject>Biological and medical sciences</subject><subject>Blood Flow Velocity</subject><subject>Blood vessels and receptors</subject><subject>Femoral Artery - physiology</subject><subject>Fluorescent Dyes</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Hindlimb</subject><subject>Laser-Doppler Flowmetry</subject><subject>Ligation</subject><subject>Mice</subject><subject>Mice, Inbred Strains</subject><subject>Mice, Knockout</subject><subject>Mice, Nude</subject><subject>Microspheres</subject><subject>Models, Animal</subject><subject>Neovascularization, Physiologic - physiology</subject><subject>Receptors, Tumor Necrosis Factor - deficiency</subject><subject>Receptors, Tumor Necrosis Factor - genetics</subject><subject>Receptors, Tumor Necrosis Factor - metabolism</subject><subject>Receptors, Tumor Necrosis Factor, Type I</subject><subject>Receptors, Tumor Necrosis Factor, Type II</subject><subject>Signal Transduction - physiology</subject><subject>Tumor Necrosis Factor-alpha - deficiency</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Tumor Necrosis Factor-alpha - metabolism</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7322</issn><issn>1524-4539</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkNtKxDAQQIMoul5-QYqgb62ZXNrUN1lXVxAE0eeQTSdLpNtq0gp-lj_iN5nVhQXnIcOQMzPJIeQMaAFQwiWFYnr_VNB1gKhVVXCmSlmo2Q6ZgGQiF5LXu2SS7uu84owdkMMYX1NZ8krukwOAWlAp6ITMb3xAO2T44RvsLGauD9kwrtLZoQ199DFzxg59yL-_suiXnWl9t8x8l5kwYPD9EjtM1DHZc6aNeLLJR-TldvY8necPj3f30-uH3AoFQ84aShcWjawWVjkmnTOUp0JIBYwyJlQplHINNo2Q0irVsEoygIXhjQO0_Ihc_M19C_37iHHQKx8ttq3psB-jrkDWEpRM4Nk_8LUfQ3p-1AxYJRRXNEFXf9D6qzGg02_Br0z41ED1WramoJNsvZWtf2VrNUvNp5sN42KFzbZ1YzcB5xvARGtaF0xnfdxyvARWl5T_AN3BiDE</recordid><startdate>20020409</startdate><enddate>20020409</enddate><creator>HOEFER, Imo E</creator><creator>VAN ROYEN, Niels</creator><creator>RECTENWALD, John E</creator><creator>BRAY, Elizabeth J</creator><creator>ABOUHAMZE, Zaher</creator><creator>MOLDAWER, Lyle L</creator><creator>VOSKUIL, Michiel</creator><creator>PIEK, Jan J</creator><creator>BUSCHMANN, Ivo R</creator><creator>OZAKI, C. Keith</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</general><scope>IQODW</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>K9.</scope><scope>NAPCQ</scope><scope>U9A</scope><scope>7X8</scope></search><sort><creationdate>20020409</creationdate><title>Direct evidence for tumor necrosis factor-α signaling in arteriogenesis</title><author>HOEFER, Imo E ; VAN ROYEN, Niels ; RECTENWALD, John E ; BRAY, Elizabeth J ; ABOUHAMZE, Zaher ; MOLDAWER, Lyle L ; VOSKUIL, Michiel ; PIEK, Jan J ; BUSCHMANN, Ivo R ; OZAKI, C. Keith</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c481t-2d00bcea57bc8f25ffa0357b45812022486488fdedd455c88d275211ba3df1ec3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Antigens, CD - genetics</topic><topic>Antigens, CD - metabolism</topic><topic>Biological and medical sciences</topic><topic>Blood Flow Velocity</topic><topic>Blood vessels and receptors</topic><topic>Femoral Artery - physiology</topic><topic>Fluorescent Dyes</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Hindlimb</topic><topic>Laser-Doppler Flowmetry</topic><topic>Ligation</topic><topic>Mice</topic><topic>Mice, Inbred Strains</topic><topic>Mice, Knockout</topic><topic>Mice, Nude</topic><topic>Microspheres</topic><topic>Models, Animal</topic><topic>Neovascularization, Physiologic - physiology</topic><topic>Receptors, Tumor Necrosis Factor - deficiency</topic><topic>Receptors, Tumor Necrosis Factor - genetics</topic><topic>Receptors, Tumor Necrosis Factor - metabolism</topic><topic>Receptors, Tumor Necrosis Factor, Type I</topic><topic>Receptors, Tumor Necrosis Factor, Type II</topic><topic>Signal Transduction - physiology</topic><topic>Tumor Necrosis Factor-alpha - deficiency</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Tumor Necrosis Factor-alpha - metabolism</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HOEFER, Imo E</creatorcontrib><creatorcontrib>VAN ROYEN, Niels</creatorcontrib><creatorcontrib>RECTENWALD, John E</creatorcontrib><creatorcontrib>BRAY, Elizabeth J</creatorcontrib><creatorcontrib>ABOUHAMZE, Zaher</creatorcontrib><creatorcontrib>MOLDAWER, Lyle L</creatorcontrib><creatorcontrib>VOSKUIL, Michiel</creatorcontrib><creatorcontrib>PIEK, Jan J</creatorcontrib><creatorcontrib>BUSCHMANN, Ivo R</creatorcontrib><creatorcontrib>OZAKI, C. Keith</creatorcontrib><collection>Pascal-Francis</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 Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HOEFER, Imo E</au><au>VAN ROYEN, Niels</au><au>RECTENWALD, John E</au><au>BRAY, Elizabeth J</au><au>ABOUHAMZE, Zaher</au><au>MOLDAWER, Lyle L</au><au>VOSKUIL, Michiel</au><au>PIEK, Jan J</au><au>BUSCHMANN, Ivo R</au><au>OZAKI, C. Keith</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Direct evidence for tumor necrosis factor-α signaling in arteriogenesis</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-04-09</date><risdate>2002</risdate><volume>105</volume><issue>14</issue><spage>1639</spage><epage>1641</epage><pages>1639-1641</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Arteriogenesis serves as an efficient mechanism for flow restoration after arterial occlusion. This process is associated with inflammatory mediators such as tumor necrosis factor-alpha (TNF-alpha), although their role in arteriogenesis remains unclear. We hypothesized that arteriogenesis is reduced in mice lacking functional TNF-alpha or p55 receptor. To test this hypothesis, we developed a novel microsphere-based murine model of hindlimb perfusion measurement.
Unilateral femoral arteries of nude (n=9), TNF-alpha(-/-) (n=9), TNF-alpha receptor p55(-/-) (n=8), and p75(-/-) (n=8) mice as well as their appropriate genetic background controls were occluded. The nude mice underwent laser Doppler hindlimb flux measurements preoperatively, postoperatively, and after 7 days. Seven days after ligation, all animals underwent tissue perfusion determinations using fluorescent microspheres. Laser Doppler findings confirmed acute decrease in flux with falsely normal values after 1 week. Microsphere results from control mice showed perfusion restoration to values approximately 50% of normal within 7 days. TNF-alpha(-/-) mice demonstrated a significant reduction (45.1%) in collateral artery perfusion compared with controls (TNF-alpha(-/-) 22.4+/-5.1% versus B6x129 49.7+/-9.3%; P<0.01). p55(-/-) mice exhibited an almost identical 45.8% reduction in collateral artery formation (p55(-/-) 28.3+/-4.3% versus C57BL/6J 61.8+/-9.1%; P<0.01), whereas p75(-/-) mice were equivalent to controls (p75(-/-) 54.5+/-5.5%; P=0.13).
Microsphere techniques in mice offer a tool for the molecular dissection of arteriogenesis mechanisms. These results suggest that TNF-alpha positively modulates arteriogenesis probably via signaling through its p55 receptor.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>11940540</pmid><doi>10.1161/01.CIR.0000014987.32865.8E</doi><tpages>3</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals |
| subjects | Animals Antigens, CD - genetics Antigens, CD - metabolism Biological and medical sciences Blood Flow Velocity Blood vessels and receptors Femoral Artery - physiology Fluorescent Dyes Fundamental and applied biological sciences. Psychology Hindlimb Laser-Doppler Flowmetry Ligation Mice Mice, Inbred Strains Mice, Knockout Mice, Nude Microspheres Models, Animal Neovascularization, Physiologic - physiology Receptors, Tumor Necrosis Factor - deficiency Receptors, Tumor Necrosis Factor - genetics Receptors, Tumor Necrosis Factor - metabolism Receptors, Tumor Necrosis Factor, Type I Receptors, Tumor Necrosis Factor, Type II Signal Transduction - physiology Tumor Necrosis Factor-alpha - deficiency Tumor Necrosis Factor-alpha - genetics Tumor Necrosis Factor-alpha - metabolism Vertebrates: cardiovascular system |
| title | Direct evidence for tumor necrosis factor-α signaling in arteriogenesis |
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