S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release
Peroxynitrite generated from nitric oxide (NO) and superoxide (O2-) contributes to ischemia/reperfusion (I/R) injury. Feedback inhibition of endothelial NO synthase by NO may inhibit O2- production generated also by endothelial NO synthase at diminished local L-arginine concentrations accompanying I...
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| Veröffentlicht in: | Circulation (New York, N.Y.) N.Y.), 2002-06, Vol.105 (25), p.3032-3038 |
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| creator | HALLSTRÖM, Seth GASSER, Harald NEUMAYER, Christoph FÜGL, Alexander NANOBASHVILI, Joseph JAKUBOWSKI, Andrzej HUK, Ihor SCHLAG, Günther MALINSKI, Tadeusz |
| description | Peroxynitrite generated from nitric oxide (NO) and superoxide (O2-) contributes to ischemia/reperfusion (I/R) injury. Feedback inhibition of endothelial NO synthase by NO may inhibit O2- production generated also by endothelial NO synthase at diminished local L-arginine concentrations accompanying I/R.
During hindlimb I/R (2.5 hours/2 hours), in vivo NO was monitored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione (chromatography), and I/R injury were measured intermittently. Rabbits receiving human serum albumin (HSA) (controls) were compared with those receiving S-nitroso human serum albumin (S-NO-HSA) beginning 30 minutes before reperfusion for 1 hour or 30 minutes before ischemia for 3.5 hours (0.1 micromol x kg(-1) x h(- 1)). The onset of ischemia led to a rapid increase of NO from its basal level (50+/-12 nmol/L) to 120+/-20 and 220+/-15 nmol/L in the control and S-NO-HSA-treated groups, respectively. In control animals, NO dropped below basal levels at the end of ischemia and to undetectable levels ( |
| doi_str_mv | 10.1161/01.CIR.0000018745.11739.9B |
| format | Article |
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During hindlimb I/R (2.5 hours/2 hours), in vivo NO was monitored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione (chromatography), and I/R injury were measured intermittently. Rabbits receiving human serum albumin (HSA) (controls) were compared with those receiving S-nitroso human serum albumin (S-NO-HSA) beginning 30 minutes before reperfusion for 1 hour or 30 minutes before ischemia for 3.5 hours (0.1 micromol x kg(-1) x h(- 1)). The onset of ischemia led to a rapid increase of NO from its basal level (50+/-12 nmol/L) to 120+/-20 and 220+/-15 nmol/L in the control and S-NO-HSA-treated groups, respectively. In control animals, NO dropped below basal levels at the end of ischemia and to undetectable levels (<1 nmol/L) during reperfusion. In S-NO-HSA-treated animals, maximal NO levels never decreased below basal concentration and on reperfusion were 100+/-15 nmol/L (S-NO-HSA preischemia group, 175+/-15 nmol/L). NO supplementation by S-NO-HSA led to partial and in the preischemia group to total preservation of high-energy phosphates and glutathione status in reperfused muscle (eg, preischemia groups: ATP, 30.23+/-5.02 micromol/g versus control, 15.75+/-4.33 micromol/g, P<0.0005; % oxidized glutathione, 4.49+/- 1.87% versus control, 22.84+/-6.39%, P<0.0001). S-NO-HSA treatment in all groups led to protection from vasoconstriction and reduced edema formation after reperfusion (eg, preischemia groups: interfiber area, 12.94+/-1.36% versus control, 27.83+/-1.95%, P< 0.00001).
Long-lasting release of NO by S-NO-HSA provides significant protection of skeletal muscle from I/R injury.</description><identifier>ISSN: 0009-7322</identifier><identifier>EISSN: 1524-4539</identifier><identifier>DOI: 10.1161/01.CIR.0000018745.11739.9B</identifier><identifier>PMID: 12081999</identifier><identifier>CODEN: CIRCAZ</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Adenosine Triphosphate - analysis ; Animals ; Atherosclerosis (general aspects, experimental research) ; Biological and medical sciences ; Blood and lymphatic vessels ; Capillaries - pathology ; Cardiology. Vascular system ; Glutathione - analysis ; Hindlimb - drug effects ; Hindlimb - metabolism ; Kinetics ; Male ; Medical sciences ; Muscle, Skeletal - drug effects ; Muscle, Skeletal - metabolism ; Muscle, Skeletal - pathology ; Nitric Oxide - biosynthesis ; Nitroso Compounds ; Phosphocreatine - analysis ; Rabbits ; Reperfusion Injury - drug therapy ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Serum Albumin, Bovine - pharmacology ; Serum Albumin, Bovine - therapeutic use</subject><ispartof>Circulation (New York, N.Y.), 2002-06, Vol.105 (25), p.3032-3038</ispartof><rights>2002 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jun 25, 2002</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c524t-d13cb9548c9c84accb1f32ef04497a2d76366826e95d77fb4366db1368dab3b53</citedby><cites>FETCH-LOGICAL-c524t-d13cb9548c9c84accb1f32ef04497a2d76366826e95d77fb4366db1368dab3b53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13764122$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12081999$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HALLSTRÖM, Seth</creatorcontrib><creatorcontrib>GASSER, Harald</creatorcontrib><creatorcontrib>NEUMAYER, Christoph</creatorcontrib><creatorcontrib>FÜGL, Alexander</creatorcontrib><creatorcontrib>NANOBASHVILI, Joseph</creatorcontrib><creatorcontrib>JAKUBOWSKI, Andrzej</creatorcontrib><creatorcontrib>HUK, Ihor</creatorcontrib><creatorcontrib>SCHLAG, Günther</creatorcontrib><creatorcontrib>MALINSKI, Tadeusz</creatorcontrib><title>S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>Peroxynitrite generated from nitric oxide (NO) and superoxide (O2-) contributes to ischemia/reperfusion (I/R) injury. Feedback inhibition of endothelial NO synthase by NO may inhibit O2- production generated also by endothelial NO synthase at diminished local L-arginine concentrations accompanying I/R.
During hindlimb I/R (2.5 hours/2 hours), in vivo NO was monitored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione (chromatography), and I/R injury were measured intermittently. Rabbits receiving human serum albumin (HSA) (controls) were compared with those receiving S-nitroso human serum albumin (S-NO-HSA) beginning 30 minutes before reperfusion for 1 hour or 30 minutes before ischemia for 3.5 hours (0.1 micromol x kg(-1) x h(- 1)). The onset of ischemia led to a rapid increase of NO from its basal level (50+/-12 nmol/L) to 120+/-20 and 220+/-15 nmol/L in the control and S-NO-HSA-treated groups, respectively. In control animals, NO dropped below basal levels at the end of ischemia and to undetectable levels (<1 nmol/L) during reperfusion. In S-NO-HSA-treated animals, maximal NO levels never decreased below basal concentration and on reperfusion were 100+/-15 nmol/L (S-NO-HSA preischemia group, 175+/-15 nmol/L). NO supplementation by S-NO-HSA led to partial and in the preischemia group to total preservation of high-energy phosphates and glutathione status in reperfused muscle (eg, preischemia groups: ATP, 30.23+/-5.02 micromol/g versus control, 15.75+/-4.33 micromol/g, P<0.0005; % oxidized glutathione, 4.49+/- 1.87% versus control, 22.84+/-6.39%, P<0.0001). S-NO-HSA treatment in all groups led to protection from vasoconstriction and reduced edema formation after reperfusion (eg, preischemia groups: interfiber area, 12.94+/-1.36% versus control, 27.83+/-1.95%, P< 0.00001).
Long-lasting release of NO by S-NO-HSA provides significant protection of skeletal muscle from I/R injury.</description><subject>Adenosine Triphosphate - analysis</subject><subject>Animals</subject><subject>Atherosclerosis (general aspects, experimental research)</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Capillaries - pathology</subject><subject>Cardiology. Vascular system</subject><subject>Glutathione - analysis</subject><subject>Hindlimb - drug effects</subject><subject>Hindlimb - metabolism</subject><subject>Kinetics</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Muscle, Skeletal - drug effects</subject><subject>Muscle, Skeletal - metabolism</subject><subject>Muscle, Skeletal - pathology</subject><subject>Nitric Oxide - biosynthesis</subject><subject>Nitroso Compounds</subject><subject>Phosphocreatine - analysis</subject><subject>Rabbits</subject><subject>Reperfusion Injury - drug therapy</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Serum Albumin, Bovine - pharmacology</subject><subject>Serum Albumin, Bovine - therapeutic use</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>eNpdkd1u3CAQhVHVqNmkfYUKRWruvPGADaZ3zSptI0WK1J9rhPFYYWvwFkzSvH3ZZqWVys1o4JsZ5hxCLqBeAwi4qmG9uf22rvcHOtm05VpytVbXr8gKWtZUTcvVa7Iq76qSnLFTcpbStqSCy_YNOQVWd6CUWpGn71VwS5zTTB-yN4EmjNlTM_XZu0CXiGbxGBYaccgWE3XJPqB35iriDuOYk5sDdWGb43MJNP3CCRczUZ-TnZA-OkP3A5yl8x83YOkzoUn4lpyMZkr47hDPyc_PNz82X6u7-y-3m093lS17LNUA3PaqbTqrbNcYa3sYOcOxbholDRuk4EJ0TKBqBynHvinp0AMX3WB63rf8nFy-9N3F-XfGtGhfNsBpMgHnnLSEThQN9-DFf-B2zjGUv2kGrIgsAQr08QWyRbEUcdS76LyJzxpqvfdG16CLN_rojf7njVbXpfj9YULuPQ7H0oMZBfhwAEyyZhqjCdalI8elaIAx_hcdtJmk</recordid><startdate>20020625</startdate><enddate>20020625</enddate><creator>HALLSTRÖM, Seth</creator><creator>GASSER, Harald</creator><creator>NEUMAYER, Christoph</creator><creator>FÜGL, Alexander</creator><creator>NANOBASHVILI, Joseph</creator><creator>JAKUBOWSKI, Andrzej</creator><creator>HUK, Ihor</creator><creator>SCHLAG, Günther</creator><creator>MALINSKI, Tadeusz</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>20020625</creationdate><title>S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release</title><author>HALLSTRÖM, Seth ; GASSER, Harald ; NEUMAYER, Christoph ; FÜGL, Alexander ; NANOBASHVILI, Joseph ; JAKUBOWSKI, Andrzej ; HUK, Ihor ; SCHLAG, Günther ; MALINSKI, Tadeusz</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c524t-d13cb9548c9c84accb1f32ef04497a2d76366826e95d77fb4366db1368dab3b53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Adenosine Triphosphate - analysis</topic><topic>Animals</topic><topic>Atherosclerosis (general aspects, experimental research)</topic><topic>Biological and medical sciences</topic><topic>Blood and lymphatic vessels</topic><topic>Capillaries - pathology</topic><topic>Cardiology. Vascular system</topic><topic>Glutathione - analysis</topic><topic>Hindlimb - drug effects</topic><topic>Hindlimb - metabolism</topic><topic>Kinetics</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Muscle, Skeletal - drug effects</topic><topic>Muscle, Skeletal - metabolism</topic><topic>Muscle, Skeletal - pathology</topic><topic>Nitric Oxide - biosynthesis</topic><topic>Nitroso Compounds</topic><topic>Phosphocreatine - analysis</topic><topic>Rabbits</topic><topic>Reperfusion Injury - drug therapy</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Serum Albumin, Bovine - pharmacology</topic><topic>Serum Albumin, Bovine - therapeutic use</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HALLSTRÖM, Seth</creatorcontrib><creatorcontrib>GASSER, Harald</creatorcontrib><creatorcontrib>NEUMAYER, Christoph</creatorcontrib><creatorcontrib>FÜGL, Alexander</creatorcontrib><creatorcontrib>NANOBASHVILI, Joseph</creatorcontrib><creatorcontrib>JAKUBOWSKI, Andrzej</creatorcontrib><creatorcontrib>HUK, Ihor</creatorcontrib><creatorcontrib>SCHLAG, Günther</creatorcontrib><creatorcontrib>MALINSKI, Tadeusz</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>HALLSTRÖM, Seth</au><au>GASSER, Harald</au><au>NEUMAYER, Christoph</au><au>FÜGL, Alexander</au><au>NANOBASHVILI, Joseph</au><au>JAKUBOWSKI, Andrzej</au><au>HUK, Ihor</au><au>SCHLAG, Günther</au><au>MALINSKI, Tadeusz</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>2002-06-25</date><risdate>2002</risdate><volume>105</volume><issue>25</issue><spage>3032</spage><epage>3038</epage><pages>3032-3038</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>Peroxynitrite generated from nitric oxide (NO) and superoxide (O2-) contributes to ischemia/reperfusion (I/R) injury. Feedback inhibition of endothelial NO synthase by NO may inhibit O2- production generated also by endothelial NO synthase at diminished local L-arginine concentrations accompanying I/R.
During hindlimb I/R (2.5 hours/2 hours), in vivo NO was monitored continuously (porphyrinic sensor), and high-energy phosphates, reduced and oxidized glutathione (chromatography), and I/R injury were measured intermittently. Rabbits receiving human serum albumin (HSA) (controls) were compared with those receiving S-nitroso human serum albumin (S-NO-HSA) beginning 30 minutes before reperfusion for 1 hour or 30 minutes before ischemia for 3.5 hours (0.1 micromol x kg(-1) x h(- 1)). The onset of ischemia led to a rapid increase of NO from its basal level (50+/-12 nmol/L) to 120+/-20 and 220+/-15 nmol/L in the control and S-NO-HSA-treated groups, respectively. In control animals, NO dropped below basal levels at the end of ischemia and to undetectable levels (<1 nmol/L) during reperfusion. In S-NO-HSA-treated animals, maximal NO levels never decreased below basal concentration and on reperfusion were 100+/-15 nmol/L (S-NO-HSA preischemia group, 175+/-15 nmol/L). NO supplementation by S-NO-HSA led to partial and in the preischemia group to total preservation of high-energy phosphates and glutathione status in reperfused muscle (eg, preischemia groups: ATP, 30.23+/-5.02 micromol/g versus control, 15.75+/-4.33 micromol/g, P<0.0005; % oxidized glutathione, 4.49+/- 1.87% versus control, 22.84+/-6.39%, P<0.0001). S-NO-HSA treatment in all groups led to protection from vasoconstriction and reduced edema formation after reperfusion (eg, preischemia groups: interfiber area, 12.94+/-1.36% versus control, 27.83+/-1.95%, P< 0.00001).
Long-lasting release of NO by S-NO-HSA provides significant protection of skeletal muscle from I/R injury.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>12081999</pmid><doi>10.1161/01.CIR.0000018745.11739.9B</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Adenosine Triphosphate - analysis Animals Atherosclerosis (general aspects, experimental research) Biological and medical sciences Blood and lymphatic vessels Capillaries - pathology Cardiology. Vascular system Glutathione - analysis Hindlimb - drug effects Hindlimb - metabolism Kinetics Male Medical sciences Muscle, Skeletal - drug effects Muscle, Skeletal - metabolism Muscle, Skeletal - pathology Nitric Oxide - biosynthesis Nitroso Compounds Phosphocreatine - analysis Rabbits Reperfusion Injury - drug therapy Reperfusion Injury - metabolism Reperfusion Injury - pathology Serum Albumin, Bovine - pharmacology Serum Albumin, Bovine - therapeutic use |
| title | S-nitroso human serum albumin treatment reduces ischemia/reperfusion injury in skeletal muscle via nitric oxide release |
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