Loading…
Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis
Pharmacologic preconditioning represents an attractive myocardial protection strategy. Tumor necrosis factor-alpha plays an important role in myocardial ischemia-reperfusion injury. We aimed to determine the effect of Monophosphoryl lipid A-induced delayed preconditioning on diastolic and systolic l...
Saved in:
| Published in: | European journal of cardio-thoracic surgery 2005-03, Vol.27 (3), p.501-507 |
|---|---|
| Main Authors: | , , , , , , , |
| Format: | Article |
| Language: | English |
| Subjects: | |
| Citations: | Items that cite this one |
| Online Access: | Get full text |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| cited_by | cdi_FETCH-LOGICAL-c283t-f5455f9c86b8dd24c3ffb8f1e6b10a107466c602ae2f64bc48539cd30dec1ed33 |
|---|---|
| cites | |
| container_end_page | 507 |
| container_issue | 3 |
| container_start_page | 501 |
| container_title | European journal of cardio-thoracic surgery |
| container_volume | 27 |
| creator | SHARONY, Ram FROLKIS, Inna FROYLICH, Dvir WILDHIRT, Stephan M SHAPIRA, Itzhak REICHART, Bruno NESHER, Nahum URETZKY, Gideon |
| description | Pharmacologic preconditioning represents an attractive myocardial protection strategy. Tumor necrosis factor-alpha plays an important role in myocardial ischemia-reperfusion injury. We aimed to determine the effect of Monophosphoryl lipid A-induced delayed preconditioning on diastolic and systolic left ventricular function and tumor necrosis factor-alpha synthesis during ischemia and reperfusion.
Rats (n=10) were pretreated with Monophosphoryl lipid A (350 microg/kg) or vehicle (n=9). Twenty-four hours later, the hearts were isolated and perfused on a Langendorff apparatus. Hemodynamic measurements, tumor necrosis factor-alpha mRNA expression and protein content were studied after stabilization (baseline), after 35 min of global ischemia and at 40 min of reperfusion.
Left ventricular developed pressure and peak rate of left ventricular developed pressure (dP/dt) rise were comparable between the animals in the control and Monophosphoryl lipid A treated groups during baseline but were higher in Monophosphoryl lipid A group at reperfusion (74+/-4 vs 51+/-5 mmHg, 3340+/-172 vs 2240+/-156 mmHg/s, respectively, P |
| doi_str_mv | 10.1016/j.ejcts.2004.11.033 |
| format | article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_67480676</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>67480676</sourcerecordid><originalsourceid>FETCH-LOGICAL-c283t-f5455f9c86b8dd24c3ffb8f1e6b10a107466c602ae2f64bc48539cd30dec1ed33</originalsourceid><addsrcrecordid>eNpFkE1v1DAQhi0EoqXwC5CQL3BLGMeOnT2iigJSBRyKxM1y_NF45dghkwXtH-B346Ur9TCaOTzvq9FDyGsGLQMm3-9bv7cbth2AaBlrgfMn5JINijeKi59P6w0MGrUTcEFeIO4BQPJOPScXrFcCdpJfkr_fJ7POxpZU7qM1iS6rtyW7uMWSY76nf-I20bnkskwF66zHRFNcoqOGxnlZy2-PdCm40Yh28nO01EWDW0n1CodsT0XUZFdLXAyx0ndfbxqTlslQPOZt8hjxJXkWTEL_6ryvyI-bj3fXn5vbb5--XH-4bWw38K0Jvej7sLODHAfnOmF5COMQmJcjA8NACSmthM74LkgxWjH0fGcdB-ct847zK_Luobc-_uvgcdNzfdunZLIvB9RSiQGkkhXkD6BdC-Lqg17WOJv1qBnok3691__165N-zZiu-mvqzbn-MM7ePWbOvivw9gwYrLbDarKN-MgNjPNedfwfN4-T5g</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>67480676</pqid></control><display><type>article</type><title>Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis</title><source>Oxford Journals Online</source><creator>SHARONY, Ram ; FROLKIS, Inna ; FROYLICH, Dvir ; WILDHIRT, Stephan M ; SHAPIRA, Itzhak ; REICHART, Bruno ; NESHER, Nahum ; URETZKY, Gideon</creator><creatorcontrib>SHARONY, Ram ; FROLKIS, Inna ; FROYLICH, Dvir ; WILDHIRT, Stephan M ; SHAPIRA, Itzhak ; REICHART, Bruno ; NESHER, Nahum ; URETZKY, Gideon</creatorcontrib><description>Pharmacologic preconditioning represents an attractive myocardial protection strategy. Tumor necrosis factor-alpha plays an important role in myocardial ischemia-reperfusion injury. We aimed to determine the effect of Monophosphoryl lipid A-induced delayed preconditioning on diastolic and systolic left ventricular function and tumor necrosis factor-alpha synthesis during ischemia and reperfusion.
Rats (n=10) were pretreated with Monophosphoryl lipid A (350 microg/kg) or vehicle (n=9). Twenty-four hours later, the hearts were isolated and perfused on a Langendorff apparatus. Hemodynamic measurements, tumor necrosis factor-alpha mRNA expression and protein content were studied after stabilization (baseline), after 35 min of global ischemia and at 40 min of reperfusion.
Left ventricular developed pressure and peak rate of left ventricular developed pressure (dP/dt) rise were comparable between the animals in the control and Monophosphoryl lipid A treated groups during baseline but were higher in Monophosphoryl lipid A group at reperfusion (74+/-4 vs 51+/-5 mmHg, 3340+/-172 vs 2240+/-156 mmHg/s, respectively, P<0.01). dP/dt fall was significantly lower in the MLA group (2630+/-225v 1580+/-210 mmHg/s, P<0.01) at 40 min of reperfusion as well as end diastolic pressure. Baseline tumor necrosis factor-alpha mRNA (expressed as arbitrary densitometry units) were higher in the Monophosphoryl lipid A group (1.3+/-0.1 vs 0.5+/-0.03, P<0.05) but remained constant after ischemia and reperfusion (1.3+/-0.1 and 1.4+/-0.03, P=0.2), while further increase was observed in the control group (from 1.0+/-0.1 to 1.4+/-0.1, P<0.05). Tumor necrosis factor-alpha protein content from heart effluent in the control group was increased during reperfusion (79+/-30 and 200+/-22pg/ml, P<0.05) but was undetectable in the Monophosphoryl lipid A group. Marked TNF-alpha immunostaining of left ventricular tissue was observed only in the control group but no TNF-alpha staining was evident in the Monophosphoryl lipid A treated group at 40 min of reperfusion.
Monophosphoryl lipid A-induced preconditioning renders the heart more tolerant to ischemia-reperfusion in terms of left ventricular diastolic and systolic function, and prevents tumor necrosis factor-alpha production during ischemia, through aborting the translation phase of tumor necrosis factor-alpha synthesis.</description><identifier>ISSN: 1010-7940</identifier><identifier>EISSN: 1873-734X</identifier><identifier>DOI: 10.1016/j.ejcts.2004.11.033</identifier><identifier>PMID: 15740963</identifier><identifier>CODEN: EJCSE7</identifier><language>eng</language><publisher>Amsterdam: Elsevier Science</publisher><subject>Animals ; Biological and medical sciences ; Cardiology. Vascular system ; Coronary Circulation - drug effects ; Gene Expression Regulation - drug effects ; Hemodynamics - drug effects ; Ischemic Preconditioning, Myocardial - methods ; Lipid A - analogs & derivatives ; Lipid A - therapeutic use ; Male ; Medical sciences ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention & control ; Organ Culture Techniques ; Pneumology ; Rats ; Rats, Sprague-Dawley ; Reverse Transcriptase Polymerase Chain Reaction - methods ; RNA, Messenger - genetics ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the heart ; Tumor Necrosis Factor-alpha - biosynthesis ; Tumor Necrosis Factor-alpha - genetics ; Ventricular Function, Left - drug effects</subject><ispartof>European journal of cardio-thoracic surgery, 2005-03, Vol.27 (3), p.501-507</ispartof><rights>2006 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c283t-f5455f9c86b8dd24c3ffb8f1e6b10a107466c602ae2f64bc48539cd30dec1ed33</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=18133572$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/15740963$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>SHARONY, Ram</creatorcontrib><creatorcontrib>FROLKIS, Inna</creatorcontrib><creatorcontrib>FROYLICH, Dvir</creatorcontrib><creatorcontrib>WILDHIRT, Stephan M</creatorcontrib><creatorcontrib>SHAPIRA, Itzhak</creatorcontrib><creatorcontrib>REICHART, Bruno</creatorcontrib><creatorcontrib>NESHER, Nahum</creatorcontrib><creatorcontrib>URETZKY, Gideon</creatorcontrib><title>Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis</title><title>European journal of cardio-thoracic surgery</title><addtitle>Eur J Cardiothorac Surg</addtitle><description>Pharmacologic preconditioning represents an attractive myocardial protection strategy. Tumor necrosis factor-alpha plays an important role in myocardial ischemia-reperfusion injury. We aimed to determine the effect of Monophosphoryl lipid A-induced delayed preconditioning on diastolic and systolic left ventricular function and tumor necrosis factor-alpha synthesis during ischemia and reperfusion.
Rats (n=10) were pretreated with Monophosphoryl lipid A (350 microg/kg) or vehicle (n=9). Twenty-four hours later, the hearts were isolated and perfused on a Langendorff apparatus. Hemodynamic measurements, tumor necrosis factor-alpha mRNA expression and protein content were studied after stabilization (baseline), after 35 min of global ischemia and at 40 min of reperfusion.
Left ventricular developed pressure and peak rate of left ventricular developed pressure (dP/dt) rise were comparable between the animals in the control and Monophosphoryl lipid A treated groups during baseline but were higher in Monophosphoryl lipid A group at reperfusion (74+/-4 vs 51+/-5 mmHg, 3340+/-172 vs 2240+/-156 mmHg/s, respectively, P<0.01). dP/dt fall was significantly lower in the MLA group (2630+/-225v 1580+/-210 mmHg/s, P<0.01) at 40 min of reperfusion as well as end diastolic pressure. Baseline tumor necrosis factor-alpha mRNA (expressed as arbitrary densitometry units) were higher in the Monophosphoryl lipid A group (1.3+/-0.1 vs 0.5+/-0.03, P<0.05) but remained constant after ischemia and reperfusion (1.3+/-0.1 and 1.4+/-0.03, P=0.2), while further increase was observed in the control group (from 1.0+/-0.1 to 1.4+/-0.1, P<0.05). Tumor necrosis factor-alpha protein content from heart effluent in the control group was increased during reperfusion (79+/-30 and 200+/-22pg/ml, P<0.05) but was undetectable in the Monophosphoryl lipid A group. Marked TNF-alpha immunostaining of left ventricular tissue was observed only in the control group but no TNF-alpha staining was evident in the Monophosphoryl lipid A treated group at 40 min of reperfusion.
Monophosphoryl lipid A-induced preconditioning renders the heart more tolerant to ischemia-reperfusion in terms of left ventricular diastolic and systolic function, and prevents tumor necrosis factor-alpha production during ischemia, through aborting the translation phase of tumor necrosis factor-alpha synthesis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cardiology. Vascular system</subject><subject>Coronary Circulation - drug effects</subject><subject>Gene Expression Regulation - drug effects</subject><subject>Hemodynamics - drug effects</subject><subject>Ischemic Preconditioning, Myocardial - methods</subject><subject>Lipid A - analogs & derivatives</subject><subject>Lipid A - therapeutic use</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Organ Culture Techniques</subject><subject>Pneumology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Reverse Transcriptase Polymerase Chain Reaction - methods</subject><subject>RNA, Messenger - genetics</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the heart</subject><subject>Tumor Necrosis Factor-alpha - biosynthesis</subject><subject>Tumor Necrosis Factor-alpha - genetics</subject><subject>Ventricular Function, Left - drug effects</subject><issn>1010-7940</issn><issn>1873-734X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2005</creationdate><recordtype>article</recordtype><recordid>eNpFkE1v1DAQhi0EoqXwC5CQL3BLGMeOnT2iigJSBRyKxM1y_NF45dghkwXtH-B346Ur9TCaOTzvq9FDyGsGLQMm3-9bv7cbth2AaBlrgfMn5JINijeKi59P6w0MGrUTcEFeIO4BQPJOPScXrFcCdpJfkr_fJ7POxpZU7qM1iS6rtyW7uMWSY76nf-I20bnkskwF66zHRFNcoqOGxnlZy2-PdCm40Yh28nO01EWDW0n1CodsT0XUZFdLXAyx0ndfbxqTlslQPOZt8hjxJXkWTEL_6ryvyI-bj3fXn5vbb5--XH-4bWw38K0Jvej7sLODHAfnOmF5COMQmJcjA8NACSmthM74LkgxWjH0fGcdB-ct847zK_Luobc-_uvgcdNzfdunZLIvB9RSiQGkkhXkD6BdC-Lqg17WOJv1qBnok3691__165N-zZiu-mvqzbn-MM7ePWbOvivw9gwYrLbDarKN-MgNjPNedfwfN4-T5g</recordid><startdate>200503</startdate><enddate>200503</enddate><creator>SHARONY, Ram</creator><creator>FROLKIS, Inna</creator><creator>FROYLICH, Dvir</creator><creator>WILDHIRT, Stephan M</creator><creator>SHAPIRA, Itzhak</creator><creator>REICHART, Bruno</creator><creator>NESHER, Nahum</creator><creator>URETZKY, Gideon</creator><general>Elsevier Science</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>7X8</scope></search><sort><creationdate>200503</creationdate><title>Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis</title><author>SHARONY, Ram ; FROLKIS, Inna ; FROYLICH, Dvir ; WILDHIRT, Stephan M ; SHAPIRA, Itzhak ; REICHART, Bruno ; NESHER, Nahum ; URETZKY, Gideon</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c283t-f5455f9c86b8dd24c3ffb8f1e6b10a107466c602ae2f64bc48539cd30dec1ed33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2005</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cardiology. Vascular system</topic><topic>Coronary Circulation - drug effects</topic><topic>Gene Expression Regulation - drug effects</topic><topic>Hemodynamics - drug effects</topic><topic>Ischemic Preconditioning, Myocardial - methods</topic><topic>Lipid A - analogs & derivatives</topic><topic>Lipid A - therapeutic use</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Organ Culture Techniques</topic><topic>Pneumology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Reverse Transcriptase Polymerase Chain Reaction - methods</topic><topic>RNA, Messenger - genetics</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the heart</topic><topic>Tumor Necrosis Factor-alpha - biosynthesis</topic><topic>Tumor Necrosis Factor-alpha - genetics</topic><topic>Ventricular Function, Left - drug effects</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>SHARONY, Ram</creatorcontrib><creatorcontrib>FROLKIS, Inna</creatorcontrib><creatorcontrib>FROYLICH, Dvir</creatorcontrib><creatorcontrib>WILDHIRT, Stephan M</creatorcontrib><creatorcontrib>SHAPIRA, Itzhak</creatorcontrib><creatorcontrib>REICHART, Bruno</creatorcontrib><creatorcontrib>NESHER, Nahum</creatorcontrib><creatorcontrib>URETZKY, Gideon</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>MEDLINE - Academic</collection><jtitle>European journal of cardio-thoracic surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>SHARONY, Ram</au><au>FROLKIS, Inna</au><au>FROYLICH, Dvir</au><au>WILDHIRT, Stephan M</au><au>SHAPIRA, Itzhak</au><au>REICHART, Bruno</au><au>NESHER, Nahum</au><au>URETZKY, Gideon</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis</atitle><jtitle>European journal of cardio-thoracic surgery</jtitle><addtitle>Eur J Cardiothorac Surg</addtitle><date>2005-03</date><risdate>2005</risdate><volume>27</volume><issue>3</issue><spage>501</spage><epage>507</epage><pages>501-507</pages><issn>1010-7940</issn><eissn>1873-734X</eissn><coden>EJCSE7</coden><abstract>Pharmacologic preconditioning represents an attractive myocardial protection strategy. Tumor necrosis factor-alpha plays an important role in myocardial ischemia-reperfusion injury. We aimed to determine the effect of Monophosphoryl lipid A-induced delayed preconditioning on diastolic and systolic left ventricular function and tumor necrosis factor-alpha synthesis during ischemia and reperfusion.
Rats (n=10) were pretreated with Monophosphoryl lipid A (350 microg/kg) or vehicle (n=9). Twenty-four hours later, the hearts were isolated and perfused on a Langendorff apparatus. Hemodynamic measurements, tumor necrosis factor-alpha mRNA expression and protein content were studied after stabilization (baseline), after 35 min of global ischemia and at 40 min of reperfusion.
Left ventricular developed pressure and peak rate of left ventricular developed pressure (dP/dt) rise were comparable between the animals in the control and Monophosphoryl lipid A treated groups during baseline but were higher in Monophosphoryl lipid A group at reperfusion (74+/-4 vs 51+/-5 mmHg, 3340+/-172 vs 2240+/-156 mmHg/s, respectively, P<0.01). dP/dt fall was significantly lower in the MLA group (2630+/-225v 1580+/-210 mmHg/s, P<0.01) at 40 min of reperfusion as well as end diastolic pressure. Baseline tumor necrosis factor-alpha mRNA (expressed as arbitrary densitometry units) were higher in the Monophosphoryl lipid A group (1.3+/-0.1 vs 0.5+/-0.03, P<0.05) but remained constant after ischemia and reperfusion (1.3+/-0.1 and 1.4+/-0.03, P=0.2), while further increase was observed in the control group (from 1.0+/-0.1 to 1.4+/-0.1, P<0.05). Tumor necrosis factor-alpha protein content from heart effluent in the control group was increased during reperfusion (79+/-30 and 200+/-22pg/ml, P<0.05) but was undetectable in the Monophosphoryl lipid A group. Marked TNF-alpha immunostaining of left ventricular tissue was observed only in the control group but no TNF-alpha staining was evident in the Monophosphoryl lipid A treated group at 40 min of reperfusion.
Monophosphoryl lipid A-induced preconditioning renders the heart more tolerant to ischemia-reperfusion in terms of left ventricular diastolic and systolic function, and prevents tumor necrosis factor-alpha production during ischemia, through aborting the translation phase of tumor necrosis factor-alpha synthesis.</abstract><cop>Amsterdam</cop><pub>Elsevier Science</pub><pmid>15740963</pmid><doi>10.1016/j.ejcts.2004.11.033</doi><tpages>7</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1010-7940 |
| ispartof | European journal of cardio-thoracic surgery, 2005-03, Vol.27 (3), p.501-507 |
| issn | 1010-7940 1873-734X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_67480676 |
| source | Oxford Journals Online |
| subjects | Animals Biological and medical sciences Cardiology. Vascular system Coronary Circulation - drug effects Gene Expression Regulation - drug effects Hemodynamics - drug effects Ischemic Preconditioning, Myocardial - methods Lipid A - analogs & derivatives Lipid A - therapeutic use Male Medical sciences Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Organ Culture Techniques Pneumology Rats Rats, Sprague-Dawley Reverse Transcriptase Polymerase Chain Reaction - methods RNA, Messenger - genetics Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the heart Tumor Necrosis Factor-alpha - biosynthesis Tumor Necrosis Factor-alpha - genetics Ventricular Function, Left - drug effects |
| title | Pharmacological preconditioning with monophosphoryl lipid a improves post ischemic diastolic function and modifies TNF-alpha synthesis |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T02%3A50%3A16IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Pharmacological%20preconditioning%20with%20monophosphoryl%20lipid%20a%20improves%20post%20ischemic%20diastolic%20function%20and%20modifies%20TNF-alpha%20synthesis&rft.jtitle=European%20journal%20of%20cardio-thoracic%20surgery&rft.au=SHARONY,%20Ram&rft.date=2005-03&rft.volume=27&rft.issue=3&rft.spage=501&rft.epage=507&rft.pages=501-507&rft.issn=1010-7940&rft.eissn=1873-734X&rft.coden=EJCSE7&rft_id=info:doi/10.1016/j.ejcts.2004.11.033&rft_dat=%3Cproquest_cross%3E67480676%3C/proquest_cross%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c283t-f5455f9c86b8dd24c3ffb8f1e6b10a107466c602ae2f64bc48539cd30dec1ed33%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=67480676&rft_id=info:pmid/15740963&rfr_iscdi=true |