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Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats
Previous findings have shown that hypotensive doses of losartan prevent the excess of apoptosis present in the hypertrophied left ventricle of adult spontaneously hypertensive rats (SHR). This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR...
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| Published in: | Hypertension (Dallas, Tex. 1979) Tex. 1979), 2000-12, Vol.36 (6), p.1065-1071 |
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| container_end_page | 1071 |
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| container_title | Hypertension (Dallas, Tex. 1979) |
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| creator | Ravassa, Susana Fortuño, María Antonia González, Arantxa López, Begoña Zalba, Guillermo Fortuño, Ana Díez, Javier |
| description | Previous findings have shown that hypotensive doses of losartan prevent the excess of apoptosis present in the hypertrophied left ventricle of adult spontaneously hypertensive rats (SHR). This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR. Primary cultures of ventricular cardiomyocytes from 30-week-old normotensive Wistar-Kyoto rats (WKY) and SHR with left ventricular hypertrophy were exposed to 10 mol/L angiotensin II for 24 hours. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase assay and confirmed by Annexin V detection. The expression of Bax-α, Bcl-2, p53 , and caspase-3 proteins was assessed by Western blot assays. The expression of BAX gene was assessed by Northern blot. Angiotensin II increased (P |
| doi_str_mv | 10.1161/01.hyp.36.6.1065 |
| format | article |
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This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR. Primary cultures of ventricular cardiomyocytes from 30-week-old normotensive Wistar-Kyoto rats (WKY) and SHR with left ventricular hypertrophy were exposed to 10 mol/L angiotensin II for 24 hours. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase assay and confirmed by Annexin V detection. The expression of Bax-α, Bcl-2, p53 , and caspase-3 proteins was assessed by Western blot assays. The expression of BAX gene was assessed by Northern blot. Angiotensin II increased (P <0.01) cardiomyocyte apoptosis, and this effect was higher (P <0.001) in SHR cells than in WKY cells. Whereas losartan (10 mol/L) blocked the apoptotic effect of the octapeptide in cells from the two strains of rats, PD123319 (10 mol/L) inhibited angiotensin II–mediated apoptosis only in SHR cells. Angiotensin II stimulated (P <0.01) Bax-α protein, and this effect was higher (P <0.01) in SHR cells than in WKY cells. Angiotensin II did not modify Bcl-2, p53, and BAX mRNA in cells from the two strains of rats. Angiotensin II induced a similar increase (P <0.05) in the ratio caspase-3/procaspase-3 (an index of caspase-3 activation) in cardiomyocytes from the two strains of rats. The present in vitro results indicate that SHR cardiomyocytes exhibit enhanced susceptibility to angiotensin II–induced apoptosis. Ligand binding to angiotensin II type 1 and type 2 receptors leading to changes in posttranscriptional processing of Bax-α and accumulation of this proapoptotic protein may be involved in the abnormal response of SHR cardiomyocytes. These data support a role for angiotensin II in apoptosis observed in the left ventricle of these rats.</description><identifier>ISSN: 0194-911X</identifier><identifier>EISSN: 1524-4563</identifier><identifier>DOI: 10.1161/01.hyp.36.6.1065</identifier><identifier>PMID: 11116126</identifier><identifier>CODEN: HPRTDN</identifier><language>eng</language><publisher>Philadelphia, PA: American Heart Association, Inc</publisher><subject>Angiotensin II - pharmacology ; Animals ; Apoptosis ; Arterial hypertension. Arterial hypotension ; bcl-2-Associated X Protein ; Biological and medical sciences ; Blood and lymphatic vessels ; Blood Pressure ; Cardiology. Vascular system ; Caspase 3 ; Caspases - metabolism ; Cells, Cultured ; Enzyme Activation ; Experimental diseases ; Heart - drug effects ; Heart Ventricles - drug effects ; Heart Ventricles - pathology ; Hypertension - complications ; Hypertension - pathology ; Hypertrophy, Left Ventricular - etiology ; Hypertrophy, Left Ventricular - pathology ; Male ; Medical sciences ; Myocardium - pathology ; Proto-Oncogene Proteins - genetics ; Proto-Oncogene Proteins - metabolism ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Rats, Inbred SHR ; Rats, Inbred WKY ; RNA, Messenger - metabolism ; Tumor Suppressor Protein p53 - metabolism</subject><ispartof>Hypertension (Dallas, Tex. 1979), 2000-12, Vol.36 (6), p.1065-1071</ispartof><rights>2000 American Heart Association, Inc.</rights><rights>2001 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Dec 2000</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5457-b31b209a49a2a5a0176642a6358b593a301a95e7e1f4eea6cc038dedd243badc3</citedby><cites>FETCH-LOGICAL-c5457-b31b209a49a2a5a0176642a6358b593a301a95e7e1f4eea6cc038dedd243badc3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,778,782,27907,27908</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=857957$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11116126$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ravassa, Susana</creatorcontrib><creatorcontrib>Fortuño, María Antonia</creatorcontrib><creatorcontrib>González, Arantxa</creatorcontrib><creatorcontrib>López, Begoña</creatorcontrib><creatorcontrib>Zalba, Guillermo</creatorcontrib><creatorcontrib>Fortuño, Ana</creatorcontrib><creatorcontrib>Díez, Javier</creatorcontrib><title>Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>Previous findings have shown that hypotensive doses of losartan prevent the excess of apoptosis present in the hypertrophied left ventricle of adult spontaneously hypertensive rats (SHR). This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR. Primary cultures of ventricular cardiomyocytes from 30-week-old normotensive Wistar-Kyoto rats (WKY) and SHR with left ventricular hypertrophy were exposed to 10 mol/L angiotensin II for 24 hours. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase assay and confirmed by Annexin V detection. The expression of Bax-α, Bcl-2, p53 , and caspase-3 proteins was assessed by Western blot assays. The expression of BAX gene was assessed by Northern blot. Angiotensin II increased (P <0.01) cardiomyocyte apoptosis, and this effect was higher (P <0.001) in SHR cells than in WKY cells. Whereas losartan (10 mol/L) blocked the apoptotic effect of the octapeptide in cells from the two strains of rats, PD123319 (10 mol/L) inhibited angiotensin II–mediated apoptosis only in SHR cells. Angiotensin II stimulated (P <0.01) Bax-α protein, and this effect was higher (P <0.01) in SHR cells than in WKY cells. Angiotensin II did not modify Bcl-2, p53, and BAX mRNA in cells from the two strains of rats. Angiotensin II induced a similar increase (P <0.05) in the ratio caspase-3/procaspase-3 (an index of caspase-3 activation) in cardiomyocytes from the two strains of rats. The present in vitro results indicate that SHR cardiomyocytes exhibit enhanced susceptibility to angiotensin II–induced apoptosis. Ligand binding to angiotensin II type 1 and type 2 receptors leading to changes in posttranscriptional processing of Bax-α and accumulation of this proapoptotic protein may be involved in the abnormal response of SHR cardiomyocytes. These data support a role for angiotensin II in apoptosis observed in the left ventricle of these rats.</description><subject>Angiotensin II - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Arterial hypertension. Arterial hypotension</subject><subject>bcl-2-Associated X Protein</subject><subject>Biological and medical sciences</subject><subject>Blood and lymphatic vessels</subject><subject>Blood Pressure</subject><subject>Cardiology. Vascular system</subject><subject>Caspase 3</subject><subject>Caspases - metabolism</subject><subject>Cells, Cultured</subject><subject>Enzyme Activation</subject><subject>Experimental diseases</subject><subject>Heart - drug effects</subject><subject>Heart Ventricles - drug effects</subject><subject>Heart Ventricles - pathology</subject><subject>Hypertension - complications</subject><subject>Hypertension - pathology</subject><subject>Hypertrophy, Left Ventricular - etiology</subject><subject>Hypertrophy, Left Ventricular - pathology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Myocardium - pathology</subject><subject>Proto-Oncogene Proteins - genetics</subject><subject>Proto-Oncogene Proteins - metabolism</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats</subject><subject>Rats, Inbred SHR</subject><subject>Rats, Inbred WKY</subject><subject>RNA, Messenger - metabolism</subject><subject>Tumor Suppressor Protein p53 - metabolism</subject><issn>0194-911X</issn><issn>1524-4563</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2000</creationdate><recordtype>article</recordtype><recordid>eNpdkc-O0zAQxiMEYsvCnROKQOKW4vG_NMeqAlppEYgFBCfLcabUS2pnbYdVbrwAJ96QJ8HdViAxkmcs-fd9mvEUxWMgcwAJLwjMd9MwZ3Iu50CkuFPMQFBecSHZ3WJGoOFVA_D5rHgQ4xUhwDmv7xdnAAc5lbPi5xs0O-1s3MfSb8uNMwF1xK68HKPBIdnW9jZNZfLl0n21PqGL1pWbze8fvzauG01Gl4Mfko82lvnlE7oUrBl7HcqVDp31-8mbKeGt_-XgXdIO_Rj7qVxPA4Zbx-9YvtcpPizubXUf8dGpnhcfX738sFpXF29fb1bLi8oILuqqZdBS0mjeaKqFJlBLyamWTCxa0TDNCOhGYI2w5YhaGkPYosOuo5y1ujPsvHh-9B2Cvx4xJrW3edy-P7amasprATXL4NP_wCs_Bpd7U5QIRgjliwyRI2SCjzHgVg3B7nWYFBB1-GhFQK2_vFNMKqkOe8qSJyffsd1j909wWkwGnp0AHY3ut0E7Y-NfbiHqRtSZ4kfqxvcJQ_zWjzcY1A51n3aK5OBULiqaL3BIVT60Zn8Ae_SuTA</recordid><startdate>200012</startdate><enddate>200012</enddate><creator>Ravassa, Susana</creator><creator>Fortuño, María Antonia</creator><creator>González, Arantxa</creator><creator>López, Begoña</creator><creator>Zalba, Guillermo</creator><creator>Fortuño, Ana</creator><creator>Díez, Javier</creator><general>American Heart Association, Inc</general><general>Lippincott</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>7X8</scope></search><sort><creationdate>200012</creationdate><title>Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats</title><author>Ravassa, Susana ; Fortuño, María Antonia ; González, Arantxa ; López, Begoña ; Zalba, Guillermo ; Fortuño, Ana ; Díez, Javier</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5457-b31b209a49a2a5a0176642a6358b593a301a95e7e1f4eea6cc038dedd243badc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2000</creationdate><topic>Angiotensin II - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Arterial hypertension. 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Vascular system</topic><topic>Caspase 3</topic><topic>Caspases - metabolism</topic><topic>Cells, Cultured</topic><topic>Enzyme Activation</topic><topic>Experimental diseases</topic><topic>Heart - drug effects</topic><topic>Heart Ventricles - drug effects</topic><topic>Heart Ventricles - pathology</topic><topic>Hypertension - complications</topic><topic>Hypertension - pathology</topic><topic>Hypertrophy, Left Ventricular - etiology</topic><topic>Hypertrophy, Left Ventricular - pathology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Myocardium - pathology</topic><topic>Proto-Oncogene Proteins - genetics</topic><topic>Proto-Oncogene Proteins - metabolism</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats</topic><topic>Rats, Inbred SHR</topic><topic>Rats, Inbred WKY</topic><topic>RNA, Messenger - metabolism</topic><topic>Tumor Suppressor Protein p53 - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Ravassa, Susana</creatorcontrib><creatorcontrib>Fortuño, María Antonia</creatorcontrib><creatorcontrib>González, Arantxa</creatorcontrib><creatorcontrib>López, Begoña</creatorcontrib><creatorcontrib>Zalba, Guillermo</creatorcontrib><creatorcontrib>Fortuño, Ana</creatorcontrib><creatorcontrib>Díez, Javier</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>MEDLINE - Academic</collection><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ravassa, Susana</au><au>Fortuño, María Antonia</au><au>González, Arantxa</au><au>López, Begoña</au><au>Zalba, Guillermo</au><au>Fortuño, Ana</au><au>Díez, Javier</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats</atitle><jtitle>Hypertension (Dallas, Tex. 1979)</jtitle><addtitle>Hypertension</addtitle><date>2000-12</date><risdate>2000</risdate><volume>36</volume><issue>6</issue><spage>1065</spage><epage>1071</epage><pages>1065-1071</pages><issn>0194-911X</issn><eissn>1524-4563</eissn><coden>HPRTDN</coden><abstract>Previous findings have shown that hypotensive doses of losartan prevent the excess of apoptosis present in the hypertrophied left ventricle of adult spontaneously hypertensive rats (SHR). This study was designed to determine whether angiotensin II facilitates apoptosis in cardiomyocytes of adult SHR. Primary cultures of ventricular cardiomyocytes from 30-week-old normotensive Wistar-Kyoto rats (WKY) and SHR with left ventricular hypertrophy were exposed to 10 mol/L angiotensin II for 24 hours. Apoptotic cells were assessed by terminal deoxynucleotidyl transferase assay and confirmed by Annexin V detection. The expression of Bax-α, Bcl-2, p53 , and caspase-3 proteins was assessed by Western blot assays. The expression of BAX gene was assessed by Northern blot. Angiotensin II increased (P <0.01) cardiomyocyte apoptosis, and this effect was higher (P <0.001) in SHR cells than in WKY cells. Whereas losartan (10 mol/L) blocked the apoptotic effect of the octapeptide in cells from the two strains of rats, PD123319 (10 mol/L) inhibited angiotensin II–mediated apoptosis only in SHR cells. Angiotensin II stimulated (P <0.01) Bax-α protein, and this effect was higher (P <0.01) in SHR cells than in WKY cells. Angiotensin II did not modify Bcl-2, p53, and BAX mRNA in cells from the two strains of rats. Angiotensin II induced a similar increase (P <0.05) in the ratio caspase-3/procaspase-3 (an index of caspase-3 activation) in cardiomyocytes from the two strains of rats. The present in vitro results indicate that SHR cardiomyocytes exhibit enhanced susceptibility to angiotensin II–induced apoptosis. Ligand binding to angiotensin II type 1 and type 2 receptors leading to changes in posttranscriptional processing of Bax-α and accumulation of this proapoptotic protein may be involved in the abnormal response of SHR cardiomyocytes. These data support a role for angiotensin II in apoptosis observed in the left ventricle of these rats.</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>11116126</pmid><doi>10.1161/01.hyp.36.6.1065</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Angiotensin II - pharmacology Animals Apoptosis Arterial hypertension. Arterial hypotension bcl-2-Associated X Protein Biological and medical sciences Blood and lymphatic vessels Blood Pressure Cardiology. Vascular system Caspase 3 Caspases - metabolism Cells, Cultured Enzyme Activation Experimental diseases Heart - drug effects Heart Ventricles - drug effects Heart Ventricles - pathology Hypertension - complications Hypertension - pathology Hypertrophy, Left Ventricular - etiology Hypertrophy, Left Ventricular - pathology Male Medical sciences Myocardium - pathology Proto-Oncogene Proteins - genetics Proto-Oncogene Proteins - metabolism Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Rats, Inbred SHR Rats, Inbred WKY RNA, Messenger - metabolism Tumor Suppressor Protein p53 - metabolism |
| title | Mechanisms of Increased Susceptibility to Angiotensin II–Induced Apoptosis in Ventricular Cardiomyocytes of Spontaneously Hypertensive Rats |
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