Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig
Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of...
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Englisch |
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1996 |
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7 |
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Springer Online Journal Archives 1860-2002 |
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in: Basic research in cardiology - 1937, 91(1996) vom: Apr., Seite 289-295 |
Übergeordnetes Werk: |
volume:91 ; year:1996 ; month:04 ; pages:289-295 ; extent:7 |
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520 | |a Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. | ||
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(DE-627)NLEJ208631844 DE-627 ger DE-627 rakwb eng Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig 1996 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. Springer Online Journal Archives 1860-2002 Tønnessen, T. oth Ilebekk, A. oth Naess, P. A. oth Christensen, G. oth in Basic research in cardiology 1937 91(1996) vom: Apr., Seite 289-295 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:91 year:1996 month:04 pages:289-295 extent:7 http://dx.doi.org/10.1007/BF00789301 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 91 1996 4 289-295 7 |
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(DE-627)NLEJ208631844 DE-627 ger DE-627 rakwb eng Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig 1996 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. Springer Online Journal Archives 1860-2002 Tønnessen, T. oth Ilebekk, A. oth Naess, P. A. oth Christensen, G. oth in Basic research in cardiology 1937 91(1996) vom: Apr., Seite 289-295 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:91 year:1996 month:04 pages:289-295 extent:7 http://dx.doi.org/10.1007/BF00789301 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 91 1996 4 289-295 7 |
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(DE-627)NLEJ208631844 DE-627 ger DE-627 rakwb eng Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig 1996 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. Springer Online Journal Archives 1860-2002 Tønnessen, T. oth Ilebekk, A. oth Naess, P. A. oth Christensen, G. oth in Basic research in cardiology 1937 91(1996) vom: Apr., Seite 289-295 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:91 year:1996 month:04 pages:289-295 extent:7 http://dx.doi.org/10.1007/BF00789301 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 91 1996 4 289-295 7 |
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(DE-627)NLEJ208631844 DE-627 ger DE-627 rakwb eng Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig 1996 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. Springer Online Journal Archives 1860-2002 Tønnessen, T. oth Ilebekk, A. oth Naess, P. A. oth Christensen, G. oth in Basic research in cardiology 1937 91(1996) vom: Apr., Seite 289-295 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:91 year:1996 month:04 pages:289-295 extent:7 http://dx.doi.org/10.1007/BF00789301 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 91 1996 4 289-295 7 |
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(DE-627)NLEJ208631844 DE-627 ger DE-627 rakwb eng Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig 1996 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. Springer Online Journal Archives 1860-2002 Tønnessen, T. oth Ilebekk, A. oth Naess, P. A. oth Christensen, G. oth in Basic research in cardiology 1937 91(1996) vom: Apr., Seite 289-295 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:91 year:1996 month:04 pages:289-295 extent:7 http://dx.doi.org/10.1007/BF00789301 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 91 1996 4 289-295 7 |
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Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. |
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Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. |
abstract_unstemmed |
Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">NLEJ208631844</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707021428.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1996 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ208631844</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Inhibition of granulocyte-derived proteases reduces the increase in plasma endothelin associated with myocardial ischemia in the pig</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1996</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">7</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Abstract Plasma endothelin (ET) is increased in association with myocardial infarction. The aim of the present study was to get insight into the mechanisms behind this ischemiainduced increase in plasma ET. Since granulocytes increase ET production in vitro, we examined to what extent inhibition of granulocyte-derived proteases could reduce the increase in plasma ET observed in association with myocardial ischemia. We infused Eglin C, a selective inhibitor of the granulocyte-derived proteases elastase, cathepsin G, and chymotrypsin, in pigs subjected to 90 min left anterior descending coronary artery occlusion followed by 210 min reperfusion (n=7). Arterial plasma ET increased in an untreated control group (n=7) from 5.0±0.6 (mean ±SEM) fmol· ml−1 before myocardial ischemia to 6.1±0.6 fmol·ml−1 at 90 min ischemia and reached a maximum of 6.8±0.9 fmol·ml−1 at 90 min reperfusion. The increase in plasma ET associated with myocardial ischemia was almost completely abolished in the Eglin C treated group (p=0.005). Plasma ET in the Eglin C treated animals was 4.7±0.4,4.7±0.4, and 4.6±0.4 fmol· ml−1 before myocardial ischemia, at 90 min ischemia, and at 90 min reperfusion, respectively. Our study suggests a role for granulocytederived proteases in the increase in plasma ET associated with myocardial ischemia. We have shown that the increase in plasma ET associated with myocardial ischemia was reduced by inhibition of granulocytederived proteases using the selective protease inhibitor Eglin C.</subfield></datafield><datafield tag="533" ind1=" " ind2=" "><subfield code="f">Springer Online Journal Archives 1860-2002</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Tønnessen, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ilebekk, A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Naess, P. A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Christensen, G.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Basic research in cardiology</subfield><subfield code="d">1937</subfield><subfield code="g">91(1996) vom: Apr., Seite 289-295</subfield><subfield code="w">(DE-627)NLEJ188985204</subfield><subfield code="w">(DE-600)1458470-0</subfield><subfield code="x">1435-1803</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:91</subfield><subfield code="g">year:1996</subfield><subfield code="g">month:04</subfield><subfield code="g">pages:289-295</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF00789301</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">ZDB-1-SOJ</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_NL_ARTICLE</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">91</subfield><subfield code="j">1996</subfield><subfield code="c">4</subfield><subfield code="h">289-295</subfield><subfield code="g">7</subfield></datafield></record></collection>
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