Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN)
Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been...
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Englisch |
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2000 |
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7 |
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Springer Online Journal Archives 1860-2002 |
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in: Experimental brain research - 1966, 130(2000) vom: Jan., Seite 60-66 |
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volume:130 ; year:2000 ; month:01 ; pages:60-66 ; extent:7 |
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| 520 | |a Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. | ||
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(DE-627)NLEJ202255069 DE-627 ger DE-627 rakwb eng Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. Springer Online Journal Archives 1860-2002 Schmid-Elsaesser, R. oth Hungerhuber, E. oth Zausinger, S. oth Baethmann, A. oth Reulen, H. -J. oth in Experimental brain research 1966 130(2000) vom: Jan., Seite 60-66 (DE-627)NLEJ188991840 (DE-600)1459099-2 1432-1106 nnns volume:130 year:2000 month:01 pages:60-66 extent:7 http://dx.doi.org/10.1007/s002210050006 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 130 2000 1 60-66 7 |
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(DE-627)NLEJ202255069 DE-627 ger DE-627 rakwb eng Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. Springer Online Journal Archives 1860-2002 Schmid-Elsaesser, R. oth Hungerhuber, E. oth Zausinger, S. oth Baethmann, A. oth Reulen, H. -J. oth in Experimental brain research 1966 130(2000) vom: Jan., Seite 60-66 (DE-627)NLEJ188991840 (DE-600)1459099-2 1432-1106 nnns volume:130 year:2000 month:01 pages:60-66 extent:7 http://dx.doi.org/10.1007/s002210050006 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 130 2000 1 60-66 7 |
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(DE-627)NLEJ202255069 DE-627 ger DE-627 rakwb eng Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. Springer Online Journal Archives 1860-2002 Schmid-Elsaesser, R. oth Hungerhuber, E. oth Zausinger, S. oth Baethmann, A. oth Reulen, H. -J. oth in Experimental brain research 1966 130(2000) vom: Jan., Seite 60-66 (DE-627)NLEJ188991840 (DE-600)1459099-2 1432-1106 nnns volume:130 year:2000 month:01 pages:60-66 extent:7 http://dx.doi.org/10.1007/s002210050006 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 130 2000 1 60-66 7 |
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(DE-627)NLEJ202255069 DE-627 ger DE-627 rakwb eng Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. Springer Online Journal Archives 1860-2002 Schmid-Elsaesser, R. oth Hungerhuber, E. oth Zausinger, S. oth Baethmann, A. oth Reulen, H. -J. oth in Experimental brain research 1966 130(2000) vom: Jan., Seite 60-66 (DE-627)NLEJ188991840 (DE-600)1459099-2 1432-1106 nnns volume:130 year:2000 month:01 pages:60-66 extent:7 http://dx.doi.org/10.1007/s002210050006 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 130 2000 1 60-66 7 |
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(DE-627)NLEJ202255069 DE-627 ger DE-627 rakwb eng Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. Springer Online Journal Archives 1860-2002 Schmid-Elsaesser, R. oth Hungerhuber, E. oth Zausinger, S. oth Baethmann, A. oth Reulen, H. -J. oth in Experimental brain research 1966 130(2000) vom: Jan., Seite 60-66 (DE-627)NLEJ188991840 (DE-600)1459099-2 1432-1106 nnns volume:130 year:2000 month:01 pages:60-66 extent:7 http://dx.doi.org/10.1007/s002210050006 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 130 2000 1 60-66 7 |
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Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) |
| abstract |
Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. |
| abstractGer |
Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. |
| abstract_unstemmed |
Abstract Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified. |
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Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN) |
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http://dx.doi.org/10.1007/s002210050006 |
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Schmid-Elsaesser, R. Hungerhuber, E. Zausinger, S. Baethmann, A. Reulen, H. -J. |
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Schmid-Elsaesser, R. Hungerhuber, E. Zausinger, S. Baethmann, A. Reulen, H. -J. |
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NLEJ188991840 |
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2024-07-06T07:22:45.246Z |
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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">NLEJ202255069</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230506102748.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070527s2000 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ202255069</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">Neuroprotective effects of the novel brain-penetrating antioxidant U-101033E and the spin-trapping agent α-phenyl-N-tert-butyl nitrone (PBN)</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2000</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 Literature on the therapeutic efficacy of free radical scavengers suggests that drugs that are able to cross the blood-brain barrier are more effective in protecting the brain from ischemic damage. However, the exact mechanisms by which brain-penetrating antioxidants act have yet not been delineated. We compared the neuroprotective potential of the newly discovered pyrrolopyrimidine U-101033E with that of α-phenyl-N-tert-butyl nitrone (PBN) and investigated their influence on cerebral blood flow. Thirty male Sprague-Dawley rats were subjected to 90 min of middle cerebral artery (MCA) occlusion by an intraluminal filament. Local cerebral blood flow (LCBF) was bilaterally recorded by laser Doppler flowmetry. Neurological deficits were quantified daily. Infarct volume was assessed after 7 days. MCA occlusion reduced ipsilateral LCBF to 20–30% of baseline. After reperfusion, postischemic hyperemia was followed by a decrease in LCBF to about 70% of baseline. There was no difference in LCBF among groups. U-101033E improved neurological function and reduced infarct volume by 52% (P<0.05). Improvement of neurological function and reduction of infarct volume (–25%) in animals treated with PBN was not significant. We conclude that U-101033E has superior neuroprotective properties compared with PBN. Neither drug improves blood flow during ischemia and 1 h of reperfusion. The mechanisms by which these brain-penetrating antioxidants act remain to be clarified.</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">Schmid-Elsaesser, R.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hungerhuber, E.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zausinger, S.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Baethmann, A.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Reulen, H. -J.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Experimental brain research</subfield><subfield code="d">1966</subfield><subfield code="g">130(2000) vom: Jan., Seite 60-66</subfield><subfield code="w">(DE-627)NLEJ188991840</subfield><subfield code="w">(DE-600)1459099-2</subfield><subfield code="x">1432-1106</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:130</subfield><subfield code="g">year:2000</subfield><subfield code="g">month:01</subfield><subfield code="g">pages:60-66</subfield><subfield code="g">extent:7</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/s002210050006</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">130</subfield><subfield code="j">2000</subfield><subfield code="c">1</subfield><subfield code="h">60-66</subfield><subfield code="g">7</subfield></datafield></record></collection>
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