Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries
Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, usin...
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
1989 |
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| Umfang: |
6 |
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Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Acta neurochirurgica - 1950, 97(1989) vom: Jan./Feb., Seite 77-82 |
| Übergeordnetes Werk: |
volume:97 ; year:1989 ; month:01/02 ; pages:77-82 ; extent:6 |
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NLEJ208134824 |
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| 520 | |a Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. | ||
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(DE-627)NLEJ208134824 DE-627 ger DE-627 rakwb eng Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. Springer Online Journal Archives 1860-2002 Nakagomi, T. oth Kassell, N. F. oth Sasaki, T. oth Hongo, K. oth Fujiwara, Sh. oth Lehman, R. M. oth Vollmer, D. G. oth in Acta neurochirurgica 1950 97(1989) vom: Jan./Feb., Seite 77-82 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:97 year:1989 month:01/02 pages:77-82 extent:6 http://dx.doi.org/10.1007/BF01577744 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 97 1989 1/2 77-82 6 |
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(DE-627)NLEJ208134824 DE-627 ger DE-627 rakwb eng Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. Springer Online Journal Archives 1860-2002 Nakagomi, T. oth Kassell, N. F. oth Sasaki, T. oth Hongo, K. oth Fujiwara, Sh. oth Lehman, R. M. oth Vollmer, D. G. oth in Acta neurochirurgica 1950 97(1989) vom: Jan./Feb., Seite 77-82 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:97 year:1989 month:01/02 pages:77-82 extent:6 http://dx.doi.org/10.1007/BF01577744 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 97 1989 1/2 77-82 6 |
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(DE-627)NLEJ208134824 DE-627 ger DE-627 rakwb eng Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. Springer Online Journal Archives 1860-2002 Nakagomi, T. oth Kassell, N. F. oth Sasaki, T. oth Hongo, K. oth Fujiwara, Sh. oth Lehman, R. M. oth Vollmer, D. G. oth in Acta neurochirurgica 1950 97(1989) vom: Jan./Feb., Seite 77-82 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:97 year:1989 month:01/02 pages:77-82 extent:6 http://dx.doi.org/10.1007/BF01577744 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 97 1989 1/2 77-82 6 |
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(DE-627)NLEJ208134824 DE-627 ger DE-627 rakwb eng Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. Springer Online Journal Archives 1860-2002 Nakagomi, T. oth Kassell, N. F. oth Sasaki, T. oth Hongo, K. oth Fujiwara, Sh. oth Lehman, R. M. oth Vollmer, D. G. oth in Acta neurochirurgica 1950 97(1989) vom: Jan./Feb., Seite 77-82 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:97 year:1989 month:01/02 pages:77-82 extent:6 http://dx.doi.org/10.1007/BF01577744 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 97 1989 1/2 77-82 6 |
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(DE-627)NLEJ208134824 DE-627 ger DE-627 rakwb eng Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries 1989 6 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. Springer Online Journal Archives 1860-2002 Nakagomi, T. oth Kassell, N. F. oth Sasaki, T. oth Hongo, K. oth Fujiwara, Sh. oth Lehman, R. M. oth Vollmer, D. G. oth in Acta neurochirurgica 1950 97(1989) vom: Jan./Feb., Seite 77-82 (DE-627)NLEJ188985085 (DE-600)1464215-3 0942-0940 nnns volume:97 year:1989 month:01/02 pages:77-82 extent:6 http://dx.doi.org/10.1007/BF01577744 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 97 1989 1/2 77-82 6 |
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effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries |
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Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries |
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Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. |
| abstractGer |
Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. |
| abstract_unstemmed |
Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid. |
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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">NLEJ208134824</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20210707005422.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">070528s1989 xx |||||o 00| ||eng c</controlfield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)NLEJ208134824</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">Effect of hypoxia on endothelium-dependent relaxation of canine and rabbit basilar arteries</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">1989</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">6</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">Summary An important role of endothelium-dependent relaxation in the local regulation of vascular tone has been suggested. In the present study, the effect of hypoxia on endothelium-dependent relaxation was investigated in canine and rabbit basilar and in rabbit common carotid arteriesin vitro, using an isometric tension recording method. Hypoxia was introduced by changing the gas mixture in thein vitro chamber from 95% O2-5% CO2 to 95% N2-5% CO2. Thrombin and acetylcholine were used to induce endothelium-dependent relaxation. Thrombin at 0.1 and 1.0U/ml, respectively, caused dose-dependent relaxation of the canine basilar artery precontracted by 10−6M prostaglandin F2α. Acetylcholine also evoked dose-dependent relaxation of rabbit basilar and common carotid arteries precontracted by serotonin. Under hypoxic conditions, the relaxing effect of thrombin or acetylcholine decreased both in canine and in rabbit arteries, although it was not significant in rabbit basilar arteries. It has been postulated that following subarachnoid haemorrhage, diffusion of oxygen to the walls of the major cerebral arteries might be impaired by the subarachnoid clot. This could cause hypoxia of the arteries and contribute to vasospasm by suppressing endothelium-dependent relaxation, as well as by enhancing the contractile responses of the cerebral arteries to the vasoconstrictor agents in the bloody cerebrospinal fluid.</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">Nakagomi, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Kassell, N. F.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Sasaki, T.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hongo, K.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Fujiwara, Sh.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lehman, R. M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Vollmer, D. G.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">in</subfield><subfield code="t">Acta neurochirurgica</subfield><subfield code="d">1950</subfield><subfield code="g">97(1989) vom: Jan./Feb., Seite 77-82</subfield><subfield code="w">(DE-627)NLEJ188985085</subfield><subfield code="w">(DE-600)1464215-3</subfield><subfield code="x">0942-0940</subfield><subfield code="7">nnns</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:97</subfield><subfield code="g">year:1989</subfield><subfield code="g">month:01/02</subfield><subfield code="g">pages:77-82</subfield><subfield code="g">extent:6</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">http://dx.doi.org/10.1007/BF01577744</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">97</subfield><subfield code="j">1989</subfield><subfield code="c">1/2</subfield><subfield code="h">77-82</subfield><subfield code="g">6</subfield></datafield></record></collection>
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