أعرض تسجيلة المادة بشكل مبسط
| dc.contributor |
Widrick, Jeffrey J. |
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| dc.contributor |
Wilcox, Anthony |
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| dc.contributor |
Bella, Deborah |
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| dc.contributor |
Levenson, Rick |
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| dc.date |
2006-05-23T17:29:31Z |
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| dc.date |
2006-05-23T17:29:31Z |
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| dc.date |
2006-04-06 |
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| dc.date |
2006-05-23T17:29:31Z |
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| dc.date.accessioned |
2013-10-16T07:36:04Z |
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| dc.date.available |
2013-10-16T07:36:04Z |
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| dc.date.issued |
2013-10-16 |
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| dc.identifier |
http://hdl.handle.net/1957/1940 |
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| dc.identifier.uri |
http://koha.mediu.edu.my:8181/xmlui/handle/1957/1940 |
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| dc.description |
Graduation date: 2006 |
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| dc.description |
We hypothesized that calpain activity is elevated in response to muscle damage. To test this hypothesis, we examined the degradation of α-fodrin into its 150 and 145 kDa fragments following either 20 eccentric or isometric contractions. In addition, experiments were performed in the presence or absence of E-64-d, a calpain inhibitor. Both EDL and SOL muscles displayed significant differences (p<0.003 and p<0.002 respectively) between the raw and normalized 150 and 145 kDa α-fodrin fragments of the DMSO + E-64-d compared to the other bath treatments. Based on our model of exercise-induced muscle damage, we expected to see greater levels of 150 and 145 kDa α-fodrin fragments in those muscles that performed the eccentric protocol. However, there was no evidence that eccentric muscle damage increased the levels of 150 and 145 kDa α-fodrin fragments over the levels observed in the isometric trials. These findings suggest that the magnitude of damage was insufficient to activate calpains. |
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| dc.language |
en_US |
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| dc.subject |
calpain |
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| dc.subject |
E-64-d |
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| dc.subject |
eccentric muscle damage |
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| dc.title |
Effect of the calpain inhibitor E-64-d on the degradation of α-fodrin in damaged muscle |
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| dc.type |
Thesis |
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الملفات في هذه المادة
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لا توجد أي ملفات مرتبطة بهذه المادة.
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هذه المادة تبدو في المجموعات التالية:
أعرض تسجيلة المادة بشكل مبسط