Disruption of sarcolemmal dystrophin and beta-dystroglycan may be a potential mechanism for myocardial dysfunction in severe sepsis.
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Disruption of calcium homeostasis in cardiomyocytes underlies cardiac structural and functional changes in severe sepsis.Activation of Both the Calpain and Ubiquitin-Proteasome Systems Contributes to Septic Cardiomyopathy through Dystrophin Loss/Disruption and mTOR InhibitionInhibition of Coxsackievirus-associated dystrophin cleavage prevents cardiomyopathy.Loss of duplexmiR-223 (5p and 3p) aggravates myocardial depression and mortality in polymicrobial sepsis.Early dystrophin loss is coincident with the transition of compensated cardiac hypertrophy to heart failure.Pathophysiology, echocardiographic evaluation, biomarker findings, and prognostic implications of septic cardiomyopathy: a review of the literature.
P2860
Disruption of sarcolemmal dystrophin and beta-dystroglycan may be a potential mechanism for myocardial dysfunction in severe sepsis.
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2010 nî lūn-bûn
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2010年の論文
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2010年学术文章
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2010年学术文章
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2010年学术文章
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2010年学术文章
@zh-my
2010年学术文章
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2010年學術文章
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2010年學術文章
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2010年學術文章
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name
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@en
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@nl
type
label
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@en
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@nl
prefLabel
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@en
Disruption of sarcolemmal dyst ...... dysfunction in severe sepsis.
@nl
P2093
P2860
P50
P356
P1476
Disruption of sarcolemmal dyst ...... l dysfunction in severe sepsis
@en
P2093
Diego Torres-Dueñas
Erica C Campos
Lygia M Malvestio
Marcos A Rossi
Simone G Ramos
Valdecir Blefari
P2860
P2888
P304
P356
10.1038/LABINVEST.2010.3
P577
2010-02-08T00:00:00Z