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Impaired autophagy,...
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Banduseela, VarunaUppsala universitet,Klinisk neurofysiologi
(author)
Impaired autophagy, chaperone expression, and protein synthesis in response to critical illness interventions in porcine skeletal muscle
- Article/chapterEnglish2013
Publisher, publication year, extent ...
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American Physiological Society,2013
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printrdacarrier
Numbers
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LIBRIS-ID:oai:DiVA.org:uu-183955
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https://urn.kb.se/resolve?urn=urn:nbn:se:uu:diva-183955URI
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https://doi.org/10.1152/physiolgenomics.00141.2012DOI
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http://kipublications.ki.se/Default.aspx?queryparsed=id:127066052URI
Supplementary language notes
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Language:English
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Summary in:English
Part of subdatabase
Classification
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Subject category:ref swepub-contenttype
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Subject category:art swepub-publicationtype
Notes
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Critical illness myopathy (CIM) is characterized by a preferential loss of the motor protein myosin, muscle wasting, and impaired muscle function in critically ill intensive care unit (ICU) patients. CIM is associated with severe morbidity and mortality and has a significant negative socioeconomic effect. Neuromuscular blocking agents, corticosteroids, sepsis, mechanical ventilation, and immobilization have been implicated as important risk factors, but the causal relationship between CIM and the risk factors has not been established. A porcine ICU model has been used to determine the immediate molecular and cellular cascades that may contribute to the pathogenesis prior to myosin loss and extensive muscle wasting. Expression profiles have been compared between pigs exposed to the ICU interventions, i.e., mechanically ventilated, sedated, and immobilized for 5 days, with pigs exposed to critical illness interventions, i.e., neuromuscular blocking agents, corticosteroids, and induced sepsis in addition to the ICU interventions for 5 days. Impaired autophagy as well as impaired chaperone expression and protein synthesis were observed in the skeletal muscle in response to critical illness interventions. A novel finding in this study is impaired core autophagy machinery in response to critical illness interventions, which when in concert with downregulated chaperone expression and protein synthesis may collectively affect the proteostasis in skeletal muscle and may exacerbate the disease progression in CIM.
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Added entries (persons, corporate bodies, meetings, titles ...)
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Chen, Yi-wen
(author)
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Göransson Kultima, HannaUppsala universitet,Cancerfarmakologi och beräkningsmedicin(Swepub:uu)hagor102
(author)
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Norman, HollyUppsala universitet,Klinisk neurofysiologi,Department of Medicine, University of Wisconsin, Madison, Wisconsin
(author)
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Aare, SudhakarUppsala universitet,Klinisk neurofysiologi(Swepub:uu)sudaa881
(author)
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Radell, PeterKarolinska Institutet
(author)
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Eriksson, LarsKarolinska Institutet
(author)
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Hoffman, Eric
(author)
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Larsson, LarsUppsala universitet,Klinisk neurofysiologi,Department of Biobehavioral Health, The Pennsylvania State University, University Park, Pennsylvania(Swepub:uu)lalar021
(author)
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Uppsala universitetKlinisk neurofysiologi
(creator_code:org_t)
Related titles
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In:Physiological Genomics: American Physiological Society45:12, s. 477-4861094-83411531-2267
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