O Friedrich

Summary

Affiliation: University of Heidelberg
Country: Germany

Publications

  1. Friedrich O, Both M, Weber C, Schurmann S, Teichmann M, von Wegner F, et al. Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle. Biophys J. 2010;98:606-16 pubmed publisher
  2. Friedrich O. Critical illness myopathy: what is happening?. Curr Opin Clin Nutr Metab Care. 2006;9:403-9 pubmed
    ..Targets for treatment or prevention of critical illness myopathy include systemic inflammatory response, increased proteolysis and reduced antioxidative capacitance in critically ill patients. ..
  3. Friedrich O. Critical illness myopathy: sepsis-mediated failure of the peripheral nervous system. Eur J Anaesthesiol Suppl. 2008;42:73-82 pubmed publisher
    ..This can open a series of new possible trials to test specific therapeutic strategies in the future. ..
  4. Friedrich O, Weber C, von Wegner F, Chamberlain J, Fink R. Unloaded speed of shortening in voltage-clamped intact skeletal muscle fibers from wt, mdx, and transgenic minidystrophin mice using a novel high-speed acquisition system. Biophys J. 2008;94:4751-65 pubmed publisher
    ..In mdx muscle, MLC-1f was significantly increased and MLC-2f and MLC-3f somewhat reduced. Fast initial active shortening seems almost unaffected in mdx muscle. ..
  5. Friedrich O, von Wegner F, Chamberlain J, Fink R, Rohrbach P. L-type Ca2+ channel function is linked to dystrophin expression in mammalian muscle. PLoS ONE. 2008;3:e1762 pubmed publisher
    ..g. impaired L-type Ca2+ currents. In regenerating mdx muscle, 'revertant' fibres restore dystrophin expression. Their functionality involving DHPR-Ca2+-channels is elusive...