O Friedrich

Summary

Affiliation: University of Heidelberg
Country: Germany

Publications

  1. pmc Inhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expression
    Martin D H Teichmann
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    PLoS ONE 3:e3644. 2008
  2. pmc Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    Biophys J 98:606-16. 2010
  3. ncbi Critical illness myopathy: what is happening?
    Oliver Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, Ruprecht Karls University of Heidelberg, Heidelberg, Germany
    Curr Opin Clin Nutr Metab Care 9:403-9. 2006
  4. ncbi [Critical illness myopathy in intensive care patients. Pathogenetic concepts and clinical management]
    O Friedrich
    Medizinische Biophysik, Abt Systemphysioligie, Institut fur Physiologie und Pathophysiologie, Ruprecht Karls Universitat, Im Neuenheimer Feld 326, 69120 Heidelberg
    Anaesthesist 55:1271-80. 2006
  5. ncbi NA+- and K+-channels as molecular targets of the alkaloid ajmaline in skeletal muscle fibres
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, University Heidelberg, Heidelberg, Germany
    Br J Pharmacol 151:82-93. 2007
  6. doi Critical illness myopathy: sepsis-mediated failure of the peripheral nervous system
    O Friedrich
    Ruprecht Karls University, Institute of Physiology and Pathophysiology, Department of System Physiology, Medical Biophysics, Heidelberg, Germany
    Eur J Anaesthesiol Suppl 42:73-82. 2008
  7. pmc 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
    O Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    Biophys J 94:4751-65. 2008
  8. pmc L-type Ca2+ channel function is linked to dystrophin expression in mammalian muscle
    Oliver Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, Heidelberg, Germany
    PLoS ONE 3:e1762. 2008
  9. doi Enhanced muscle shortening and impaired Ca2+ channel function in an acute septic myopathy model
    Oliver Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, INF 326, 69120, Heidelberg, Germany
    J Neurol 257:546-55. 2010
  10. pmc Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, INF 326, Ruprecht Karls University, 69120 Heidelberg, Germany
    J Physiol 555:251-65. 2004

Collaborators

Detail Information

Publications30

  1. pmc Inhibitory control over Ca(2+) sparks via mechanosensitive channels is disrupted in dystrophin deficient muscle but restored by mini-dystrophin expression
    Martin D H Teichmann
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    PLoS ONE 3:e3644. 2008
    ..They may be related to mechanosensitive pathways but the mechanisms are elusive. Also, it is not known whether truncated dystrophins can correct the dystrophic disinhibition...
  2. pmc Microarchitecture is severely compromised but motor protein function is preserved in dystrophic mdx skeletal muscle
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    Biophys J 98:606-16. 2010
    ....
  3. ncbi Critical illness myopathy: what is happening?
    Oliver Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, Ruprecht Karls University of Heidelberg, Heidelberg, Germany
    Curr Opin Clin Nutr Metab Care 9:403-9. 2006
    ..Trends and concepts of clinical diagnosis and handling will be evaluated and their implications for muscle physiology and nutritional/metabolic intervention discussed...
  4. ncbi [Critical illness myopathy in intensive care patients. Pathogenetic concepts and clinical management]
    O Friedrich
    Medizinische Biophysik, Abt Systemphysioligie, Institut fur Physiologie und Pathophysiologie, Ruprecht Karls Universitat, Im Neuenheimer Feld 326, 69120 Heidelberg
    Anaesthesist 55:1271-80. 2006
    ..This article focuses on current concepts and results revealing the pathomechanism(s) of CIM and some simple therapeutic or preventive measures have been deduced which are summarized and discussed...
  5. ncbi NA+- and K+-channels as molecular targets of the alkaloid ajmaline in skeletal muscle fibres
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, University Heidelberg, Heidelberg, Germany
    Br J Pharmacol 151:82-93. 2007
    ..Ajmaline is a widely used antiarrhythmic drug. Its action on voltage-gated ion channels in skeletal muscle is not well documented and we have here elucidated its effects on Na(+) and K(+) channels...
  6. doi Critical illness myopathy: sepsis-mediated failure of the peripheral nervous system
    O Friedrich
    Ruprecht Karls University, Institute of Physiology and Pathophysiology, Department of System Physiology, Medical Biophysics, Heidelberg, Germany
    Eur J Anaesthesiol Suppl 42:73-82. 2008
    ..This can open a series of new possible trials to test specific therapeutic strategies in the future...
  7. pmc 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
    O Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, Ruprecht Karls University, Heidelberg, Germany
    Biophys J 94:4751-65. 2008
    ..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...
  8. pmc L-type Ca2+ channel function is linked to dystrophin expression in mammalian muscle
    Oliver Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, Heidelberg, Germany
    PLoS ONE 3:e1762. 2008
    ..g. impaired L-type Ca2+ currents. In regenerating mdx muscle, 'revertant' fibres restore dystrophin expression. Their functionality involving DHPR-Ca2+-channels is elusive...
  9. doi Enhanced muscle shortening and impaired Ca2+ channel function in an acute septic myopathy model
    Oliver Friedrich
    Medical Biophysics, Department of Systems Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, INF 326, 69120, Heidelberg, Germany
    J Neurol 257:546-55. 2010
    ..The acute challenge model is also robust against atrophy or fibre type changes that ordinarily would have to be considered in chronic sepsis models...
  10. pmc Mini-dystrophin restores L-type calcium currents in skeletal muscle of transgenic mdx mice
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, INF 326, Ruprecht Karls University, 69120 Heidelberg, Germany
    J Physiol 555:251-65. 2004
    ..This linkage seems to be fully restored in the presence of mini-dystrophin...
  11. ncbi Prolonged high-pressure treatments in mammalian skeletal muscle result in loss of functional sodium channels and altered calcium channel kinetics
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, INF 326, Ruprecht Karls University, Heidelberg, Germany
    Cell Biochem Biophys 45:71-83. 2006
    ..Based on these results, a model of high pressure-induced alterations to the channel conformation is proposed...
  12. pmc Numerical analysis of Ca2+ depletion in the transverse tubular system of mammalian muscle
    O Friedrich
    Institute of Physiology and Pathophysiology, Medical Biophysics, University of Heidelberg, INF 326, D-69120 Heidelberg, Germany
    Biophys J 80:2046-55. 2001
    ..From our findings, we conclude that ion depletion in the tubular system may be one of the major effects for the I(Ca) decline measured in isotonic physiological solution under voltage clamp conditions...
  13. ncbi 'In situ' high pressure confocal Ca(2+)-fluorescence microscopy in skeletal muscle: a new method to study pressure limits in mammalian cells
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, INF 326, Ruprecht Karls University, Heidelberg, Germany
    Undersea Hyperb Med 33:181-95. 2006
    ..The pressure induced disturbance of Ca2+ homeostasis might have important implications for the pressure exposure limits and/or dive profiles of deep sea mammals...
  14. ncbi Elementary Ca2+ release events in mammalian skeletal muscle: effects of the anaesthetic drug thiopental
    F v Wegner
    Medical Biophysics, Institute for Physiology and Pathophysiology, University of Heidelberg, INF 326, D 69120, Heidelberg, Germany
    J Muscle Res Cell Motil 27:315-26. 2006
    ..In summary, thiopental seems to be a potent RyR1 agonist and substantially alters the gating mechanisms of RyR Ca2+ release channel clusters already in clinically relevant doses, i.e. doses administered during general anaesthesia...
  15. ncbi Critical illness myopathy serum fractions affect membrane excitability and intracellular calcium release in mammalian skeletal muscle
    Oliver Friedrich
    Medical Biophysics Institute of Physiology and Pathophysiology, Ruprecht Karls University, Im Neuenheimer Feld 326, Heidelberg, Germany
    J Neurol 251:53-65. 2004
    ....
  16. ncbi Reversibility of high pressure effects on the contractility of skeletal muscle
    K R Kress
    Institute of Physiology and Pathophysiology, Ruprecht-Karls-University, Heidelberg, Germany
    J Muscle Res Cell Motil 22:379-89. 2001
    ..e. Troponin T, shown by SDS gel electrophoresis. However, the general stability of the other bands does not indicate a substantial increase of unspecific protease activity following a high pressure treatment up to 25 MPa...
  17. ncbi Membrane ion conductances of mammalian skeletal muscle in the post-decompression state after high-pressure treatment
    O Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, Ruprecht Karls University, INF 326, 69120 Heidelberg, Germany
    J Membr Biol 188:11-22. 2002
    ..For higher pressure applications (e.g., 25 MPa), there seemed to be a marked loss of membrane integrity and INa, IK and ICa almost disappeared...
  18. doi Orai1 and Stim1 regulate normal and hypertrophic growth in cardiomyocytes
    Mirko Voelkers
    Department of Internal Medicine III, Laboratory for Molecular and Translational Cardiology, Division of Cardiology, INF 350, University of Heidelberg, 69120 Heidelberg, Germany
    J Mol Cell Cardiol 48:1329-34. 2010
    ..This study shows for the first time that both Orai1 and Stim1 have a key role in cardiomyocyte SOCE regulating both normal and hypertrophic postnatal cardiac growth in vitro...
  19. doi Motor protein function in skeletal muscle-a multiple scale approach to contractility
    Frederic von Wegner
    Medical Biophysics Group, Institute of Physiology, University of Heidelberg, 69120 Heidelberg, Germany
    IEEE Trans Med Imaging 28:1632-42. 2009
    ..Our approach is feasible to explain the possible underlying mechanisms that contribute to different shortening velocities at different scales and complexities...
  20. ncbi Second harmonic imaging of intrinsic signals in muscle fibers in situ
    Martin Both
    Ruprecht Karls Universitat, Institut fur Physiologie und Pathophysiologie, Medical Biophysics Unit, Im Neuenheimer Feld 326, D 69120 Heidelberg, Germany
    J Biomed Opt 9:882-92. 2004
    ....
  21. ncbi Fast XYT imaging of elementary calcium release events in muscle with multifocal multiphoton microscopy and wavelet denoising and detection
    Frederic von Wegner
    Medical Biophysics Group, Institute of Physiology and Pathophysiology, University of Heidelberg, Heidelberg BW 69120, Germany
    IEEE Trans Med Imaging 26:925-34. 2007
    ..The proposed method allows a detailed spatiotemporal analysis of elementary Ca2+ release events underlying the excitation-contraction coupling process in muscle...
  22. ncbi Understanding critical illness myopathy: approaching the pathomechanism
    Oliver Friedrich
    Medical Biophysics, Institute of Physiology and Pathophysiology, University of Heidelberg, INF 326, 69120 Heidelberg, Germany
    J Nutr 135:1813S-1817S. 2005
    ..Establishing the interactions in the excitation-contraction cascade in CIM is a challenging task, not only to clarify its pathomechanism but also to deduce clinical interventions...
  23. doi Resting membrane potentials recorded on-site in intact skeletal muscles from deep sea fish (Sigmops gracile) salvaged from depths up to 1.000 m
    Frederic von Wegner
    Medical Biophysics Unit, Department of Systems Physiology, Institute of Physiology and Pathophysiology, University of Heidelberg, Heidelberg, Germany
    Mar Biotechnol (NY) 10:478-86. 2008
    ..These data are expected to more realistically reflect the physiological state of biological preparations residing in the deep sea...
  24. doi Velocity distributions of single F-actin trajectories from a fluorescence image series using trajectory reconstruction and optical flow mapping
    Frederic von Wegner
    University of Heidelberg, Institute of Physiology and Pathophysiology, Medical Biophysics Group, Im Neuenheimer Feld 326, 69120 Heidelberg, Germany
    J Biomed Opt 13:054018. 2008
    ..The presented approach may prove helpful to identify actin filament subpopulations and to analyze actin-myosin interaction kinetics under biochemical regulation...
  25. ncbi Ketamine stereoselectively inhibits spontaneous Ca2+-oscillations in cultured hippocampal neurons
    Barbara Sinner
    Department of Anesthesiology, University of Heidelberg, Im Neuenheimer Feld 110, 69120 Heidelberg, Germany
    Anesth Analg 100:1660-6. 2005
    ....
  26. ncbi S100A1 decreases calcium spark frequency and alters their spatial characteristics in permeabilized adult ventricular cardiomyocytes
    Mirko Völkers
    Department of Internal Medicine III, Laboratory for Cardiac Stem Cell and Gene Therapy, Division of Cardiology, INF 350, University of Heidelberg, 69120 Heidelberg, Germany
    Cell Calcium 41:135-43. 2007
    ..6) remained unaltered by S100A1. Hence, we propose S100A1 as a novel inhibitory modulator of RyR2 function at diastolic Ca2+-concentrations in rabbit ventricular cardiomyocytes...
  27. doi Deficient zebrafish ether-à-go-go-related gene channel gating causes short-QT syndrome in zebrafish reggae mutants
    David Hassel
    Department of Internal Medicine III, University Hospital Heidelberg, Im Neuenheimer Feld 410, 69120 Heidelberg, Germany
    Circulation 117:866-75. 2008
    ..Genetic predisposition is believed to be responsible for most clinically significant arrhythmias; however, suitable genetic animal models to study disease mechanisms and evaluate new treatment strategies are largely lacking...
  28. ncbi Evidence for activation of endogenous transporters in Xenopus laevis oocytes expressing the Plasmodium falciparum chloroquine resistance transporter, PfCRT
    Susanne Nessler
    Hygiene Institut, Abteilung Parasitologie, Universitatsklinikum Heidelberg, Im Neuenheimer Feld 324, D 69120 Heidelberg, Germany
    J Biol Chem 279:39438-46. 2004
    ..laevis oocytes, supports a model in which PfCRT activates transport systems. Our data suggest that PfCRT plays a role as a direct or indirect activator or modulator of other transporters...
  29. ncbi Depolarisation of the plasma membrane in the arsenic trioxide (As2O3)-and anti-CD95-induced apoptosis in myeloid cells
    Florian Nolte
    Department of Transfusion Medicine, University of Ulm, Institute for Clinical Transfusion Medicine and Immunogenetics, Ulm, Germany
    FEBS Lett 578:85-9. 2004
    ..However, none of these ions contributed significantly to anti-Fas induced depolarisation. This indicates the existence of different mechanisms for apoptotic plasma membrane depolarisation within one cell type...
  30. ncbi Quantitative calcium measurements in subcellular compartments of Plasmodium falciparum-infected erythrocytes
    Petra Rohrbach
    Hygiene Institut, Abteilung Parasitologie, Universitatsklinikum Heidelberg, Im Neuenheimer Feld 324, D 69120 Heidelberg, Germany
    J Biol Chem 280:27960-9. 2005
    ..Our data suggest that the food vacuole contains only moderate amounts of Ca2+, disfavoring a role as a major intracellular Ca2+ store...