Michael Haug
University of Erlangen-Nuremberg
21 Papers
17 Citations
Michael Haug is an academic researcher from University of Erlangen-Nuremberg. The author has contributed to research in topics: Skeletal muscle & Myofibril. The author has an hindex of 5, co-authored 13 publications.
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Papers
Optofluidic rotation of living cells for single-cell tomography.
TL;DR: An optofluidic device that combines a microfluidic system with a dual beam trap allows for the rotation of single cells in a continuous flow, around an axis perpendicular to the imaging plane, and enables the tomographic reconstruction of the 3D structure of the cell.
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Early signs of architectural and biomechanical failure in isolated myofibers and immortalized myoblasts from desmin-mutant knock-in mice
Stefanie Diermeier,Julian Iberl,Kristina Vetter,Michael Haug,Charlotte Pollmann,Barbara Reischl,Andreas Buttgereit,Sebastian Schürmann,Marina Spörrer,Wolfgang H. Goldmann,Ben Fabry,Fatiha Elhamine,Robert Stehle,Gabriele Pfitzer,Lilli Winter,Christoph S. Clemen,Christoph S. Clemen,Harald Herrmann,Rolf Schröder,Oliver Friedrich +19 more
TL;DR: It is demonstrated that mutant desmin alters myofibrillar cytoarchitecture, markedly disrupts the lateral sarcomere lattice and distorts myofbrillar angular axial orientation, and suggests that mutated desmin already markedly impedes myocyte structure and function at pre-symptomatic stages of myofBRillar myopathies.
Impact of prolonged sepsis on neural and muscular components of muscle contractions in a mouse model
Chloë Goossens,Ruben Weckx,Sarah Derde,Lawrence Van Helleputte,Lawrence Van Helleputte,Dominik Schneidereit,Michael Haug,Barbara Reischl,Oliver Friedrich,Ludo Van Den Bosch,Ludo Van Den Bosch,Greet Van den Berghe,Lies Langouche +12 more
TL;DR: In this article, the authors used a fluid-resuscitated, antibiotic-treated, parenterally fed murine model of prolonged (5-days) sepsis-induced muscle weakness (caecal ligation and puncture).
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Myofibrillar Lattice Remodeling Is a Structural Cytoskeletal Predictor of Diaphragm Muscle Weakness in a Fibrotic mdx (mdx Cmah−/−) Model
Paul Ritter,Stefanie Nübler,Andreas Buttgereit,Lucas R. Smith,Alexander Mühlberg,Julian Bauer,Mena Michael,Lucas Kreiß,Michael Haug,Elisabeth R. Barton,Oliver Friedrich +10 more
TL;DR: The results show that the mdx Cmah−/− genotype reproduces DMD-like fibrosis but is not associated with changes in passive visco-elastic muscle stiffness, and detriments in active isometric force are compatible with the pronounced myofibrillar disarray of the dystrophic background.
Absence of the Z-disc protein α-actinin-3 impairs the mechanical stability of Actn3KO mouse fast-twitch muscle fibres without altering their contractile properties or twitch kinetics
Michael Haug,Barbara Reischl,Stefanie Nübler,Leonit Kiriaev,Davi A. G. Mázala,Peter J. Houweling,Kathryn N. North,Oliver Friedrich,Stewart I. Head +8 more
TL;DR: In this article , single fast-twitch skeletal muscle fibres from the Actn3KO mouse were separated from the intact muscle by a collagenase digest procedure, and the absence of α-actinin-3 does not affect the visco-elastic properties or myofibrillar force production.