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Annette Zippelius
Researcher at University of Göttingen
Publications - 174
Citations - 3593
Annette Zippelius is an academic researcher from University of Göttingen. The author has contributed to research in topics: Critical exponent & Amorphous solid. The author has an hindex of 29, co-authored 170 publications receiving 3342 citations. Previous affiliations of Annette Zippelius include Kavli Institute for Theoretical Physics & Max Planck Society.
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Relaxational dynamics of the Edwards-Anderson model and the mean-field theory of spin-glasses
TL;DR: In this article, an exact uniform Lagrangian for the average dynamic correlation and response functions is derived for arbitrary range of random exchange, using a functional-integral method proposed by De Dominicis.
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Energy Landscape of a Lennard-Jones Liquid: Statistics of Stationary Points
TL;DR: Molecular dynamics simulations are used to generate an ensemble of saddles of the potential energy of a Lennard-Jones liquid, classifying all extrema by their potential energy u and number of unstable directions k, and a well-defined relation k(u) is revealed.
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Mechanical Properties of Spider Dragline Silk: Humidity, Hysteresis, and Relaxation
TL;DR: It is found that the relaxation process is well described by a stretched exponential decay, which makes it plausible that the variation in the literature values can to a large extent be attributed to changes in RH.
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Heterogeneous Presynaptic Release Probabilities: Functional Relevance for Short-Term Plasticity
Julia Trommershäuser,Julia Trommershäuser,Ralf Schneggenburger,Annette Zippelius,Erwin Neher +4 more
TL;DR: It is concluded that synaptic transmission cannot be accurately described unless heterogeneity of synaptic release probability is taken into account.
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Impairment of mitochondrial calcium handling in a mtSOD1 cell culture model of motoneuron disease
Manoj Kumar Jaiswal,Wolf-Dieter Zech,Miriam Goos,Christine Leutbecher,Alberto Ferri,Annette Zippelius,Maria Teresa Carrì,Roland Nau,Bernhard U. Keller +8 more
TL;DR: The present evidence supports a hypothesis that mitochondria are a target of mutant SOD1-mediated toxicity in familial amyotrophic lateral sclerosis (fALS) and intracellular alterations of cytosolic and mitochondrial calcium might aggravate the course of this neurodegenerative disease.