The origin of stiffening in cross-linked semiflexible networks

Strain stiffening of protein networks is explored by means of a finite strain analysis of a two-dimensional network model of cross-linked semiflexible filaments. The results show that stiffening is caused by non-affine network rearrangements that govern a transition from a bending dominated response at small strains to a stretching dominated response at large strains. Thermally-induced filament undulations only have a minor effect; they merely postpone the transition.Comment: 5 pages, 5 figure

Anisotropic plastic deformation by viscous flow in ion tracks

A model describing the origin of ion beam-induced anisotropic plastic deformation is derived and discussed. It is based on a viscoelastic thermal spike model for viscous flow in single ion tracks derived by Trinkaus and Ryazanov. Deviatoric (shear) stresses, brought about by the rapid thermal expansion of the thermal spike, relax at ion track temperatures beyond a certain flow temperature. Shear stress relaxation is accompanied by the generation of viscous strains. The model introduces differential equations describing the time evolution of the radial and axial stresses, enabling an exact derivation of the viscous strains for any ion track temperature history T(t). It is shown that the viscous strains effectively freeze in for large track cooling rates, whereas reverse viscous flow reduces the net viscous strains in the ion track for smaller cooling rates. The model is extended to include finite-size effects that occur for ion tracks close to the sample edge, enabling a comparison with experimental results for systems with small size. The "effective flow temperature approach" that was earlier introduced by Trinkaus and Ryazanov by making use of Eshelby's theory of elastic inclusions, follows directly from the viscoelastic model as a limiting case. We show that the viscous strains in single ion tracks are the origin of the macroscopic anisotropic deformation process. The macroscopic deformation rate can be directly found by superposing the effects of single ion impacts. By taking realistic materials parameters, model calculations are performed for experimentally studied cases. Qualitative agreement is observed

Three-dimensional cross-linked F-actin networks:Relation between network architecture and mechanical behavior

Numerical simulations are reported for the response of three-dimensional cross-linked F-actin networks when subjected to large deformations. In addition to the physiological parameters such as actin and cross-linker concentration, the model explicitly accounts for filament properties and network architecture. Complementary to two-dimensional studies, we find that the strain-stiffening characteristics depend on network architecture through the local topology around cross-links

Aligned gold nanorods in silica made by ion irradiation of core-shell colloidal particles

Colloidal particles with a 14 nm diameter Au core surrounded by a 72 nm thick silica shell have been irradiated with 30 MeV heavy ions. The shell deforms into an oblate ellipsoid, while the core becomes rod-shaped (aspect ratio up to 9) with the major axis along the beam. Optical extinction measurements show evidence for split plasmon bands, characteristic for anisotropic metal nanoparticles

Controlled Anisotropic Deformation of Ag Nanoparticles by Si Ion Irradiation

The shape and alignment of silver nanoparticles embedded in a glass matrix is controlled using silicon ion irradiation. Symmetric silver nanoparticles are transformed into anisotropic particles whose larger axis is along the ion beam. Upon irradiation, the surface plasmon resonance of symmetric particles splits into two resonances whose separation depends on the fluence of the ion irradiation. Simulations of the optical absorbance show that the anisotropy is caused by the deformation and alignment of the nanoparticles, and that both properties are controlled with the irradiation fluence.Comment: Submitted to Phys. Rev. Lett. (October 14, 2005

Anisotropic colloids through non-trivial buckling

We present a study on buckling of colloidal particles, including experimental, theoretical and numerical developments. Oil-filled thin shells prepared by emulsion templating show buckling in mixtures of water and ethanol, due to dissolution of the core in the external medium. This leads to conformations with a single depression, either axisymmetric or polygonal depending on the geometrical features of the shells. These conformations could be theoretically and/or numerically reproduced in a model of homogeneous spherical thin shells with bending and stretching elasticity, submitted to an isotropic external pressure.Comment: submitted to EPJ

Mutated CTSF in adult-onset neuronal ceroid lipofuscinosis and FTD

OBJECTIVE: To investigate the molecular basis of a Belgian family with autosomal recessive adult-onset neuronal ceroid lipofuscinosis (ANCL or Kufs disease [KD]) with pronounced frontal lobe involvement and to expand the findings to a cohort of unrelated Belgian patients with frontotemporal dementia (FTD). METHODS: Genetic screening in the ANCL family and FTD cohort (n = 461) was performed using exome sequencing and targeted massive parallel resequencing. RESULTS: We identified a homozygous mutation (p.Ile404Thr) in the Cathepsin F (CTSF) gene cosegregating in the ANCL family. No other mutations were found that could explain the disease in this family. All 4 affected sibs developed motor symptoms and early-onset dementia with prominent frontal features. Two of them evolved to akinetic mutism. Disease presentation showed marked phenotypic variation with the onset ranging from 26 to 50 years. Myoclonic epilepsy in one of the sibs was suggestive for KD type A, while epilepsy was not present in the other sibs who presented with clinical features of KD type B. In a Belgian cohort of unrelated patients with FTD, the same heterozygous p.Arg245His mutation was identified in 2 patients who shared a common haplotype. CONCLUSIONS: A homozygous CTSF mutation was identified in a recessive ANCL pedigree. In contrast to the previous associations of CTSF with KD type B, our findings suggest that CTSF genetic testing should also be considered in patients with KD type A as well as in early-onset dementia with prominent frontal lobe and motor symptoms