Tunneling-percolation origin of nonuniversality: theory and experiments

A vast class of disordered conducting-insulating compounds close to the percolation threshold is characterized by nonuniversal values of transport critical exponent t, in disagreement with the standard theory of percolation which predicts t = 2.0 for all three dimensional systems. Various models have been proposed in order to explain the origin of such universality breakdown. Among them, the tunneling-percolation model calls into play tunneling processes between conducting particles which, under some general circumstances, could lead to transport exponents dependent of the mean tunneling distance a. The validity of such theory could be tested by changing the parameter a by means of an applied mechanical strain. We have applied this idea to universal and nonuniversal RuO2-glass composites. We show that when t > 2 the measured piezoresistive response \Gamma, i. e., the relative change of resistivity under applied strain, diverges logarithmically at the percolation threshold, while for t = 2, \Gamma does not show an appreciable dependence upon the RuO2 volume fraction. These results are consistent with a mean tunneling dependence of the nonuniversal transport exponent as predicted by the tunneling-percolation model. The experimental results are compared with analytical and numerical calculations on a random-resistor network model of tunneling-percolation.Comment: 13 pages, 12 figure

Piezoresistivity and conductance anisotropy of tunneling-percolating systems

Percolating networks based on interparticle tunneling conduction are shown to yield a logarithmic divergent piezoresistive response close to the critical point as long as the electrical conductivity becomes nonuniversal. At the same time, the piezoresistivity or, equivalently, the conductivity anisotropy exponent $\lambda$ remains universal also when the conductive exponent is not, suggesting a purely geometric origin of $\lambda$. We discuss our results in relation to the nature of transport for a variety of materials such as carbon-black--polymer composites and RuO_2-glass systems which show nonuniversal transport properties and coexistence between tunneling and percolating behaviors.Comment: 6 pages, 3 figures, Added discussion on experiment

Bonding to aged surfaces: A thermally-aged epoxy

It is common experience that aged surfaces are often difficult to bond to. We report an examination of bonding to thermally-aged epoxy surfaces, using as the adhesive the same epoxy as that of the aged surface. The cured and postcured epoxy was aged at 200 ° C, with the ageing time varying from 2 to 8 h. The fracture energy of the bond line was measured by mode I cleavage under conditions of relatively slow crack growth. The bondline fracture energy was found to decrease logarithmically with ageing time. The fracture energies for bonds to surfaces aged for 2, 4, and 8 h at 200 ° C were 0.077, 0.059, and 0.050 kJ M −2 , respectively. These compare to 0.13 kJ M −2 for a bond to an unaged surface and 0.21 kJ m −2 for bulk fracture. Fracture surfaces resulting from both slow and rapid fracture were examined by optical and scanning electron microscopy. Fracture features different from those arising from bulk fracture were found. Areas with ‘good’ adhesion occurred amidst fields of featureless fracture surface; the frequency and size of these areas decreased with increased ageing time. Evidence of plastic deformation was found, always occurring on the new side of the bond: ridges parallel with crack propagation at high crack speeds and subsurface undulations perpendicular to crack propagation at low speeds. The bond has the effect of channelling the crack along the bondline, but fracture does not always remain exactly at the interface. Fracture often occurred a relatively constant distance away from the interface, suggesting that the presence of the interface was felt for some distance.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44698/1/10853_2004_Article_BF00584867.pd

Decrease of CD68 Synovial Macrophages in Celastrol Treated Arthritic Rats

Rheumatoid arthritis (RA) is a chronic immune-mediated inflammatory disease characterized by cellular infiltration into the joints, hyperproliferation of synovial cells and bone damage. Available treatments for RA only induce remission in around 30% of the patients, have important adverse effects and its use is limited by their high cost. Therefore, compounds that can control arthritis, with an acceptable safety profile and low production costs are still an unmet need. We have shown, in vitro, that celastrol inhibits both IL-1β and TNF, which play an important role in RA, and, in vivo, that celastrol has significant anti-inflammatory properties. Our main goal in this work was to test the effect of celastrol in the number of sublining CD68 macrophages (a biomarker of therapeutic response for novel RA treatments) and on the overall synovial tissue cellularity and joint structure in the adjuvant-induced rat model of arthritis (AIA).FCT fellowship: (SFRH/BPD/92860/2013)