The present paper considers the mechanical and fracture properties of four different epoxy polymers containing 0, 10 and 20 wt% of well-dispersed silica nanoparticles. Firstly, it was found that, for any given epoxy polymer, their Young's modulus steadily increased as the volume fraction, v f, of the silica nanoparticles was increased. Modelling studies showed that the measured moduli of the different silica-nanoparticle filled epoxy-polymers lay between upper-bound values set by the Halpin-Tsai and the Nielsen 'no-slip' models, and lower-bound values set by the Nielsen 'slip' model; with the last model being the more accurate at relatively high values of v f . Secondly, the presence of silica nanoparticles always led to an increase in the toughness of the epoxy polymer. However, to what extent a given epoxy polymer could be so toughened was related to structure/property relationships which were governed by (a) the values of glass transition temperature, T g , and molecular weight, M c , between cross-links of the epoxy polymer, and (b) the adhesion acting at the silicananoparticle/epoxy-polymer interface. Thirdly, the two toughening mechanisms which were operative in all the epoxy polymers containing silica nanoparticles were identified to be (a) localised shear-bands initiated by the stress concentrations around the periphery of the silica nanoparticles, and (b) debonding of the silica nanoparticles followed by subsequent plastic void-growth of the epoxy polymer. Finally, the toughening mechanisms have been quantitatively modelled and there was good agreement between the experimentally measured values and the predicted values of the fracture energy, G c , for all the epoxy polymers modified by the presence of silica nanoparticles. The modelling studies have emphasised the important roles of the stress versus strain behaviour of the epoxy polymer and the silica-nanoparticle/epoxy-polymer interfacial adhesion in influencing the extent of the two toughening mechanisms, and hence the overall fracture energy, G c , of the nanoparticle-filled polymers.

The present paper investigates the effect of adding silica nanoparticles to an anhydride-cured epoxy polymer in bulk and when used as the matrix of carbon-and glass-fibre reinforced composites. The formation of 'hybrid' epoxy polymers, containing both silica nanoparticles and carboxyl-terminated butadiene-acrylonitrile (CTBN) rubber microparticles, is also discussed. The structure/property relationships are considered, with an emphasis on the toughness and the toughening mechanisms. The fracture energy of the bulk epoxy polymer was increased from 77 to 212 J/m 2 by the presence of 20 wt.% of silica nanoparticles. The observed toughening mechanisms that were operative were (a) plastic shear-yield bands, and (b) debonding of the matrix from the silica nanoparticles, followed by plastic void-growth of the epoxy. The largest increases in toughness observed were for the 'hybrid' materials. Here a maximum fracture energy of 965 J/m 2 was measured for a 'hybrid' epoxy polymer containing 9 wt.% and 15 wt.% of the rubber microparticles and silica nanoparticles, respectively. Most noteworthy was the observation that these increases in the toughness of the bulk polymers were found to be transferred to the fibre composites. Indeed, the interlaminar fracture energies for the fibre-composites materials were increased even further by a fibre-bridging toughening mechanism. The present work also extends an existing model to predict the toughening effect of the nanoparticles in a thermoset polymer. There was excellent agreement between the predictions and the experimental data for the epoxy containing the silica nanoparticles, and for epoxy polymers containing micrometre-sized glass particles. The latter, relatively large, glass particles were investigated to establish whether a 'nanoeffect', with respect to increasing the toughness of the epoxy bulk polymers, did indeed exist.

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Multi-walled carbon nanotubes, with a typical length of 140 lm and a diameter of 120 nm, have been used to modify an anhydride-cured epoxy polymer. The modulus, fracture energy and the fatigue performance of the modified polymers have been investigated. Microscopy showed that these long nanotubes were agglomerated, and that increasing the nanotube content increased the severity of the agglomeration. The addition of nanotubes increased the modulus of the epoxy, but the glass transition temperature was unaffected. The measured fracture energy was also increased, from 133 to 223 J/m 2 with the addition of 0.5 wt% of nanotubes. The addition of the carbon nanotubes also resulted in an increase in the fatigue performance. The threshold strain-energy release-rate, G th , increased from 24 J/m 2 for the unmodified material to 73 J/m 2 for the epoxy with 0.5 wt% of nanotubes. Electron microscopy of the fracture surfaces showed clear evidence of nanotube debonding and pull-out, plus void growth around the nanotubes, in both the fracture and fatigue tests. The modelling study showed that the modified Halpin-Tsai equation can fit very well with the measured values of the Young's modulus, when the orientation and agglomeration of the nanotubes are considered. The fracture energy of the nanotube-modified epoxies was predicted, by considering the contributions of the toughening mechanisms of nanotube debonding, nanotube pull-out and plastic void growth of the epoxy. This indicated that debonding and pull-out contribute to the toughening effect, but the contribution of void growth is not significant. There was excellent agreement between the predictions and the experimental results.

The circadian clock gene Period2 (PER2) has been suggested to be a tumor suppressor. However, detailed mechanistic evidence has not been provided to support this hypothesis. We found that loss of PER2 enhanced invasion and activated expression of epithelialmesenchymal transition (EMT) genes including TWIST1, SLUG, and SNAIL. This finding was corroborated by clinical observation that PER2 down-regulation was associated with poor prognosis in breast cancer patients. We further demonstrated that PER2 served as a transcriptional corepressor, which recruited polycomb proteins EZH2 and SUZ12 as well as HDAC2 to octamer transcription factor 1 (OCT1) (POU2F1) binding sites of the TWIST1 and SLUG promoters to repress expression of these EMT genes. Hypoxia, a condition commonly observed in tumors, caused PER2 degradation and disrupted the PER2 repressor complex, leading to activation of EMT gene expression. This result was further supported by clinical data showing a significant negative correlation between hypoxia and PER2. Thus, our findings clearly demonstrate the tumor suppression function of PER2 and elucidate a pathway by which hypoxia promotes EMT via degradation of PER2.HIF1alpha | breast cancer stem cell