Fracture behaviour of unmodified and rubber-modified epoxies under hydrostatic pressure

The fracture toughness and uniaxial tensile yield strengths of unmodified and CTBN-rubber-modified epoxies were measured under hydrostatic pressure. The purpose of these experiments was to learn how suppressing cavitation in rubber particles affects the deformation mechanisms and the fracture toughness of rubber-modified epoxy. It was found that the cavitation of CTBN-rubber could be suppressed at a relatively low pressure (between 30 and 38 M Pa). With cavitation suppressed, the rubber particles are unable to induce massive shearyielding in the epoxy matrix, and the fracture toughness of the rubber-modified epoxy is no higher than that of the unmodified epoxy in the pressure range studied. Unmodified epoxy shows a brittle-to-ductile transition in fracture toughness test. The reason for this transition is the postponement of the cracking process by applied pressure.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44734/1/10853_2005_Article_BF01154701.pd

Thermal effects in high density polyethylene and low density polyethylene at high hydrostatic pressures

The temperature changes as a result of rapid hydrostatic pressure applications are reported for high density polyethylene (HDPE) and low density polyethylene (LDPE) in the reference temperature range from 298 to 423 K and in the pressure range from 13.8 to 200 MN m −2 . The adiabatic temperature changes were found to be a function of pressure and temperature. A curve fitting analysis showed that the empirical curve (∂/∂ P ) = ab (Δ P ) b−1 described the experimental thermoelastic coefficients obtained from the experiments. The data were analyzed by determining the predicted thermoelastic coefficients derived from the Thomson equation (∂/∂ P ) θ = α T 0 /ϱ C p . The experimental and predicted Grüneisen parameter γ T were also determined.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/44687/1/10853_2005_Article_BF01132919.pd

Nicotinamide reverses behavioral impairments and provides neuroprotection in 3-nitropropionic acid induced animal model ofHuntington's disease: implication of oxidative stress- poly(ADP- ribose) polymerase pathway

Huntington's disease (HD) is characterized by cognitive and psychiatric impairment caused by neuronal degeneration in the brain. Several studies have supported the hypothesis that oxidative stress is the main pathogenic factor in HD. The current study aims to determine the possible neuroprotective effects of nicotinamide on 3-nitropropionic acid (3-NP) induced HD. Male Wistar albino rats were divided into six groups. Group I was the vehicle-treated control, group II received 3-NP (20\ua0mg/kg, intraperitoneally (i.p.) for 4\ua0days, group III received nicotinamide (500\ua0mg/kg, i.p.). The remaining groups received a combination of 3-NP plus nicotinamide 100, 300 or 500\ua0mg/kg, i.p. respectively for 8\ua0days. Afterward, the motor function and hind paw activity in the limb withdrawal were tested; rats were then euthanized for biochemical and histopathological analyses. Treatment of rats with 3-NP altered the motor function, elevated oxidative stress and caused significant histopathological changes in the brain. The treatment of rats with nicotinamide (100, 300 and 500\ua0mg/kg) improved the motor function tested by locomotor activity test, movement analysis, and limb withdrawal test, which was associated with decreased oxidative stress markers (malondialdehyde, nitrites) and increased antioxidant enzyme (glutathione) levels. In addition, nicotinamide treatment decreased lactate dehydrogenase and prevented neuronal death in the striatal region. Our study, therefore, concludes that antioxidant drugs like nicotinamide might slow progression of clinical HD and may improve the motor functions in HD patients. To the best of our knowledge, this study is the first to explore the neuroprotective effects of nicotinamide on 3-NP-induced HD