Fracture initiation at a crack or notch in a viscoplastic material under high rate loading

The two-dimensional problem of an edge crack in a half space or plate is considered. The body is loaded by a suddenly applied, spatially uniform normal velocity imposed on the plane boundary of the body on one side of the edge crack. Otherwise, the boundary of the body, including the crack faces, is traction free. Both cases of an initially sharp crack tip and a narrow notch with small but nonzero notch root radius are considered. The material is modeled as elastic viscoplastic, including strain hardening, rate sensitivity and thermal softening. The applied loading produces predominantly mode II loading in the crack tip region. Under these conditions it is possible to nucleate an adiabatic shear band at the crack tip as a precursor to a mode II fracture. On the other hand, because of the rate sensitivity of the material and the high rate of loading, it may be possible under certain conditions to generate tensile stresses in the crack tip region sufficiently large to nucleate brittle tensile fracture. The problem is solved numerically by means of the finite element method in order to investigate the competition between these two possible fracture initiation mechanisms. The magnitude of the impact velocity imposed on the edge of the plate and the notch tip acuity have an effect on processes near the crack tip. For given material, the inception of crack growth is determined by the competition between a stress-based brittle fracture condition, associated with rate sensitivity and strain hardening, and a strain based criterion, associated with high strain rate and thermal softening.     

Envelope glycoprotein gp120 of human immunodeficiency virus type 1 alters ion transport in astrocytes: implications for AIDS dementia complex

Infection by human immunodeficiency virus type 1 (HIV-1) is often complicated by a variety of neurological abnormalities. The most common clinical syndrome, termed acquired immunodeficiency syndrome (AIDS) dementia complex, presents as a subcortical dementia with cognitive, motor, and behavioral disturbances and is unique to HIV-1 infection. The pathogenesis of this syndrome is poorly understood but is believed to involve interactions among virally infected macrophages/microglia, astrocytes, and neurons. In this study, we show that exposure of primary rat and human astrocytes to heat-activated HIV-1 virions, or to eukaryotically expressed HIV-1 and HIV-2 envelope glycoproteins (gp120) stimulates amiloride-sensitive Na+/H+ antiport, potassium conductance, and glutamate efflux. These effects are blocked specifically by amiloride, an inhibitor of Na+/H+ antiport and by the selective removal of gp120 with immobilized monoclonal antibody. As a result of modulation of astrocytic function by gp120, the ensuing neuronal depolarization and glutamate exposure could activate both voltage-gated and N-methyl-D-aspartate-regulated Ca2+ channels, leading to increases in intraneuronal Ca2+ and neuronal death. These findings implicate the astrocyte directly in the pathogenesis of AIDS dementia complex.