Calpain-mediated cleavage of DARPP-32 in Alzheimer's disease.

Toxicity induced by aberrant protein aggregates in Alzheimer's disease (AD) causes synaptic disconnection and concomitant progressive neurodegeneration that eventually impair cognitive function. cAMP-response element-binding protein (CREB) is a transcription factor involved in the molecular switch that converts short-term to long-term memory. Although disturbances in CREB function have been suggested to cause memory deficits in both AD and AD animal models, the mechanism of CREB dysfunction is still unclear.

The growth of a low defect InAs HEMT structure on Si by using an AlGaSb buffer layer containing InSb quantum dots for dislocation termination.

It is found that the surface migration and nucleation behaviors of InSb quantum dots on AlSb/Si substrates, formed by molecular beam epitaxy in Stranski-Krastanov (SK) growth mode, are dependent on the substrate temperature. At relatively high temperatures above 430 degrees C, quantum dots are migrated and preferentially assembled onto the surface steps of high defect AlSb layers grown on Si substrates, while they are uniformly distributed on the surface at lower temperatures below 400 degrees C. It is also found that quantum dots located on the defect sites lead to effective termination of the propagation of micro-twin-induced structural defects into overlying layers, resulting in the low defect material grown on a largely mismatched substrate.