3 results match your criteria: "DrexelUniversity[Affiliation]"

Finite curvature-mediated ferroelectricity.

Nano Lett

February 2010

Department of Materials Science and Engineering, DrexelUniversity, Philadelphia, Pennsylvania 19104, USA.

We demonstrate that ferroelectric (FE) polarizations oriented along the finite thickness direction in ultrathin films are enhanced by the introduction of extreme curvature, thereby suppressing the finite-size-driven evolution of the FE phase transition temperature T(C). The measured responses within individual nanoshells possess magnitudes nearly three times that for their planar counterparts while exhibiting finite curvature-dependent offsets in FE switching hystereses. In stark contrast to the expected scaling of a depression of T(C) with inverse thickness, results based on modified Landau-Ginzburg model calculations indicate geometric curvature-driven polarization gradients in ultrathin films result in significant increases in T(C).

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Approximation modeling for the online performance management of distributed computing systems.

IEEE Trans Syst Man Cybern B Cybern

October 2008

Electrical and Computer Engineering Department, DrexelUniversity, Philadelphia, PA 19104, USA.

A promising method of automating management tasks in computing systems is to formulate them as control or optimization problems in terms of performance metrics. For an online optimization scheme to be of practical value in a distributed setting, however, it must successfully tackle the curses of dimensionality and modeling. This paper develops a hierarchical control framework to solve performance management problems in distributed computing systems operating in a data center.

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Mechanisms of cell death and neuroprotection by poloxamer 188 after mechanical trauma.

FASEB J

February 2006

School of Biomedical Engineering, Science, and Health Systems, DrexelUniversity, Philadelphia, Pennsylvania 19104, USA.

The mechanisms of cell death and the progressive degeneration of neural tissue following traumatic brain injury (TBI) have come under intense investigation. However, the complex interactions among the evolving pathologies in multiple cell types obscure the causal relationships between the initial effects of the mechanical trauma at the cellular level and the long-term dysfunction and neuronal death. We used an in vitro model of neuronal injury to study the mechanisms of cell death in response to a well-defined mechanical insult and found that the majority of dead cells were apoptotic.

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