Constitutive equations for thermomechanical deformations of glassy polymers

AbstractPoly-Carbonate (PC) and Poly-Methyl-Methacrylate (PMMA) are lightweight and mechanically tough transparent glassy polymers. Their mechanical behavior at low to moderate strain rates has been well characterized; however, that at high strain rates needs additional work. We propose two modifications to existing pressure-dependent viscoplastic constitutive equations that enable one to simulate better mechanical deformations of PC and PMMA at high strain rates. First, the elastic moduli are taken to depend upon the current temperature and the current effective strain rate. Second, two internal variables are introduced to better characterize the strain softening of the material at high strain rates. A technique to find values of newly introduced material parameters is described. We compute the local temperature rise due to energy dissipated during plastic deformations. The true axial stress vs. the true axial strain curves in uniaxial compression from numerical simulations of the test configurations at high strain rates using the proposed constitutive equations are found to agree well with the experimental results available in the literature

Reduced-order models for microelectromechanical rectangular and circular plates incorporating the Casimir force

AbstractWe consider the von Kármán nonlinearity and the Casimir force to develop reduced-order models for prestressed clamped rectangular and circular electrostatically actuated microplates. Reduced-order models are derived by taking flexural vibration mode shapes as basis functions for the transverse displacement. The in-plane displacement vector is decomposed as the sum of displacements for irrotational and isochoric waves in a two-dimensional medium. Each of these two displacement vector fields satisfies an eigenvalue problem analogous to that of transverse vibrations of a linear elastic membrane. Basis functions for the transverse and the in-plane displacements are related by using the nonlinear equation governing the plate in-plane motion. The reduced-order model is derived from the equation yielding the transverse deflection of a point. For static deformations of a plate, the pull-in parameters are found by using the displacement iteration pull-in extraction method. Reduced-order models are also used to study linear vibrations about a predeformed configuration. It is found that 9 basis functions for a rectangular plate give a converged solution, while 3 basis functions give pull-in parameters with an error of at most 4%. For a circular plate, 3 basis functions give a converged solution while the pull-in parameters computed with 2 basis functions have an error of at most 3%. The value of the Casimir force at the onset of pull-in instability is used to compute device size that can be safely fabricated

Retroviral gene transfer is inhibited by chondroitin sulfate proteoglycans/glycosaminoglycans in malignant pleural effusions

Gene therapy may be an important adjuvant for treating cancer in the pleural space. The initial results of retroviral gene transfer to cancer cells in malignant pleural effusions revealed that transduction was markedly inhibited, and studies to characterize the inhibitory factor(s) were performed. The inhibition was contained within the soluble, rather than cellular, components of the effusions and was demonstrated with amphotropic, gibbon ape leukemia virus, and vesicular stomatitis virus-glycoprotein pseudotyped retroviral vectors. After excluding complement proteins, a series of studies identified chondroitin sulfates (CSs) as the inhibitory substances. First, treatment of the effusions with mammalian hyaluronidase or chondroitinases, but not Streptomyces hyaluronidase, abolished the inhibitory activity. Second, addition of exogenous CS glycosaminoglycans mimicked the inhibition observed with pleural effusions. Third, immunoassays and biochemical analyses of malignant pleural effusion specimens revealed CS in relevant concentrations within pleural fluid. Fourth, proteoglycans/glycosaminoglycans isolated from the effusions inhibited retroviral gene transfer. Analyses of the mechanism of inhibition indicate that the chondroitin sulfates interact with vector in solution rather than at the target cell surface. These results suggest that drainage of the malignant pleural effusion, and perhaps enzymatic pretreatment of the pleural cavity, will be necessary for efficient retroviral vector mediated gene delivery to pleural metastases

Iκbα gene transfer is cytotoxic to squamous-cell lung cancer cells and sensitizes them to tumor necrosis factor-α-mediated cell death

Current paradigms in cancer therapy suggest that activation of nuclear factor-κB (NF-κB) by a variety of stimuli, including some cytoreductive agents, may inhibit apoptosis. Thus, inhibiting NF-κB activation may sensitize cells to anticancer therapy, thereby providing a more effective treatment for certain cancers. E-1-deleted adenoviral (Ad) vectors encoding a "superrepressor" form of the NF-κB inhibitor IκBα (AdIκBαSR) or β-galactosidase (AdLacZ) were tested alone and in combination with tumor necrosis factor-α (TNF-α) in lung cancer cells for sensitization of the cells to death. Following transduction with AdIκBαSR, lung cancer cells expressed IκBαSR in a dose-dependent manner. Probing nuclear extracts of lung cancer cells with NF-κB-sequence-specific oligonucleotides indicated that there was a minimal amount of NF-κB in the nucleus at baseline and an expected and dramatic increase in nuclear NF-κB following exposure of cells to TNF-α. Control E-1-deleted AdLacZ did not promote NF-κB activation. Importantly, AdIκBαSR-mediated gene transfer resulted in the complete block of nuclear translocation of NF-κB by specific binding of its p65/relA component with transgenic IκBαSR. At the cellular level, transduction with AdIκBαSR resulted in increased cytotoxicity in lung cancer cells as opposed to transduction with equivalent doses of AdLacZ. In addition, whereas the parental cells were resistant to TNF-α-mediated cytotoxicity, IκBαSR-transduced cells could be sensitized to TNF-α. Consequently, AdIκBαSR transduction followed by exposure to TNF-α uniformly resulted in the death of non-small-cell lung cancer cells. These data suggest that novel approaches incorporating IκBα gene therapy may have a role in the treatment of lung cancer