Effect of tip profile on atomic-force microscope images: A model study

Adopting the empirical silicon interatomic potential of Stillinger and Weber, we investigate the effect of the tip profile on the atomic-force microscope images for a prototype system, Si(001)-(2×1), and conclude that the tip profile has a profound effect on the observations. We also study relaxation of the surface under the influence of the tip using a many-body energy minimization procedure and find that the force exerted by the tip should be less than 10-9 N for the atomic-force microscope to be a nondestructive tool. © 1988 The American Physical Society

Molecular-dynamics study of self-interstitials in silicon

Results of a molecular-dynamics computer simulation are presented for atomic relaxations and relaxation energies for self-interstitials in a silicon crystal. The Stillinger-Weber model potential containing two- and three-body terms is used and is expected to be more realistic than a simple Keating potential. The host crystal is represented by a cluster of 800 atoms, and the additional silicon atom was embedded in various interstitial sites near the center. The whole assembly was then periodically continued to fill the entire space. It is found that significant atomic relaxations occur in a shell of a radius 11 a.u. and decay exponentially. In fact the relaxation is oscillatory in nature and also nonuniform within some shells. The calculated formation energies of vacancy and self-interstitials at equilibrium show trends which are in agreement with the self-consistent field total-energy calculations. These energy values are also in agreement with the known self-diffusion activation energy. From calculated formation energy values, we are able to draw the conclusion that the tetrahedral-site interstitial can be most readily formed. The hexagonal-site interstitial, on the other hand, is most repulsive. The migration from tetrahedral to dumbbell interstitial site appears to be most favorable. © 1987 The American Physical Society

Some aspects of the Liouville equation in mathematical physics and statistical mechanics

This paper presents some mathematical aspects of Classical Liouville theorem and we have noted some mathematical theorems about its initial value problem. Furthermore, we have implied on the formal frame work of Stochastic Liouville equation (SLE)

Hypoxia-induced p53 modulates both apoptosis and radiosensitivity via AKT

Contains fulltext : 153027.pdf (publisher's version ) (Open Access)Restoration of hypoxia-induced apoptosis in tumors harboring p53 mutations has been proposed as a potential therapeutic strategy; however, the transcriptional targets that mediate hypoxia-induced p53-dependent apoptosis remain elusive. Here, we demonstrated that hypoxia-induced p53-dependent apoptosis is reliant on the DNA-binding and transactivation domains of p53 but not on the acetylation sites K120 and K164, which, in contrast, are essential for DNA damage-induced, p53-dependent apoptosis. Evaluation of hypoxia-induced transcripts in multiple cell lines identified a group of genes that are hypoxia-inducible proapoptotic targets of p53, including inositol polyphosphate-5-phosphatase (INPP5D), pleckstrin domain-containing A3 (PHLDA3), sulfatase 2 (SULF2), B cell translocation gene 2 (BTG2), cytoplasmic FMR1-interacting protein 2 (CYFIP2), and KN motif and ankyrin repeat domains 3 (KANK3). These targets were also regulated by p53 in human cancers, including breast, brain, colorectal, kidney, bladder, and melanoma cancers. Downregulation of these hypoxia-inducible targets associated with poor prognosis, suggesting that hypoxia-induced apoptosis contributes to p53-mediated tumor suppression and treatment response. Induction of p53 targets, PHLDA3, and a specific INPP5D transcript mediated apoptosis in response to hypoxia through AKT inhibition. Moreover, pharmacological inhibition of AKT led to apoptosis in the hypoxic regions of p53-deficient tumors and consequently increased radiosensitivity. Together, these results identify mediators of hypoxia-induced p53-dependent apoptosis and suggest AKT inhibition may improve radiotherapy response in p53-deficient tumors