Surface optical Raman modes in InN nanostructures

Raman spectroscopic investigations are carried out on one-dimensional nanostructures of InN,such as nanowires and nanobelts synthesized by chemical vapor deposition. In addition to the optical phonons allowed by symmetry; A1, E1 and E2(high) modes, two additional Raman peaks are observed around 528 cm-1 and 560 cm-1 for these nanostructures. Calculations for the frequencies of surface optical (SO) phonon modes in InN nanostructures yield values close to those of the new Raman modes. A possible reason for large intensities for SO modes in these nanostructures is also discussed.Comment: 13 pages, 4 figures, Submitted in Journa

Confined Acoustic Phonon in CdS1-xSex Nanoparticles in Borosilicate Glass

We calculate low-frequency Raman scattering from the confined acoustic phonon modes of CdS1-xSex nanoparticles embedded in borosilicate glass. The calculation of the Raman scattering by acoustic phonons in nanoparticles has been performed by using third-order perturbation theory. The deformation potential approximation is used to describe the electronphonon interaction. The Raman-Brillouin electronic density and the electron-phonon interaction are found to increases with decreasing size of nanoparticle. A good agreement between the calculated and reported low-frequency Raman spectra is found.Comment: 13 pages, 3 figures. Journal of Nanoscience and Nanotechnology (In Press

Computational Modeling and Analysis of Insulin Induced Eukaryotic Translation Initiation

Insulin, the primary hormone regulating the level of glucose in the bloodstream, modulates a variety of cellular and enzymatic processes in normal and diseased cells. Insulin signals are processed by a complex network of biochemical interactions which ultimately induce gene expression programs or other processes such as translation initiation. Surprisingly, despite the wealth of literature on insulin signaling, the relative importance of the components linking insulin with translation initiation remains unclear. We addressed this question by developing and interrogating a family of mathematical models of insulin induced translation initiation. The insulin network was modeled using mass-action kinetics within an ordinary differential equation (ODE) framework. A family of model parameters was estimated, starting from an initial best fit parameter set, using 24 experimental data sets taken from literature. The residual between model simulations and each of the experimental constraints were simultaneously minimized using multiobjective optimization. Interrogation of the model population, using sensitivity and robustness analysis, identified an insulin-dependent switch that controlled translation initiation. Our analysis suggested that without insulin, a balance between the pro-initiation activity of the GTP-binding protein Rheb and anti-initiation activity of PTEN controlled basal initiation. On the other hand, in the presence of insulin a combination of PI3K and Rheb activity controlled inducible initiation, where PI3K was only critical in the presence of insulin. Other well known regulatory mechanisms governing insulin action, for example IRS-1 negative feedback, modulated the relative importance of PI3K and Rheb but did not fundamentally change the signal flow