Advisor: Vladimir Baranovsky
Abstract:
We begin by exploring algebraic codes created using cubic hypersurfaces. This leads to the questions of classification, realization, and construction of cubic hypersurfaces. Given the classification by Manin, Frame, Swinnerton-Dyer, etc., we will look at methods of realization and construction of these cubics. Specifically, we will focus on two approaches. The first approach involves looking at the blow-downs of cubics. The second approach involves automorphisms of well-defined cubics.
We consider the scattering of a time-harmonic plane wave incident on a two-scale heterogeneous medium, which consists of scatterers that are much smaller than the wavelength and extended scatterers that are comparable to the wavelength. A generalized Foldy-Lax formulation is proposed to capture multiple scattering among point scatterers and extended scatterers. Our formulation is given as a coupled system, which combines the original Foldy-Lax formulation for the point scatterers and the regular boundary integral equation for the extended obstacle scatterers. An efficient physically motivated Gauss-Seidel iterative method is proposed to solve the coupled system, where only a linear system of algebraic equations for point scatterers or a boundary integral equation for a single extended obstacle scatterer is required to solve at each step of iteration. In contrast to the standard inverse obstacle scattering problem, the proposed inverse scattering problem is not only to determine the shape of the extended obstacle scatterer but also to locate the point scatterers. Based on the generalized Foldy-Lax formulation and the singular value decomposition of the response matrix constructed from the far-field pattern, an imaging function is developed to visualize the location of the point scatterers and the shape of the extended obstacle scatterer.
We consider the problem of proving the existence of periodic solutions for
a second order nonautonomous Hamiltonian system in n-dimensional Euclidean
space. We assume the dynamic behavior is determined by a nonautonomous
linear term and a nonautonomous gradient term which must be continuous and
linearly bounded. By proving the existence of a critical point for a
nonlinear functional acting on an appropriate function space we find
conditions for the existence of weak solutions when neither the linear nor
the nonlinear contribution to the dynamic behavior is dominant. We
consider the case where the dynamic behavior is determined only by the
nonautonomous gradient term. We also give conditions for the existence of
classical solutions.
X_\alpha = \{f : \omega^\alpha \rightarro\powerset_{\omega_1}(\mathbb{R})| f is increasing and continuous}
and \mu_\alpha be a normal fine measure on X_\alpha. We identify X_0 with \powerset_{\omega_1}(R). Martin and Woodin independently showed that these measures exist assuming (ZF + DC_\mathbb{R}) + AD + Every set is Suslin (\mu_0's existence was originally shown by Solovay from AD_\mathbb{R}). We sketch the proof of the derived model construction giving the existence of these measures (+ AD^+) from large cardinals and the Prikry forcing construction which gives back the exact large cardinal strength from AD^+ and the measure. If time allows, we will survey some theorems on the structure theory of the model L(\mathbb{R},\mu_\alpha) assuming the model satisfies \Theta > \omega_2 and \mu_\alpha is a normal fine measure on X_\alpha. Here the main theorem is that our assumption implies L(\mathbb{R},\mu_\alpha) satisfies AD^+
Starting from a supercompact, we construct a model in which SCH fails at $\aleph_\omega$ and there is a bad scale at $\aleph_\omega$. The existence of a bad scale implies the failure of weak square. The construction uses two Prikry type forcings defined in different ground models and a suitably defined projection between them. This is joint work with Spencer Unger.
Stochasticity is a hallmark of cellular processes, and different classes of genes show large differences in their cell-to-cell variability (noise). To decipher the sources and consequences of this noise, we systematically measured pairwise correlations between large numbers of genes, including those with high variability. We find that there is substantial pathway variability shared across similarly regulated genes. This induces quantitative correlations in the expression of functionally related genes such as those involved in the Msn2/4 stress response pathway, amino acid biosynthesis, and mitochondrial maintenance. Bioinformatic analyses and genetic perturbations suggest that fluctuations in PKA and Tor signaling contribute to pathway-specific variability. Our results argue that a limited number of well-delineated ‘‘noise regulons’’ operate across a yeast cell and that such coordinated fluctuations enable a stochastic but coherent induction of functionally related genes. We discuss how this principle might be general to stress responses across different organisms and the mechanisms by which stochastic but coherent stress responses strengthen resistance to environmental insults. More broadly, our work shows that pathway noise is a quantitative tool for exploring pathway features and regulatory relationships in un-stimulated systems.