Perfect Sets and ff-Ideals

A square-free monomial ideal $I$ is called an {\it $f$-ideal}, if both $\delta_{\mathcal{F}}(I)$ and $\delta_{\mathcal{N}}(I)$ have the same $f$-vector, where $\delta_{\mathcal{F}}(I)$ ($\delta_{\mathcal{N}}(I)$, respectively) is the facet (Stanley-Reisner, respectively) complex related to $I$. In this paper, we introduce and study perfect subsets of $2^{[n]}$ and use them to characterize the $f$-ideals of degree $d$. We give a decomposition of $V(n, 2)$ by taking advantage of a correspondence between graphs and sets of square-free monomials of degree $2$, and then give a formula for counting the number of $f$-ideals of degree $2$, where $V(n, 2)$ is the set of $f$-ideals of degree 2 in $K[x_1,\ldots,x_n]$. We also consider the relation between an $f$-ideal and an unmixed monomial ideal.Comment: 15 page

On the role of global flow instability analysis in closed loop flow control

Control of linear flow instabilities has been demonstrated to be an effective theoretical flow control methodology, capable of modifying transitional flow on canonical geometries such as the plane channel and the flat-plate boundary layer

A physical mechanism of heterogeneity in stem cell, cancer and cancer stem cell

Heterogeneity is ubiquitous in stem cells (SC), cancer cells (CS), and cancer stem cells (CSC). SC and CSC heterogeneity is manifested as diverse sub-populations with self-renewing and unique regeneration capacity. Moreover, the CSC progeny possesses multiple plasticity and cancerous characteristics. Many studies have demonstrated that cancer heterogeneity is one of the greatest obstacle for therapy. This leads to the incomplete anti-cancer therapies and transitory efficacy. Furthermore, numerous micro-metastasis leads to the wide spread of the tumor cells across the body which is the beginning of metastasis. The epigenetic processes (DNA methylation or histone remodification etc.) can provide a source for certain heterogeneity. In this study, we develop a mathematical model to quantify the heterogeneity of SC, CSC and cancer taking both genetic and epigenetic effects into consideration. We uncovered the roles and physical mechanisms of heterogeneity from the three aspects (SC, CSC and cancer). In the adiabatic regime (relatively fast regulatory binding and effective coupling among genes), seven native states (SC, CSC, Cancer, Premalignant, Normal, Lesion and Hyperplasia) emerge. In non-adiabatic regime (relatively slow regulatory binding and effective weak coupling among genes), multiple meta-stable SC, CS, CSC and differentiated states emerged which can explain the origin of heterogeneity. In other words, the slow regulatory binding mimicking the epigenetics can give rise to heterogeneity. Elucidating the origin of heterogeneity and dynamical interrelationship between intra-tumoral cells has clear clinical significance in helping to understand the cellular basis of treatment response, therapeutic resistance, and tumor relapse.Comment: 7 pages, 2 figure