Exact Ground States of Large Two-Dimensional Planar Ising Spin Glasses

Studying spin-glass physics through analyzing their ground-state properties has a long history. Although there exist polynomial-time algorithms for the two-dimensional planar case, where the problem of finding ground states is transformed to a minimum-weight perfect matching problem, the reachable system sizes have been limited both by the needed CPU time and by memory requirements. In this work, we present an algorithm for the calculation of exact ground states for two-dimensional Ising spin glasses with free boundary conditions in at least one direction. The algorithmic foundations of the method date back to the work of Kasteleyn from the 1960s for computing the complete partition function of the Ising model. Using Kasteleyn cities, we calculate exact ground states for huge two-dimensional planar Ising spin-glass lattices (up to 3000x3000 spins) within reasonable time. According to our knowledge, these are the largest sizes currently available. Kasteleyn cities were recently also used by Thomas and Middleton in the context of extended ground states on the torus. Moreover, they show that the method can also be used for computing ground states of planar graphs. Furthermore, we point out that the correctness of heuristically computed ground states can easily be verified. Finally, we evaluate the solution quality of heuristic variants of the Bieche et al. approach.Comment: 11 pages, 5 figures; shortened introduction, extended results; to appear in Physical Review E 7

Antagomir-1290 suppresses CD133+ cells in non-small cell lung cancer by targeting fyn-related Src family tyrosine kinase

Cancer stem-like cells (CSLCs) are involved in cancer initiation, development, and metastasis, and microRNAs (miRNAs) play pivotal roles in regulating CSLCs. miRNA-based therapeutic strategy associated with CSLCs might promise potential new therapeutic approaches. In the present study, we found that miR-1290 was increased in CD133+ cells. Antagomir-1290 significantly suppressed tumor volume and weight initiated by CD133+ cells in vivo. Furthermore, antagomir-1290 significantly inhibited the proliferation, clonogenicity, invasion, and migration of CD133+ cells by targeting fyn-related Src family tyrosine kinase. These findings provide insights into the clinical prospect of miR-1290-based therapies for non-small cell lung cancer