Correlation Functions of Multisite Interaction Spin-S models on the Bethe-like Lattices

Multisite interaction spin-S models in an external magnetic field are studied recursively on the Bethe-like lattices. The transfer-matrix method is extended to calculate exactly the two-spin correlation functions. The exact expressions for the correlation length and magnetic susceptibility are derived for spin-1/2 models. The singularity of the correlation length with critical index $\nu =1$ and the proportionality of magnetic susceptibility to correlation length in the second order phase transition region of spin-1/2 ferromagnetic models on the Bethe-like lattices are established analytically.Comment: 13 pages, In Press Int. J. Mod. Phys.

DLC2 modulates angiogenic responses in vascular endothelial cells by regulating cell attachment and migration.

Deleted in liver cancer 1 (DLC1) is a RhoGTPase activation protein-containing tumor suppressor that associates with various types of cancer. Although DLC2 shares a similar domain structure with that of DLC1, the function of DLC2 is not well characterized. Here, we describe the expression and ablation of DLC2 in mice using a reporter-knockout approach. DLC2 is expressed in several tissues and in endothelial cells (ECs) of blood vessels. Although ECs and blood vessels show no histological abnormalities and mice appear overall healthy, DLC2-mutant mice display enhanced angiogenic responses induced by matrigel and by tumor cells. Silencing of DLC2 in human ECs has reduced cell attachment, increased migration, and tube formation. These changes are rescued by silencing of RhoA, suggesting that the process is RhoA pathway dependent. These results indicate that DLC2 is not required for mouse development and normal vessel formation, but may protect mouse from unwanted angiogenesis induced by, for example, tumor cells

Exact Solution of a Monomer-Dimer Problem: A Single Boundary Monomer on a Non-Bipartite Lattice

We solve the monomer-dimer problem on a non-bipartite lattice, the simple quartic lattice with cylindrical boundary conditions, with a single monomer residing on the boundary. Due to the non-bipartite nature of the lattice, the well-known method of a Temperley bijection of solving single-monomer problems cannot be used. In this paper we derive the solution by mapping the problem onto one on close-packed dimers on a related lattice. Finite-size analysis of the solution is carried out. We find from asymptotic expansions of the free energy that the central charge in the logarithmic conformal field theory assumes the value $c=-2$.Comment: 15 pages, 1 figure, submitted to Phy. Rev. E; v2: revised Acknowledgment

THE ECOLOGICAL SITUATION AND THE PROCESSES OF USING NATURAL RESOURCES IN UZBEKISTAN DURING INDEPENDENCE

During the years of independence, the reduction of atmospheric air pollution levels, the improvement of the main open water flows, the reduction of the application of pesticides, the improvement of the structure of cultivated areas, the involvement of international organizations in the solution of national environmental problems have been analyzed

LSD1 is essential for oocyte meiotic progression by regulating CDC25B expression in mice

Mammalian oocytes are arrested at prophase I until puberty when hormonal signals induce the resumption of meiosis I and progression to meiosis II. Meiotic progression is controlled by CDK1 activity and is accompanied by dynamic epigenetic changes. Although the signalling pathways regulating CDK1 activity are well defined, the functional significance of epigenetic changes remains largely unknown. Here we show that LSD1, a lysine demethylase, regulates histone H3 lysine 4 di-methylation (H3K4me2) in mouse oocytes and is essential for meiotic progression. Conditional deletion of Lsd1 in growing oocytes results in precocious resumption of meiosis and spindle and chromosomal abnormalities. Consequently, most Lsd1-null oocytes fail to complete meiosis I and undergo apoptosis. Mechanistically, upregulation of CDC25B, a phosphatase that activates CDK1, is responsible for precocious meiotic resumption and also contributes to subsequent spindle and chromosomal defects. Our findings uncover a functional link between LSD1 and the major signalling pathway governing meiotic progression