Realistic three-generation models from SO(32) heterotic string theory

We search for realistic supersymmetric standard-like models from SO(32) heterotic string theory on factorizable tori with multiple magnetic fluxes. Three chiral ganerations of quarks and leptons are derived from the adjoint and vector representations of SO(12) gauge groups embedded in SO(32) adjoint representation. Massless spectra of our models also include Higgs fields, which have desired Yukawa couplings to quarks and leptons at the tree-level.Comment: 29 pages, Typos corrected, references added, and Sec. 3.3 is adde

Gauge coupling unification in SO(32) heterotic string theory with magnetic fluxes

We study $SO(32)$ heterotic string theory on torus with magnetic fluxes. Non-vanishing fluxes can lead to non-universal gauge kinetic functions for $SU(3) \times SU(2) \times U(1)_Y$ which is the important features of $SO(32)$ heterotic string theory in contrast to the $E_8\times E_8$ theory. It is found that the experimental values of gauge couplings are realized with ${\cal O}(1)$ values of moduli fields based on the realistic models with the $SU(3) \times SU(2) \times U(1)_Y$ gauge symmetry and three chiral generations of quarks and leptons without chiral exotics.Comment: 20 pages, 9 figure

Therapeutic Implications of PPARγ in Cardiovascular Diseases

Peroxisome proliferator-activated receptor-γ (PPARγ) is the members of the nuclear receptor superfamily as a master transcriptional factor that promotes differentiation of preadipocytes by activating adipose-specific gene expression. Although PPARγ is expressed predominantly in adipose tissue and associated with adipocyte differentiation and glucose homeostasis, PPARγ is also present in a variety of cell types including vascular cells and cardiomyocytes. Activation of PPARγ suppresses production of inflammatory cytokines, and there is accumulating data that PPARγ ligands exert antihypertrophy of cardiomyocytes and anti-inflammatory, antioxidative, and antiproliferative effects on vascular wall cells and cardiomyocytes. In addition, activation of PPARγ is implicated in the regulation of endothelial function, proliferation and migration of vascular smooth muscle cells, and activation of macrophages. Many studies suggest that PPARγ ligands not only ameliorate insulin sensitivity, but also have pleiotropic effects on the pathophysiology of atherosclerosis, cardiac hypertrophy, ischemic heart, and myocarditis