Edge states and topological orders in the spin liquid phases of star lattice

A group of novel materials can be mapped to the star lattice, which exhibits some novel physical properties. We give the bulk-edge correspondence theory of the star lattice and study the edge states and their topological orders in different spin liquid phases. The bulk and edge-state energy structures and Chern number depend on the spin liquid phases and hopping parameters because the local spontaneous magnetic flux in the spin liquid phase breaks the time reversal and space inversion symmetries. We give the characteristics of bulk and edge energy structures and their corresponding Chern numbers in the uniform, nematic and chiral spin liquids. In particular, we obtain analytically the phase diagram of the topological orders for the chiral spin liquid states SL[\phi,\phi,-2\phi], where \phi is the magnetic flux in two triangles and a dodecagon in the unit cell. Moreover, we find the topological invariance for the spin liquid phases, SL[\phi_{1},\phi_{2},-(\phi_{1}+\phi_{2})] and SL[\phi_{2},\phi_{1},-(\phi_{1}+\phi_{2})]. The results reveal the relationship between the energy-band and edge-state structures and their topological orders of the star lattice.Comment: 7 pages, 8 figures, 1 tabl

The involvement of soluble epoxide hydrolase in the development of cardiovascular diseases through epoxyeicosatrienoic acids

Arachidonic acid (AA) has three main metabolic pathways: the cycloxygenases (COXs) pathway, the lipoxygenases (LOXs) pathway, and the cytochrome P450s (CYPs) pathway. AA produces epoxyeicosatrienoic acids (EETs) through the CYPs pathway. EETs are very unstable in vivo and can be degraded in seconds to minutes. EETs have multiple degradation pathways, but are mainly degraded in the presence of soluble epoxide hydrolase (sEH). sEH is an enzyme of bifunctional nature, and current research focuses on the activity of its C-terminal epoxide hydrolase (sEH-H), which hydrolyzes the EETs to the corresponding inactive or low activity diol. Previous studies have reported that EETs have cardiovascular protective effects, and the activity of sEH-H plays a role by degrading EETs and inhibiting their protective effects. The activity of sEH-H plays a different role in different cells, such as inhibiting endothelial cell proliferation and migration, but promoting vascular smooth muscle cell proliferation and migration. Therefore, it is of interest whether the activity of sEH-H is involved in the initiation and progression of cardiovascular diseases by affecting the function of different cells through EETs

CYP2J3 Gene Delivery Reduces Insulin Resistance via Upregulation of eNOS in Fructose-treated Rats

Accumulating evidence suggests that cytochrome P450 (CYP) epoxygenases metabolize arachidonic acid into epoxyeicosatrienoic acids (EETs) which play important roles in various pathophysiological processes. Interestingly, CYP-derived eicosanoids are vasodilatory, at least in part through their ability to activate eNOS and subsequent NO release. This study investigated the roles of eNOS in CYP2J3 gene delivery reducing blood pressure and improving insulin resistance in fructose-treated rats. CYP2J3 overexpression in vivo increased EET generation, reduced blood pressure and reversed insulin resistance as determined by insulin resistance index (HOMA-IR). Furthermore, administration of eNOS inhibitor L-NMMA significantly and partially abolished the beneficial effects of CYP2J3 gene delivery on hypertension and insulin resistance induced by fructose intake, and possible mechanism is associated with increased ET-1, ETA-receptor mRNA expression and reduced sensitivity of insulin to peripheral tissues and organs characterized by reduced activity of IRS-1/PI3K/AKT and AMPK signalling pathways. These data provide direct evidence that CYP2J3-derived EETs may alleviate insulin resistance at least in part through upregulated eNOS expression

Two-Dimensional Honeycomb Monolayer of Nitrogen Group Elements and the Related Nano-Structure: A First-Principle Study

Because of its novel physical properties, two-dimensional materials have attracted great attention. From first-principle calculations and vibration frequenceis analysis, we predict a new family of two-dimensional materials based on the idea of octet stability: honeycomb lattices of pnictogens (N, P, As, Sb, Bi). The buckled structures of materials come from the sp3 hybridization. These materials have indirect band gap ranging from 0.43eV to 3.7eV. From the analysis of projected density of states, we argue that the s and p orbitals together are sufficient to describe the electronic structure under tight-binding model, and the tight-binding parameters are obtained by fitting the band structures to first-principle results. Surprisingly large on-site spin-orbit coupling is found for all the pnictogen lattices except nitrogen. Investigation on the electronic structures of both zigzag and armchair nanoribbons reveals the possible existence of spin-polarized ferromagnetic edge states in some cases, which are rare in one-dimensional systems. These edge states and magnetism may exist under the condition of high vaccum and low temperature. This new family of materials would have promising applications in electronics, optics, sensors, and solar cells.Comment: 22 pages, 10 figure

The growth of northeastern Tibet and its relevance to large-scale continental geodynamics: A review of recent studies

Recent studies of the northeastern part of the Tibetan Plateau have called attention to two emerging views of how the Tibetan Plateau has grown. First, deformation in northern Tibet began essentially at the time of collision with India, not 10–20 Myr later as might be expected if the locus of activity migrated northward as India penetrated the rest of Eurasia. Thus, the north-south dimensions of the Tibetan Plateau were set mainly by differences in lithospheric strength, with strong lithosphere beneath India and the Tarim and Qaidam basins steadily encroaching on one another as the region between them, the present-day Tibetan Plateau, deformed, and its north-south dimension became narrower. Second, abundant evidence calls for acceleration of deformation, including the formation of new faults, in northeastern Tibet since ~15 Ma and a less precisely dated change in orientation of crustal shortening since ~20 Ma. This reorientation of crustal shortening and roughly concurrent outward growth of high terrain, which swings from NNE-SSW in northern Tibet to more NE-SW and even ENE-WSW in the easternmost part of northeastern Tibet, are likely to be, in part, a consequence of crustal thickening within the high Tibetan Plateau reaching a limit, and the locus of continued shortening then migrating to the northeastern and eastern flanks. These changes in rates and orientation also could result from removal of some or all mantle lithosphere and increased gravitational potential energy per unit area and from a weakening of crustal material so that it could flow in response to pressure gradients set by evolving differences in elevation

Mechanism of histone deacetylases in cardiac hypertrophy and its therapeutic inhibitors

Cardiac hypertrophy is a key process in cardiac remodeling development, leading to ventricle enlargement and heart failure. Recently, studies show the complicated relation between cardiac hypertrophy and epigenetic modification. Post-translational modification of histone is an essential part of epigenetic modification, which is relevant to multiple cardiac diseases, especially in cardiac hypertrophy. There is a group of enzymes related in the balance of histone acetylation/deacetylation, which is defined as histone acetyltransferase (HAT) and histone deacetylase (HDAC). In this review, we introduce an important enzyme family HDAC, a key regulator in histone deacetylation. In cardiac hypertrophy HDAC I downregulates the anti-hypertrophy gene expression, including Kruppel-like factor 4 (Klf4) and inositol-5 phosphatase f (Inpp5f), and promote the development of cardiac hypertrophy. On the contrary, HDAC II binds to myocyte-specific enhancer factor 2 (MEF2), inhibit the assemble ability to HAT and protect against cardiac hypertrophy. Under adverse stimuli such as pressure overload and calcineurin stimulation, the HDAC II transfer to cytoplasm, and MEF2 can bind to nuclear factor of activated T cells (NFAT) or GATA binding protein 4 (GATA4), mediating inappropriate gene expression. HDAC III, also known as SIRTs, can interact not only to transcription factors, but also exist interaction mechanisms to other HDACs, such as HDAC IIa. We also present the latest progress of HDAC inhibitors (HDACi), as a potential treatment target in cardiac hypertrophy