Correlated metallic state in honeycomb lattice: Orthogonal Dirac semimetal

A novel gapped metallic state coined orthogonal Dirac semimetal is proposed in the honeycomb lattice in terms of $Z_{2}$ slave-spin representation of Hubbard model. This state corresponds to the disordered phase of slave-spin and has the same thermaldynamical and transport properties as usual Dirac semimetal but its singe-particle excitation is gapped and has nontrivial topological order due to the $Z_{2}$ gauge structure. The quantum phase transition from this orthogonal Dirac semimetal to usual Dirac semimetal is described by a mean-field decoupling with complementary fluctuation analysis and its criticality falls into the universality class of 2+1D Ising model while a large anomalous dimension for the physical electron is found at quantum critical point (QCP), which could be considered as a fingerprint of our fractionalized theory when compared to other non-fractionalized approaches. As byproducts, a path integral formalism for the $Z_{2}$ slave-spin representation of Hubbard model is constructed and possible relations to other approaches and the sublattice pairing states, which has been argued to be a promising candidate for gapped spin liquid state found in the numerical simulation, are briefly discussed. Additionally, when spin-orbit coupling is considered, the instability of orthogonal Dirac semimetal to the fractionalized quantum spin Hall insulator (fractionalized topological insulator) is also expected. We hope the present work may be helpful for future studies in $Z_{2}$ slave-spin theory and related non-Fermi liquid phases in honeycomb lattice.Comment: 12 pages,no figures, more discussions added. arXiv admin note: text overlap with arXiv:1203.063

Transmission resonance in a composite plasmonic structure

The design, fabrication, and optical properties of a composite plasmonic structure, a two-dimentional array of split-ring resonators inserted into periodic square holes of a metal film, have been reported. A new type of transmission resonance, which makes a significant difference from the conventional peaks, has been suggested both theoretically and experimentally. To understand this effect, a mechanism of ring- resonance induced dipole emission is proposed.Comment: 14 pages, 4 figure

[μ-1,1′-(Butane-1,4-di­yl)di-1H-benz­imidazole-κ2 N 3:N 3′]bis­{[N,N′-bis(car­boxy­meth­yl)ethyl­enediamine-N,N′-di­acetato-κ5 O,O′,O′′,N,N′]mercury(II)} methanol disolvate

The binuclear title complex, [Hg2(C10H14N2O8)2(C18H18N4)]·2CH3OH, lies on an inversion center with the unique HgII ion coordinated in a disorted octa­hedral environment with one Hg—N bond significantly shorter than the other two. In the crystal structure, inter­molecular O—H⋯O hydrogen bonds link complex and solvent mol­ecules into a three-dimensional network

Numerical simulation of dental resurfacing of a feldspar porcelain with coarse diamond burs

Dental bioceramics are more and more attractive to both dentists and patients due to their unique biocompatibility and esthetics; they can be fabricated efficiently using chair-side CAD/CAM dental systems. However, the failure rate of ceramic prostheses is noticeable high. The major clinical failure mode lies in surface and subsurface damage in the ceramic prostheses due to their inherent brittleness. In clinical practice, ceramic prostheses are intraorally adjusted and resurfaced using dental handpieces/burs for marginal and occlusal fit. The clinical adjustments using abrasive burs produce surface and subsurface damage in prostheses. This paper will address this issue via numerical simulation. Finite element analysis was utilised to model the dental resurfacing of a feldspar porcelain with coarse diamond burs and to predict the degrees of subsurface damage of the porcelain prostheses

Hepatic senescence, the good and the bad

Gradual alterations of cell's physiology and functions due to age or exposure to various stresses lead to the conversion of normal cells to senescent cells. Once becoming senescent, the cell stops dividing permanently but remains metabolically active. Cellular senescence does not have a single marker but is characterized mainly by a combination of multiple markers, such as, morphological changes, expression of cell cycle inhibitors, senescence associated β-galactosidase activity, and changes in nuclear membrane. When cells in an organ become senescent, the entire organism can be affected. This may occur through the senescence-associated secretory phenotype (SASP). SASP may exert beneficial or harmful effects on the microenvironment of tissues. Research on senescence has become a very exciting field in cell biology since the link between age-related diseases, including cancer, and senescence has been established. The loss of regenerative and homeostatic capacity of the liver over the age is somehow connected to cellular senescence. The major contributors of senescence properties in the liver are hepatocytes and cholangiocytes. Senescent cells in the liver have been implicated in the etiology of chronic liver diseases including cirrhosis and hepatocellular carcinoma and in the interference of liver regeneration. This review summarizes recently reported findings in the understanding of the molecular mechanisms of senescence and its relationship with liver diseases

Autophagy, Metabolism, and Alcohol-Related Liver Disease: Novel Modulators and Functions

Alcohol-related liver disease (ALD) is caused by over-consumption of alcohol. ALD can develop a spectrum of pathological changes in the liver, including steatosis, inflammation, cirrhosis, and complications. Autophagy is critical to maintain liver homeostasis, but dysfunction of autophagy has been observed in ALD. Generally, autophagy is considered to protect the liver from alcohol-induced injury and steatosis. In this review, we will summarize novel modulators of autophagy in hepatic metabolism and ALD, including autophagy-mediating non-coding RNAs (ncRNAs), and crosstalk of autophagy machinery and nuclear factors. We will also discuss novel functions of autophagy in hepatocytes and non-parenchymal hepatic cells during the pathogenesis of ALD and other liver diseases