Pd2 and CoPd dimers/N-doped graphene sensors with enhanced sensitivity for CO detection: A first-principles study.

CONTEXT: The detection and monitoring of CO gas are essential to avoid human health problems. Therefore, the CO adsorption on Pd2 and PdCo dimers deposited on pyridinic Nx-doped graphene (PNxG; x = 1 - 3) was investigated employing the auxiliary density functional theory. In the most stable arrangements for the Pd2 dimer supported on PNxG, a Pd atom is in the PNxG vacancy, and the other Pd atom is placed on C atoms. For the PdCo dimer deposited on PNxG, the most stable interaction is like Pd2 dimer supported on PNxG, but with the Co atom centered over the vacancy site. Concerning the stability of the Pd2 and PdCo dimers supported on PNxG, the interaction energies (Eint) of the PdCo dimer deposited on PNxG are higher than those obtained with the Pd2 dimer. Also, the Eint of Pd2 and PdCo dimers deposited on PNxG are higher than those supported on pristine graphene. The CO adsorption energies on Pd2/PNxG and PdCo/PNxG composites are higher than those reported in the literature for pristine graphene, showing that the Pd2/PNxG and PdCo/PNxG composites have a good sensitivity toward the CO molecule. METHODS: All electronic structure calculations were performed using the auxiliary density functional theory implemented in the deMon2k program. For exchange and correlation functional, the revised PBE was used. The Pd atoms were treated with an 18-electron QECP|SD basis set, while the remaining atoms were subjected to a DZVP-GGA basis set. The GEN-A2* auxiliary-function-set was used for all computations.

Proteins involved in lipid metabolism as possible biomarkers or predisposing factors for non-alcoholic fatty liver disease.

Non-alcoholic fatty liver disease (NAFLD) is caused by the accumulation of lipids inside hepatocytes; it can be simple or it can be inflammatory. Its prevalence has been increasing in recent years and is predicted to become the most common indication for liver transplantation by 2030. NAFLD is a multifactorial disease, although patients with metabolic disorders are at higher risk of developing it, and in more severe forms. Liver fat originates from the increase of free fatty acids (FFA), from de novo lipogenesis and from diet. This review compile evidence of the involvement of unregulated enzymes in the synthesis of fatty acids (FA), the alteration of FA transport proteins, and the presence of diverse polymorphisms, which may be associated with an increased risk of NAFLD.

Molecular characterization of the hemagglutinin-neuraminidase gene of porcine rubulavirus isolates associated with neurological disorders in fattening and adult pigs.

"Blue eye disease" is a viral infection of swine endemic in Mexico, which produces fatal encephalitis accompanied by respiratory signs and corneal opacity in suckling piglets. An atypical blue eye disease outbreak presented high rates of neurological signs in fattening and adult pigs from 2000 to 2003. In order to identify the basis of increased neurovirulence, the hemagglutinin-neuraminidase (HN) gene of several porcine rubulavirus isolates were sequenced and compared with that of La Piedad Michoacan virus and other isolates that did not produce neurological disorders in weaned pigs. Nine amino acid mutations distinguished the high neurovirulent PAC6-PAC9 viruses, whereas five mutations characterized the low neurovirulent PAC2 and PAC3 viruses. HN protein three-dimensional models showed that the main conformation and functional domains were preserved, although substitutions A223T and A291D occurred in PAC2 and PAC3 viruses, as well as A511K and E514K presented in PAC6-PAC9 viruses considerably modified the properties of the HN protein surface. The increased positive charge of the HN protein of PAC6-PAC9 viruses seems to be associated with their increased neurovirulence.