Physical model of neutron scattering by clathrate hydrate and C60hosting paramagnetic oxygen molecules.

This paper describes the physical modelling of neutron scattering in two polycrystalline inclusion compounds, fully deuterated clathrate hydrate andC60, each with paramagnetic oxygen as guest molecules. For studying the suitability of these materials for neutron moderation to very low energies, the model includes, in addition to the magnetic neutron scattering by the oxygen, the nuclear scattering by all constituents. The theoretical total cross sections are calculated based on the phonon density of states obtained by density functional theory and molecular dynamics simulations.

Coulomb excitation of 104Sn and the strength of the 100Sn shell closure.

A measurement of the reduced transition probability for the excitation of the ground state to the first 2+ state in 104Sn has been performed using relativistic Coulomb excitation at GSI. 104Sn is the lightest isotope in the Sn chain for which this quantity has been measured. The result is a key point in the discussion of the evolution of nuclear structure in the proximity of the doubly magic nucleus 100Sn.

Effect of Ni(II) on inflammatory gene expression in THP1 monocytic cells.

Nickel-containing alloys are in common use for dental restorations, but tend to corrode and release Ni(II) in service. Ni(II) increases secretion of several inflammatory cytokines from activated monocytic cells, suggesting that nickel alloys may exaggerate inflammatory responses in adjacent periodontal tissues. In this work, the effects of Ni(II) on expression of inflammatory cytokine and receptor genes as well as nuclear factor-kappa B (NFκB)-related genes were assessed using quantitative real-time polymerase chain reaction (PCR) and PCR-based arrays in the human THP1 monocytic cell line pre-exposed to Ni(II) for 72 h, then activated by lipopolysaccharide.

Ni(II) alters the NFκB signaling pathway in monocytic cells.

Nickel-based alloys are used for dental restorations because of their strength, high moduli, and relatively low cost. However, these alloys corrode significantly in use, particularly in lower pH environments that are common under oral biofilms. Ni(II) corrosion products increase inflammatory cytokine secretion from activated monocytes, suggesting that nickel alloys may exacerbate inflammatory responses in adjacent periodontal tissues caused by dental plaque.

PAR1- and PAR2-induced innate immune markers are negatively regulated by PI3K/Akt signaling pathway in oral keratinocytes.

Background: Protease-Activated Receptors (PARs), members of G-protein-coupled receptors, are activated by proteolytic activity of various proteases. Activation of PAR1 and PAR2 triggers innate immune responses in human oral keratinocytes (HOKs), but the signaling pathways downstream of PAR activation in HOKs have not been clearly defined. In this study, we aimed to determine if PAR1- and PAR2-mediated signaling differs in the induction of innate immune markers CXCL3, CXCL5 and CCL20 via ERK, p38 and PI3K/Akt.