Plasma membrane calcium ATPase 4b inhibits nitric oxide generation through calcium-induced dynamic interaction with neuronal nitric oxide synthase.

The activation and deactivation of Ca(2+)- and calmodulindependent neuronal nitric oxide synthase (nNOS) in the central nervous system must be tightly controlled to prevent excessive nitric oxide (NO) generation. Considering plasma membrane calcium ATPase (PMCA) is a key deactivator of nNOS, the present investigation aims to determine the key events involved in nNOS deactivation of by PMCA in living cells to maintain its cellular context. Using time-resolved Förster resonance energy transfer (FRET), we determined the occurrence of Ca(2+)-induced protein-protein interactions between plasma membrane calcium ATPase 4b (PMCA4b) and nNOS in living cells.

Stable photoluminescent ZnO@Cd(OH)2 core-shell nanoparticles synthesized via ultrasonication-assisted sol-gel method.

Core-shell structured ZnO@Cd(OH)(2) nanoparticles with stable and improved luminescence have been prepared successfully via a facile ultrasonication-assisted sol-gel method. Their composition and structure have been confirmed by high resolution transmission electron microscopy, X-ray diffraction, energy-dispersive X-ray spectroscopy, X-ray photoelectron spectroscopy, and infrared spectra. The size of the nanoparticles decreases gradually along with the increase in the shell thickness, indicating that Cd(OH)(2) shells can hider ZnO cores growth and aggregation effectively.

ESeroS-GS modulates lipopolysaccharide-induced macrophage activation by impairing the assembly of TLR-4 complexes in lipid rafts.

The binding of lipopolysaccharides (LPS) to macrophages results in inflammatory responses. In extreme cases it can lead to endotoxic shock, often resulting in death. A broad range of antioxidants, including tocopherols, can reduce LPS activity in vitro and in vivo.

Induction of inducible nitric oxide synthase increases the production of reactive oxygen species in RAW264.7 macrophages.

Macrophages produce a large volume of ROS (reactive oxygen species) through respiratory burst. However, the influence of iNOS [inducible NOS (nitric oxide synthase)] activation on ROS production remains unclear. In the present study, the kinetic generation of ROS in RAW264.

Melatonin impairs NADPH oxidase assembly and decreases superoxide anion production in microglia exposed to amyloid-beta1-42.

Melatonin shows significant protective effects in Alzheimer's disease (AD) models in vitro and in vivo; these effects are related to its function as an antioxidant. The source of reactive oxygen species (ROS) generation in the AD brain is primarily the amyloid-beta (Abeta)- activated microglial nicotinamide adenine dinucleotide phosphate (NADPH) oxidase. However, the effects of melatonin on the activation of NADPH oxidase remain unclear.

Two-photon fluorescence measurements of reversible photodegradation in a dye-doped polymer.

We report on the dynamics of photodegradation and subsequent recovery of two-photon fluorescence in a dye-doped polymer. The energy dependence suggests that photodegradation is a linear process, while recovery is entropic. Such recovery could be useful to high-intensity devices such as two-photon absorbers, which can be used in many applications.

Pushing the hyperpolarizability to the limit.

We use numerical optimization to find a one-dimensional potential energy function that yields the largest hyperpolarizability, which we find is within 30% of the fundamental limit. Our results reveal insights into the character of the potential energy functions and wave functions that lead to the largest hyperpolarizability. We suggest that donor-acceptor molecules with a conjugated bridge with many sites of reduced conjugation to impart conjugation modulation may be the best paradigm for making materials with huge hyperpolarizabilities that approach the fundamental limit.