Silver nanoparticles supported on carbon nanotube carpets: influence of surface functionalization.

The effectiveness of nanoparticle-based functional devices depends strongly on the surface morphology and area of the support. An emerging powerful approach of increasing the available surface area without decreasing strength or increasing bulk is to attach arrays of suitable nanotubes on the surface, and to attach the necessary nanoparticles to them. Earlier publications by this team have shown that carpet-like arrays of carbon nanotubes (CNTs) can be successfully grown on a variety of larger carbon substrates such as graphite, foams and fabric, which offer hierarchical multiscale supporting architecture suitable for the attachment of silver nanoparticles (AgNPs).

A single amino acid change humanizes long-chain fatty acid binding and activation of mouse peroxisome proliferator-activated receptor α.

Peroxisome proliferator-activated receptor α (PPARα) is an important regulator of hepatic lipid metabolism which functions through ligand binding. Despite high amino acid sequence identity (>90%), marked differences in PPARα ligand binding, activation and gene regulation have been noted across species. Similar to previous observations with synthetic agonists, we have recently reported differences in ligand affinities and extent of activation between human PPARα (hPPARα) and mouse PPARα (mPPARα) in response to long chain fatty acids (LCFA).

Divergence between human and murine peroxisome proliferator-activated receptor alpha ligand specificities.

Peroxisome proliferator-activated receptor α (PPARα) belongs to the family of ligand-dependent nuclear transcription factors that regulate energy metabolism. Although there exists remarkable overlap in the activities of PPARα across species, studies utilizing exogenous PPARα ligands suggest species differences in binding, activation, and physiological effects. While unsaturated long-chain fatty acids (LCFA) and their thioesters (long-chain fatty acyl-CoA; LCFA-CoA) function as ligands for recombinant mouse PPARα (mPPARα), no such studies have been conducted with full-length human PPARα (hPPARα).

Low-dose sarin exposure produces long term changes in brain neurochemistry of mice.

Sarin is a toxic organophosphorus (OP) nerve agent that has been reported to cause long-term alterations in behavioral and neuropsychological processes. The present study was designed to investigate the effect of low dose sarin exposure on the monoamine neurotransmitter systems in various brain regions of mice. The rationale was to expand our knowledge about the noncholinergic neurochemical alterations associated with low dose exposure to this cholinesterase inhibitor.