Ultralow loading Pt nanocatalysts prepared by atomic layer deposition on carbon aerogels.

Using atomic layer deposition (ALD), we show that Pt nanoparticles can be deposited on the inner surfaces of carbon aerogels (CA). The resultant Pt-loaded materials exhibit high catalytic activity for the oxidation of CO even at loading levels as low as approximately 0.05 mg Pt/cm2. We observe a conversion efficiency of nearly 100% in the 150-250 degrees C temperatures range, and the total conversion rate seems to be limited only by the thermal stability of the CA support in ambient oxygen. The ALD approach described here is universal in nature, and can be applied to the design of new catalytic materials for a variety of applications, including fuel cells, hydrogen storage, pollution control, green chemistry, and liquid fuel production.

Nasal administration of osteopontin peptide mimetics confers neuroprotection in stroke.

Osteopontin (OPN), a large secreted glycoprotein with an arginine, glycine, aspartate (RGD) motif, can bind and signal through cellular integrin receptors. We have shown previously that OPN enhances neuronal survival in the setting of ischemia. Here, we sought to increase the neuroprotective potency of OPN and improve the method of delivery with the goal of identifying a treatment for stroke in humans. We show that thrombin cleavage of OPN improves its ability to ligate integrin receptors and its neuroprotective capacity in models of ischemia. Thrombin-cleaved OPN is a twofold more effective neuroprotectant than the untreated molecule. We also tested whether OPN could be administered intranasally and found that it is efficiently targeted to the brain via intranasal delivery. Furthermore, intranasal administration of thrombin-treated OPN confers protection against ischemic brain injury. Osteopontin mimetics based on the peptide sequences located either N or C terminal to the thrombin cleavage site were generated and tested in models of ischemia. Treatment with successively shorter N-terminal peptides and a phosphorylated C-terminal peptide provided significant neuroprotection against ischemic injury. These findings show that OPN mimetics offer promise for development into new drugs for the treatment of stroke.

Preconditioning reprograms the response to ischemic injury and primes the emergence of unique endogenous neuroprotective phenotypes: a speculative synthesis.

Ischemic tolerance in the brain, in which sub-threshold insults increase resistance to subsequent injurious ischemia, is a powerful adaptive defense that involves an endogenous program of neuroprotection. Emerging evidence from genomic studies suggests diverse stimuli that trigger preconditioning achieve neuroprotection through a common process which depends on a fundamental reprogramming of the response to injury. Such reprogramming of the genomic response to injury leads to the induction of novel neuroprotective pathways not ordinarily found in the setting of ischemia. Genomic studies also indicate that the nature of the preconditioning stimulus (eg, brief ischemia or endotoxin [lipopolysaccharide]) dictates the phenotype of neuroprotection, a phenotype that parallels protective adaptations also found in certain physiological conditions where the preconditioning stimulus exists at levels that can induce injury. The idea that preconditioning leads to a fundamental reprogramming event that confers neuroprotection is a novel and important concept in the field of ischemic tolerance. Moreover, the view that distinct preconditioning stimuli confer neuroprotection via effectors that differ according to the nature of the preconditioning stimulus offers promise that multiple, nonoverlapping pathways may be discovered as novel neuroprotective therapies.