Alzheimer's disease is a neurodegenerative disorder characterized by the extracellular deposition in the brain of aggregated ␤ -amyloid peptide, presumed to play a pathogenic role, and by preferential loss of neurons that express the 75-kD neurotrophin receptor (p75 NTR ). Using rat cortical neurons and NIH-3T3 cell line engineered to stably express p75 NTR , we find that the ␤ -amyloid peptide specifically binds the p75 NTR . Furthermore, 3T3 cells expressing p75 NTR , but not wild-type control cells lacking the receptor, undergo apoptosis in the presence of aggregated ␤ -amyloid. Normal neural crest-derived melanocytes that express physiologic levels of p75 NTR undergo apoptosis in the presence of aggregated ␤ -amyloid, but not in the presence of control peptide synthesized in reverse. These data imply that neuronal death in Alzheimer's disease is mediated, at least in part, by the interaction of ␤ -amyloid with p75 NTR , and suggest new targets for therapeutic intervention. ( J. Clin. Invest. 1997.

The application of graphene-based membranes is hindered by their poor stability under practical hydrodynamic conditions. Here, nanocarbon architectures are designed by intercalating surface-functionalized, small-diameter, multi-walled carbon nanotubes (MWCNTs) into reduced graphene oxide (rGO) sheets to create highly stable membranes with improved water permeability and enhanced membrane selectivity. With the intercalation of 10 nm diameter MWCNTs, the water permeability reaches 52.7 L m −2 h −1 bar −1 , which is 4.8 times that of pristine rGO membrane and fi ve to ten times higher than most commercial nanofi ltration membranes. The membrane also attains almost 100% rejection for three organic dyes of different charges. More importantly, the membrane can endure a turbulent hydrodynamic fl ow with cross-fl ow rates up to 2000 mL min −1 and a Reynolds number of 4667. Physicochemical characterization reveals that the inner graphitic walls of the MWCNTs can serve as spacers, while nanoscale rGO foliates on the outer walls interconnect with the assimilated rGO sheets to instill superior membrane stability. In contrast, intercalating with single-walled nanotubes fails to reproduce such stability. Overall, this nanoarchitectured design is highly versatile in creating both graphene-rich and CNT-rich all-carbon membranes with engineered nanochannels, and is regarded as a general approach in obtaining stable membranes for realizing practical applications of graphenebased membranes.

Metal oxides of earth-abundant elements are promising electrocatalysts to overcome the sluggish oxygen evolution and oxygen reduction reaction (OER/ORR) in many electrochemical energy-conversion devices. However, it is difficult to control their catalytic activity precisely. Here, a general three-stage synthesis strategy is described to produce a family of hybrid materials comprising amorphous bimetallic oxide nanoparticles anchored on N-doped reduced graphene oxide with simultaneous control of nanoparticle elemental composition, size, and crystallinity. Amorphous Fe Co O is obtained from Prussian blue analog nanocrystals, showing excellent OER activity with a Tafel slope of 30.1 mV dec and an overpotential of 257 mV for 10 mA cm and superior ORR activity with a large limiting current density of -5.25 mA cm at 0.6 V. A fabricated Zn-air battery delivers a specific capacity of 756 mA h g (corresponding to an energy density of 904 W h kg ), a peak power density of 86 mW cm and can be cycled over 120 h at 10 mA cm . Other two amorphous bimetallic, Ni Fe O and Ni Co O , are also produced to demonstrate the general applicability of this method for synthesizing binary metal oxides with controllable structures as electrocatalysts for energy conversion.

p75NTR , a nerve growth factor co-receptor that has been implicated in apoptosis of neurons, is structurally related to Fas and the receptors for tumor necrosis factor-␣ that display ligand independent assembly into trimers. Using embryonic day 17 fetal rat cortical neurons and p75 NTR -expressing NIH-3T3 cells, we now show that p75 NTR exists as a trimer as well as a monomer. Furthermore, we have reported and others have confirmed that amyloid ␤ binds p75 NTR , and that this binding leads to apoptotic cell death. We now report that amyloid ␤ binds to trimers of p75 NTR as well as to p75 NTR monomers but not to the p140 trkA , the nerve growth factor co-receptor that mediates neuronal survival. Furthermore, amyloid ␤ activates p75 NTR , strongly inducing the transcription of c-Jun mRNA and stimulating the stress-activated c-Jun NH 2 -terminal kinase, as measured by phosphorylation of its substrate (glutathione S-transferase-c-Jun-(1-79)). Our data suggest that p75 NTR may be present as a preformed trimer that binds amyloid ␤ to induce receptor activation, and support the hypothesis that p75 NTR activation by amyloid ␤ is causally related to Alzheimer's disease.