104 research outputs found

    CVD growth of carbon nanostructures from zirconia: mechanisms and a method for enhancing yield.

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    By excluding metals from synthesis, growth of carbon nanostructures via unreduced oxide nanoparticle catalysts offers wide technological potential. We report new observations of the mechanisms underlying chemical vapor deposition (CVD) growth of fibrous carbon nanostructures from zirconia nanoparticles. Transmission electron microscope (TEM) observation reveals distinct differences in morphological features of carbon nanotubes and nanofibers (CNTs and CNFs) grown from zirconia nanoparticle catalysts versus typical oxide-supported metal nanoparticle catalysts. Nanofibers borne from zirconia lack an observable graphitic cage consistently found with nanotube-bearing metal nanoparticle catalysts. We observe two distinct growth modalities for zirconia: (1) turbostratic CNTs 2-3 times smaller in diameter than the nanoparticle localized at a nanoparticle corner, and (2) nonhollow CNFs with approximately the same diameter as the nanoparticle. Unlike metal nanoparticle catalysts, zirconia-based growth should proceed via surface-bound kinetics, and we propose a growth model where initiation occurs at nanoparticle corners. Utilizing these mechanistic insights, we further demonstrate that preannealing of zirconia nanoparticles with a solid-state amorphous carbon substrate enhances growth yield.This material is based upon work supported by the National Science Foundation under Grant No. 1007793 and was also supported by Airbus group, Boeing, Embraer, Lockheed Martin, Saab AB, Hexcel, and TohoTenax through MIT’s Nano- Engineered Composite aerospace STructures (NECST) Consortium. This research was supported (in part) by the U.S. Army Research Office under Contract W911NF-13-D-0001. This work was performed in part at the Center for Nanoscale Systems (CNS), a member of the National Nanotechnology Infrastructure Network (NNIN), which is supported by the National Science Foundation under NSF Award No. ECS-0335765. CNS is part of Harvard University. This work was carried out in part through the use of MIT Microsystems Technology Laboratories. Stephan Hofmann acknowledges funding from EPSRC under grant EP/H047565/1. Piran Kidambi acknowledges the Lindemann Trust Fellowship.This is the final published version. It first appeared at http://pubs.acs.org/doi/abs/10.1021/ja509872y

    Systematic study of (n, p) reaction cross sections from the reaction threshold to 20 MeV

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    The cross sections of Cr-nat(n, x)V-52, Cr-52(n, p)V-52, Cr-nat(n, x)V-53, Cr-53(n, p)V-53, Zn-nat(n, x)Cu-66, Zn-66(n, p)Cu-66, Zn-nat(n, x)Cu-68(m), Zn-68(n, p)Cu-68(m), Mo-nat(n, x)Nb-97(g), Mo-97(n, p)Nb-97(g), Mo-nat(n, x)Nb-97(m), Mo-97(n, p)Nb-97(m), Sn-nat(n, x)In-116(m1+m2), Sn-116(n, p)In-116(m1+m2), Sn-nat(n, x)In-117(g), Sn-117(n, p)In-117(g), Sn-nat(n, x)In-118(m1+m2), Sn-118(n, p)In-118(m1+m2), Sn-nat(n, x)In-120(x), Sn-120(n, p)In-120(x), Ba-nat(n, x)Cs-138, and Ba-138(n, p)Cs-138 reactions have been measured at 14.8 MeV neutron energy. In the present work, the contributions of (n, np), (n, pn), and (n, d) reactions from heavier isotopes are subtracted. The cross sections were also estimated with the TALYS-1.2 nuclear model code using different level density models, at neutron energies varying from the reaction threshold to 20 MeV. The variations in the (n, p) cross sections with the neutron number in the isotopes of an element are also discussed in brief

    Neuroprotective effect of Cubebin: A dibenzylbutyrolactone lignan on scopolamine-induced amnesia in mice

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    Background & objectives: Acetylcholinesterase (AChE) inhibitors represent a major class of drugs which provide symptomatic relief and improvement in cognitive function in Alzheimer's disease (AD). In this study, cubebin, a dibenzylbutyrolactone lignan, was isolated from Piper cubeba and investigated for its AChE inhibitory activity in an attempt to explore its potential for memory-enhancing activities in mice. Methods: Molecular docking of cubebin was carried out followed by in vitro AChE activity. Mice were treated with cubebin (25 & 50 mg/kg; i.p.), for three days and memory impairment was induced by scopolamine (3 mg/kg; i.p.). Memory function was evaluated by Morris water maze (MWM) test. Biochemical parameters of oxidative stress and cholinergic function were estimated in brain. Results: Molecular docking study revealed that cubebin was well bound within the binding site of the AChE enzyme showing interactions such as π-π stacking and hydrogen bonding with residues present therein. Cubebin inhibited AChE enzyme in an in vitro assay with IC50value of 992 μM. Scopolamine administration caused a significant impairment of learning and memory in mice, as indicated by a marked decrease in MWM performance. Scopolamine administration also produced a significant enhancement of brain AChE activity and oxidative stress in mice brain. Pre-treatment of cubebin (25 and 50 mg/kg; i.p.) significantly prevented scopolamine-induced learning and memory deficits along with attenuation of scopolamine-induced rise in brain AChE activity and oxidative stress level. Interpretation & conclusions: Cubebin showed promising protective activity in scopolamine-induced spatial memory impairment in mice. This could be attributed to its brain AChE inhibition and antioxidant activity
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