This study deals with the dispersion of longitudinal waves in a single-walled armchair
carbon nanotube, focusing on the effect of the microstructure of the carbon nanotube on
the wave dispersion. To reveal the effect analytically, the carbon nanotube is modelled as a
non-local elastic cylindrical shell in the study. The dynamic equation of the non-local
elastic cylindrical shell is established and the corresponding dispersion relation of
longitudinal waves is derived. These analytic results are verified via molecular dynamics
simulations, based on the Terroff–Brenner potential, for the propagation of various
longitudinal waves in three single-walled armchair carbon nanotubes. The molecular
dynamics simulations indicate that the longitudinal wave dispersion predicted by the model
of the non-local elastic cylindrical shell shows a good agreement with that of
molecular dynamics simulations in a wide frequency range up to the terahertz region.
They also show that both the microstructure of the carbon nanotube and the
coupling between the longitudinal wave and the radial motion play an important
role in the dispersion of longitudinal waves in a single-walled armchair carbon
nanotube.
Nicotinic acid (niacin) has been shown to decrease myocyte injury. Because interventions that lower the cytosolic NADH/NAD(+) ratio improve glycolysis and limit infarct size, we hypothesized that 1) niacin, as a precursor of NAD(+), would lower the NADH/NAD(+) ratio, increase glycolysis, and limit ischemic injury and 2) these cardioprotective benefits of niacin would be limited in conditions that block lactate removal. Isolated rat hearts were perfused without (Ctl) or with 1 microM niacin (Nia) and subjected to 30 min of low-flow ischemia (10% of baseline flow, LF) and reperfusion. To examine the effects of limiting lactate efflux, experiments were performed with 1) Ctl and Nia groups subjected to zero-flow ischemia and 2) the Nia group treated with the lactate-H(+) cotransport inhibitor alpha-cyano-4-hydroxycinnamate under LF conditions. Measured variables included ATP, pH, cardiac function, tissue lactate-to-pyruvate ratio (reflecting NADH/NAD(+)), lactate efflux rate, and creatine kinase release. The lactate-to-pyruvate ratio was reduced by more than twofold in Nia-LF hearts during baseline and ischemic conditions (P < 0.001 and P < 0.01, respectively), with concurrent lower creatine kinase release than Ctl hearts (P < 0.05). Nia-LF hearts had significantly greater lactate release during ischemia (P < 0.05 vs. Ctl hearts) as well as higher functional recovery and a relative preservation of high-energy phosphates. Inhibiting lactate efflux with alpha-cyano-4-hydroxycinnamate and blocking lactate washout with zero flow negated some of the beneficial effects of niacin. During LF, niacin lowered the cytosolic redox state and increased lactate efflux, consistent with redox regulation of glycolysis. Niacin significantly improved functional and metabolic parameters under these conditions, providing additional rationale for use of niacin as a therapeutic agent in patients with ischemic heart disease.
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