Quantum Molecular Sieving Effects of H₂ and D₂ on Bundled and Nonbundled Single-Walled Carbon Nanotubes

The quantum molecular sieving effects of pore-structure-controlled single-walled carbon nanotubes (SWCNTs) for H₂ and D₂ were evaluated at 20, 40, and 77 K. The adsorption amounts of D₂ were larger than those of H₂. The lower the adsorption temperature, the greater the difference between the D₂ and H₂ adsorption amounts. Bundled SWCNTs with interstitial pores of diameter 0.6 nm gave the greatest adsorption difference between D₂ and H₂ per unit pore volume. Diffusion-dominated behavior was observed in the low-pressure region at 20 and 40 K as a result of lower mobility. Bundled SWCNTs with only interstitial pores provided a significant quantum molecular sieving as a result of strongly interacting potential wells

S1P3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species

金沢大学医薬保健研究域医学系Aims Sphingosine kinase 1 (SPHK1), its product sphingosine-1-phosphate (S1P), and S1P receptor subtypes have been suggested to play protective roles for cardiomyocytes in animal models of ischaemic preconditioning and cardiac ischaemia/reperfusion injury. To get more insight into roles for SPHK1 in vivo, we have generated SPHK1-transgenic (TG) mice and analysed the cardiac phenotype.Methods and results SPHK1-TG mice overexpressed SPHK1 in diverse tissues, with a nearly 20-fold increase in enzymatic activity. The TG mice grew normally with normal blood chemistry, cell counts, heart rate, and blood pressure. Unexpectedly, TG mice with high but not low expression levels of SPHK1 developed progressive myocardial degeneration and fibrosis, with upregulation of embryonic genes, elevated RhoA and Rac1 activity, stimulation of Smad3 phosphorylation, and increased levels of oxidative stress markers. Treatment of juvenile TG mice with pitavastatin, an established inhibitor of the Rho family G proteins, or deletion of S1P3, a major myocardial S1P receptor subtype that couples to Rho GTPases and transactivates Smad signalling, both inhibited cardiac fibrosis with concomitant inhibition of SPHK1-dependent Smad-3 phosphorylation. In addition, the anti-oxidant N-2-mercaptopropyonylglycine, which reduces reactive oxygen species (ROS), also inhibited cardiac fibrosis. In in vivo ischaemia/reperfusion injury, the size of myocardial infarct was 30 decreased in SPHK1-TG mice compared with wild-type mice.Conclusion These results suggest that chronic activation of SPHK1-S1P signalling results in both pathological cardiac remodelling through ROS mediated by S1P3 and favourable cardioprotective effects