Si/Ge interfacial thermal conductance enhancement through Sn nanoparticle embedding.

The improvement of interfacial thermal conductance (ITC) is a crucial aspect of the thermal management of nanodevices. In this paper, the effect of embedding Sn nanoparticles at the Si/Ge interface on ITC was investigated using non-equilibrium molecular dynamics (NEMD) simulations. It was found that although Sn has a higher atomic weight than both silicon and germanium, the ITC can be enhanced by 1.95 times when the nanoparticles reach a suitable number and diameter. The phonon transmission functions and density of states clearly indicate that an increased ITC can be attributed to the enhanced inelastic phonon scattering facilitated by Sn nanoparticles. This enhancement opens up novel channels for interfacial phonon transport. However, when the number of nanoparticles surpasses a suitable value, elastic phonons begin to dominate heat transport, leading to a subsequent decrease in the ITC. Sensitivity analysis further underscores that the ITC exhibits greater responsiveness to changes in diameter. In addition, it is also shown that with increasing temperature, a higher frequency phonon excitation occurs, increasing phonon inelastic scattering and interface transmission. These findings offer a novel strategy for enhancing ITC and deepening our comprehension of both elastic and inelastic phonon processes in interfacial phonon transport.

The effect of interface angle on the thermal conductivity of Si/Ge superlattices.

Si/Ge superlattices (SLs) are good candidates for thermoelectric materials because of their remarkable thermal insulating performance compared with their bulk counterparts. In this paper, the non-equilibrium molecular dynamics (NEMD) simulation method was applied to investigate the thermal conductivity of Si/Ge SLs containing tilted interfaces. It was found that the thermal conductivity will be 4-5 times higher than that of other angles when the period length is 4-8 atomic layers and the interface angle is 45°. This phenomenon can be attributed to the smooth arrangement of the 45° interface which induces phonon coherent transport. Meanwhile, the thermal conductivity has not been improved due to the phonon localization although the phonons satisfy the coherent transport when the interface angle is 90°. Interestingly, the thermal conductivity is almost unchanged with the increasing interface angle when the period length is large enough which exceeds 20 atomic layers. The main reason for the unchanged thermal conductivity is due to the period length which is greater than the phonon coherence length inducing the phonon incoherent transport.

The GPR120 Agonist TUG-891 Inhibits the Motility and Phagocytosis of Mouse Alveolar Macrophages.

Movement and phagocytosis characterize the fundamental actions of macrophages. Although it is known that the free fatty acid receptor GPR120 is expressed in macrophages and regulates cytokine expression to exert anti-inflammatory activities, the effects of GPR120 activation on the motility and phagocytosis of macrophages are not clear. In this study, mouse alveolar macrophages (AM) were stimulated with the GPR120 agonist TUG-891, and the changes in cell motility, intracellular Ca2+ concentration ([Ca2+]i), and the ability of phagocytosis were measured. Mouse AM in controls exhibited active movement in vitro, and TUG-891 significantly restrained AM movement. Meanwhile, TUG-891 stimulated a quick increase in [Ca2+]i in AM, which was blocked separately by the Gq protein inhibitor YM-254890, the phospholipase C (PLC) inhibitor U73122, or depletion of endoplasmic reticulum (ER) Ca2+ store by thapsigargin. The inhibition of AM movement by TUG-891 was eliminated by YM-254890, U73122, thapsigargin, and chelation of cytosolic Ca2+ by BAPTA. Moreover, TUG-891 inhibited AM phagocytosis of fluorescent microspheres, which was also blocked by YM-254890, U73122, thapsigargin, and BAPTA. In conclusion, GPR120 activation in mouse AM increases [Ca2+]i but inhibits the motility and phagocytosis via Gq protein/PLC-mediated Ca2+ release from ER Ca2+ store.

Tyrphostin AG556 increases the activity of large conductance Ca2+ -activated K+ channels by inhibiting epidermal growth factor receptor tyrosine kinase.

The present study was designed to investigate whether large conductance Ca2+ -activated K+ (BK) channels were regulated by epidermal growth factor (EGF) receptor (EGFR) tyrosine kinase. BK current and channel tyrosine phosphorylation level were measured in BK-HEK 293 cells expressing both functional α-subunits and the auxiliary ß1-subunits using electrophysiology, immunoprecipitation and Western blotting approaches, respectively, and the function of rat cerebral basilar arteries was determined with a wire myography system. We found that BK current in BK-HEK 293 cells was increased by the broad spectrum protein tyrosine kinase (PTK) inhibitor genistein and the selective EGFR tyrosine kinase inhibitor AG556, one of the known tyrphostin. The effect of genistein or AG556 was antagonized by the protein tyrosine phosphatase (PTP) inhibitor orthovanadate. On the other hand, orthovanadate or EGF decreased BK current, and the effect was counteracted by AG556. The tyrosine phosphorylation level of BK channels (α- and ß1-subunits) was increased by EGF and orthovanadate, while decreased by genistein and AG556, and the reduced tyrosine phosphorylation of BK channels by genistein or AG556 was reversed by orthovanadate. Interestingly, AG556 induced a remarkable enhancement of BK current in rat cerebral artery smooth muscle cells and relaxation of pre-contracted rat cerebral basilar arteries with denuded endothelium, and these effects were antagonized by the BK channel blocker paxilline or orthovanadate. These results demonstrate that tyrosine phosphorylation of BK channels by EGFR kinase decreases the channel activity, and inhibition of EGFR kinase by AG556 enhances the channel activity and dilates rat cerebral basilar arteries.