Metal-Organic Frameworks-Derived Mesoporous Si/SiOx @NC Nanospheres as a Long-Lifespan Anode Material for Lithium-Ion Batteries.

Silicon (Si)-based anode materials with suitable engineered nanostructures generally have improved lithium storage capabilities, which provide great promise for the electrochemical performance in lithium-ion batteries (LIBs). Herein, a metal-organic framework (MOF)-derived unique core-shell Si/SiOx @NC structure has been synthesized by a facile magnesio-thermic reduction, in which the Si and SiOx matrix were encapsulated by nitrogen (N)-doped carbon. Importantly, the well-designed nanostructure has enough space to accommodate the volume change during the lithiation/delithiation process. The conductive porous N-doped carbon was optimized through direct carbonization and reduction of SiO2 into Si/SiOx simultaneously. Benefiting from the core-shell structure, the synthesized product exhibited enhanced electrochemical performance as an anode material in LIBs. Particularly, the Si/SiOx @NC-650 anode showed the best reversible capacities up to 724 and 702 mAh g-1 even after 100 cycles. The excellent cycling stability of Si/SiOx @NC-650 may be attributed to the core-shell structure as well as the synergistic effect between the Si/SiOx and MOF-derived N-doped carbon.

Propranolol regulates cardiac transient outward potassium channel in rat myocardium via cAMP/PKA after short-term but not after long-term ischemia.

It was recently suggested that the antiarrhythmic effect of propranolol, a ss-adrenoceptor antagonist, on ischemic myocardium includes restoration of I(K1) current and Cx43 conductance; however, little is known whether effects on the transient outward current I(to) contribute. A model of myocardial infarction (MI) by ligating the left anterior descending coronary artery was established. Propranolol was given 1 h or daily for 3 months, whole-cell patch-clamp techniques were used to measure I(to). Kv4.2 and PKA levels were analyzed by Western blot and cAMP level was determined by radioimmunoassay. The results showed that propranolol decreased the incidence of arrhythmias induced by acute ischemia and mortality in 3 month MI rats. Propranolol restored the diminished I(to) density and Kv4.2 protein in MI hearts. In addition, neonatal cardiomyocyte pretreatment with propranolol or administrated after hypoxia can resume I(to) density. cAMP/PKA was enhanced in acute MI, the reason of decreased Kv4.2 expression. Treatment with propranolol prevented the increased cAMP/PKA in 1 h MI, whereas propranolol had little effect on decreased cAMP/PKA in 3 months MI. This study demonstrated that both short- and long-term propranolol administrations protect cardiomyocytes against arrhythmias and mortality caused by cardiac ischemia; the involvement of cAMP/PKA signal pathway in the regulation of propranolol on I(to) acted differently along with the ischemic progression.