One-stone, two birds: One step regeneration of discarded copper foil in zinc battery for dendrite-free lithium deposition current collector.

The ever-growing requirement for electrochemical energy storage has exacerbated the production of spent batteries, and the recycling of valuable battery components has recently received a remarkable attention. Among all battery components, copper foil is widely utilized as a current collector for stable zinc platting and stripping in zinc metal batteries (ZMBs) due to the perfect lattice matching of between metal copper and zinc, which is accompanied by the formation of multiple copper-zinc alloy components during the cycling process. Herein, a novel "two birds with one-stone" strategy through a one simple heat treatment step to revive the discarded copper foil in zinc metal battery is reported to further obtain a lithiophilic current collector (CuxZny-Cu) with multiple copper-zinc alloy components on the surface of the discarded copper foil. Such revived CuxZny-Cu current collector greatly reduces the lithium nucleation overpotential and realizes uniform lithium deposition and further inhibits lithium dendrites growth. The formed multiple CuxZny alloy phases on the surface of discarded copper foil exhibit a low Li nucleation overpotential of only 15 mV at 0.5 mA cm-2 for the first cycle. Moreover, such a CuxZny-Cu current collector could achieve stable cycle for 220 cycles at 0.5 mA cm-2 and 110 cycles at 1 mA cm-2 with a Li plating capacity of 1 mAh cm-2. Theoretical calculations indicate that, compared with pure Cu foil, the formed multiple alloy components of CuZn5, CuZn8, Cu0.61Zn0.39 and CuZn have low adsorption energy of -2.17, -2.55, -2.16 and -2.35 eV with lithium atoms, respectively, which result in reduced lithium nucleation overpotential. The full cell composed of CuxZny alloy current collector with deposition of 5 mAh cm-2 metal Li anode coupled with LiFePO4 (LFP) cathode exhibits a reversible capacity of 125.6 mAh/g after 110 cycles at a current of 0.5 C with capacity retention of 85.1 %. This work proposed a promising strategy to regenerate the discarded copper foil in rechargeable batteries.

Construction of Supercapacitor-Based Ionic Diodes with Adjustable Bias Directions by Using Poly(ionic liquid) Electrolytes.

The newly emerging supercapacitor-diode (CAPode), integrating the characteristics of a diode into an electrical-double-layer capacitor, can be employed to extend conventional supercapacitors to new technological applications and may play a crucial role in grid stabilization, signal propagation, and logic operations. However, the reported CAPodes have only been able to realize charge storage in the positive-bias direction. Here, bias-direction-adjustable CAPodes realized by using a polycation-based ionic liquid (IL) or a polyanion-based IL as electrolyte in an asymmetric carbon-based supercapacitor architecture are proposed. The resulting CAPodes exhibit charge-storage function at only the positive- or negative-bias direction with a high rectification ratio (≈80% for rectification ratio II, RRII ) and an outstanding cycling life (4500 cycles), representing a crucial breakthrough for designing high-performance capacitive ionic diodes.

Homocysteine accelerates atherosclerosis by inhibiting scavenger receptor class B member1 via DNMT3b/SP1 pathway.

Homocysteine (Hcy) is an independent risk factor for atherosclerosis, which is characterized by lipid accumulation in the atherosclerotic plaque. Increasing evidence supports that as the main receptor of high-density lipoprotein, scavenger receptor class B member 1 (SCARB1) is protective against atherosclerosis. However, the underlying mechanism regarding it in Hcy-mediated atherosclerosis remains unclear. Here, we found the remarkable inhibition of SCARB1 expression in atherosclerotic plaque and Hcy-treated foam cells, whereas overexpression of SCARB1 can suppress lipid accumulation in foam cells following Hcy treatment. Analysis of SCARB1 promoter showed that no significant change of methylation level was observed both in vivo and in vitro under Hcy treatment. Moreover, it was found that the negative regulation of DNMT3b on SCARB1 was due to the decreased recruitment of SP1 to SCARB1 promoter. Thus, we concluded that inhibition of SCARB1 expression induced by DNMT3b at least partly accelerated Hcy-mediated atherosclerosis through promoting lipid accumulation in foam cells, which was attributed to the decreased binding of SP1 to SCARB1 promoter. In our point, these findings will provide novel insight into an epigenetic mechanism for atherosclerosis.

Aberrant MFN2 transcription facilitates homocysteine-induced VSMCs proliferation via the increased binding of c-Myc to DNMT1 in atherosclerosis.

It is well-established that homocysteine (Hcy) is an independent risk factor for atherosclerosis. Hcy can promote vascular smooth muscle cell (VSMC) proliferation, it plays a key role in neointimal formation and thus contribute to arteriosclerosis. However, the molecular mechanism on VSMCs proliferation underlying atherosclerosis is not well elucidated. Mitofusin-2 (MFN2) is an important transmembrane GTPase in the mitochondrial outer membrane and it can block cells in the G0/G1 stage of the cell cycle. To investigate the contribution of aberrant MFN2 transcription in Hcy-induced VSMCs proliferation and the underlying mechanisms. Cell cycle analysis revealed a decreased proportion of VSMCs in G0/G1 and an increased proportion in S phase in atherosclerotic plaque of APOE-/- mice with hyperhomocystinaemia (HHcy) as well as in VSMCs exposed to Hcy in vitro. The DNA methylation level of MFN2 promoter was obviously increased in VSMCs treated with Hcy, leading to suppressed promoter activity and low expression of MFN2. In addition, we found that the expression of c-Myc was increased in atherosclerotic plaque and VSMCs treated with Hcy. Further study showed that c-Myc indirectly regulates MFN2 expression is duo to the binding of c-Myc to DNMT1 promoter up-regulates DNMT1 expression leading to DNA hypermethylation of MFN2 promoter, thereby inhibits MFN2 expression in VSMCs treated with Hcy. In conclusion, our study demonstrated that Hcy-induced hypermethylation of MFN2 promoter inhibits the transcription of MFN2, leading to VSMCs proliferation in plaque formation, and the increased binding of c-Myc to DNMT1 promoter is a new and relevant molecular mechanism.