A Hydrogel Electrolyte with High Adaptability over a Wide Temperature Range and Mechanical Stress for Long-Life Flexible Zinc-Ion Batteries.

Flexible zinc-ion batteries have garnered significant attention in the realm of wearable technology. However, the instability of hydrogel electrolytes in a wide-temperature range and uncontrollable side reactions of the Zn electrode have become the main problems for practical applications. Herein, N,N-dimethylformamide (DMF) to design a binary solvent (H2O-DMF) is introduced and combined it with polyacrylamide (PAM) and ZnSO4 to synthesize a hydrogel electrolyte (denoted as PZD). The synergistic effect of DMF and PAM not only guides Zn2+ deposition on Zn(002) crystal plane and isolates H2O from the Zn anode, but also breaks the hydrogen bonding network between water to improve the wide-temperature range stability of hydrogel electrolytes. Consequently, the symmetric cell utilizing PZD can stably cycle over 5600 h at 0.5 mA cm- 2@0.5 mAh cm-2. Furthermore, the Zn//PZD//MnO2 full cell exhibits favorable wide-temperature range adaptability (for 16000 cycles at 3 A g-1 under 25 °C, 750 cycles with 98 mAh g-1 at 0.1 A g-1 under -20 °C) and outstanding mechanical properties (for lighting up the LEDs under conditions of pressure, bending, cutting, and puncture). This work proposes a useful modification for designing a high-performance hydrogel electrolyte, which provides a reference for investigating the practical flexible aqueous batteries.

The Metabolism and Liver Toxicity of N,N-dimethylformamide in the Isolated Perfused Rat Liver

N,N-dimethylformamide (DMF) is metabolized by the microsomal cytochrome p-450 into mainly N-hydroxymethyl- N-methylformamide (HMMF), which further breaks down to N-methyformamide (NMF). However, the detailed mechanism of its toxicity remains unclear. We investigated the metabolism and the toxicity of DMF using the isolated perfused liver model. DMF was added to the recirculating perfusate of the isolated perfused rat liver at concentrations of 0, 10 and 25 mM. Samples were collected from the inferior vena cava at 0, 30, 45, 60, 75, and 90 minutes following addition of the DMF. The metabolites of DMF were analyzed using Gas-chromatography (GC). The changes in the rate of oxygen consumption by the DMF were monitored during perfusion. The enzyme activities (aspartic aminotransferase:AST, alanine aminotransferase:ALT, and lactic dehydrogenase:LDH)) in the perfusate were monitored to see if DMF caused hepatotoxicity. As the perfusion progressed, the DMF concentration in the perfusate decreased, but the level of NMF increased to a maximum of 1.16 mM. The rate of oxygen consumption increased at DMF concentrations of 10 mM and 25 mM. However, when a known inhibitor of cytochrome p-450, SKF 525A (300 micro M), was used to pretreat the perfusate prior to the addition of the DMF, the rate of oxygen consumption was significantly inhibited, indicating the cytochrome p-450 system was responsible for the conversion of DMF to NMF. On addition of the DMF, the activities of the enzymes AST, ALT and LDH were significantly increased a time and dose dependent manner. However, following pretreatment with SKF 525A, their releases were inhibited.