ABSTRACT
Constructing an artificial solid electrolyte interphase (ASEI) on Li metal anodes (LMAs) is a potential strategy for addressing the dendrite issues. However, the mechanical fatigue of the ASEI caused by stress accumulation under the repeated deformation from the Li plating/stripping is not taken seriously. Herein, this work introduces a mechanically interlocked [an]daisy chain network (DCMIN) into the ASEI to stabilize the Li metal/ASEI interface by combining the functions of energy dissipation and fast Li-ion transport. The DCMIN featured by large-range molecular motions is cross-linked via efficient thiol-ene click chemistry; thus, the DCMIN has flexibility and excellent mechanical properties. As an ASEI, the crown ether units in DCMIN not only interact with the dialkylammonium of a flexible chain, forming the energy dissipation behavior but also coordinate with Li ion to support the fast Li-ion transport in DCMIN. Therefore, a stable 2800 h-symmetrical cycling (1 mA cm-2) and an excellent 5 C-rate (full cell with LiFePO4) performance are achieved by DCMIN-based ASEI. Furthermore, the 1-Ah pouch cell (LiNi0.88Co0.09Mn0.03O2 cathode) with DCMIN-coated LMA exhibits improved capacity retention (88%) relative to the Control. The molecular design of DCMIN provides new insights into the optimization of an ASEI for high-energy LMAs.
ABSTRACT
The separator with high Young's modulus can avoid the danger of large-sized dendrites, but regulating the chemical behavior of lithium (Li) at the separator/anode interface can effectively eliminate the dendrite issue. Herein, a polyimine aerogel (PIA) with accurate nitrogen (N) functional design is used as the functional separator in Li metal batteries to promote uniform Li nucleation and suppress the dendrite growth. Specifically, the imine (N1) and protonated tertiary amine (N2) sites in the molecular structure of the PIA are significantly different in electron cloud density (ECD) distribution. The N1 site with higher ECD and the N2 site with lower ECD tend to attract and repulse Li+ through electrostatic interactions, respectively. This synergy effect of the PIA separator accelerates the interfacial Li+ diffusion on the Li anode to sustain a uniform two-dimensional Li nucleation behavior. Meanwhile, the well-defined nanochannels of the PIA separator show high affinity to electrolyte and bring uniform Li+ flux for Li plating/stripping. Consequently, the dendrites are effectively suppressed by the PIA separator in routine carbonate electrolyte, and the Li metal batteries with the PIA separator exhibit high Coulombic efficiency and stable high-rate cycling. These findings demonstrate that the ingenious marriage of special chemical structure designs and hierarchical pores can enable the separator to affect the interfacial Li nucleation behavior.
ABSTRACT
BACKGROUND: As a significant cause of malignancy mortality, gastric carcinoma (GC) has been well documented to be an often-fatal diagnosis. Despite the limitations of effective therapy, immunotherapy has emerged as a promising therapeutic approach capable of killing cancer cells via the immune system. The current study was conducted to investigate the effect of cytokine C-C motif chemokine ligand 21 (CCL21) on GC progression through the metastasis-associated lung adenocarcinoma transcript 1/serine arginine-rich splicing factor 1/mammalian target of rapamycin (MALAT1/SRSF1/mTOR) axis. METHODS: Bioinformatics analysis was conducted to identify the key genes associated with GC and to subsequently predict their downstream genes. The effect of CCL21, MALAT1, and SRSF1 on the malignant phenotypes and epithelial-mesenchymal transition (EMT) of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo were assessed by expression determination and plasmid transfection. Additionally, RNA pull-down and RNA binding protein immunoprecipitation experiments were performed to determine the MALAT1-microRNA-202-3p (miR-203-3p) interaction and miR-202-3p-SRSF1 interaction followed by the analysis of their effect on the mTOR pathway. RESULTS: CCL21 was identified as a key GC immune gene. Overexpressed CCL21, MALAT1, and SRSF1 along with poorly expressed miR-202-3p were identified in the GC cells. CCL21 induced the MALAT1 expression in a time- and dose-dependent manner. Functionally, MALAT1 targeted miR-202-3p but upregulated SRSF1 and activated mTOR. Crucially, evidence was obtained indicating that CCL21 promoted both the malignant phenotypes and EMT of SGC-7901 and MGC-803 cells in-vitro and the tumorigenesis of SGC-7901 and MGC-803 cells in-vivo by increasing the MALAT1-induced upregulation of SRSF1. CONCLUSIONS: Taken together, the key observations of our study provide evidence that CCL21 enhances the progression of GC via the MALAT1/SRSF1/mTOR axis, providing a novel therapeutic target for the treatment of GC.