One-Step Construction of the Positively/Negatively Charged Ultrathin Janus Nanofiltration Membrane for the Separation of Li+ and Mg2.

To coordinate the trade-off between the separation and permeation of the nanofiltration membrane for the separation of Mg2+/Li+, we regulated poly(ethyleneimine)/piperazine interface polymerization parameters to construct a positively/negatively charged ultrathin Janus nanofiltration membrane at a free aqueous-organic interface. At the optimized interfacial polymerization parameters, 0.03 wt % of piperazine reacted with trimethylbenzene chloride prior to poly(ethyleneimine), forming a primary polyamide layer with fewer defects or limiting large-scale defects of the polyamide layer. The controlled subsequent reaction of poly(ethyleneimine) and trimethylbenzene chloride results in a Janus nanofiltration membrane, with one side enriched with the carboxyl groups, the other side enriched with the amine groups, and a dense polyamide structure in the middle. Under the optimum conditions, the positive potential of the rear surface of the prepared membrane was 14.57 mV, and the water contact angle reached 71.31°, while the negative potential of the front surface was -25.48 mV, and the water contact angle was 12.93°, confirming a Janus membrane with opposite charges and large hydrophilicity differences in the front and rear surfaces. With a high cross-linking degree, a 40 nm thick polyamide layer is 29.09% more thinner than the traditional polyamide membrane. The ultrathin Janus nanofiltration membrane showed an excellent separation factor (SLi,Mg of 18.26), stability, and water permeability flux (10.6 L·m-2·h-1·bar-1). The rejections to MgCl2, CaCl2, MgSO4, and Na2SO4 are measured above 90% at a nearly constant permeability of 10.6 L·m-2·h-1·bar-1, particularly stable rejections to MgCl2 and Na2SO4.

The combination of nuclear receptor NR1D1 and ULK1 promotes mitophagy in adipocytes to ameliorate obesity.

Obesity is a severe disease worldwide. Mitochondrial autophagy (mitophagy) may be related to metabolic abnormalities in obese individuals, but the mechanism is still unclear. We aimed to investigate whether nuclear receptors NR1D1 and ULK1 influence obesity by affecting mitophagy. In vitro model was established by inducing 3T3-L1 cells differentiation. MTT was detected cell viability. ELISA was tested triglyceride (TG). Oil red O staining was performed to detect lipid droplets. Flow cytometry was measured mtROS. ChIP and Dual-luciferase reporter assay were verified NR1D1 bind to ULK1. LC3 level was detected by IF. After differentiation medium treatment, cell viability was decreased, TG content and lipid droplets were increased Moreover, NR1D1 expression was reduced in Model group. NR1D1 overexpression was increased cell viability, reduced TG content and lipid droplets. Subsequently, NR1D1 inhibited TOM20 and mtROS, whereas, Parkin and PINK1 were accelerated. NR1D1 overexpression facilitated LC3 expression, whereas ULK1 knockdown was reversed the effect of NR1D1 overexpression. Liensinine also reversed the effect of NR1D1 overexpression, that is, cell viability was reduced, mtROS, TG content and lipid droplets were increased. The combination of nuclear receptor NR1D1 and ULK1 promoted mitophagy in adipocytes to alleviate obesity, which provided new target and strategy for obesity treatment.Abbreviations: Mitochondrial autophagy (mitophagy), triglyceride (TG), Uncoordinated-51 like autophagy activating kinase 1 (ULK1), Nuclear receptor subfamily 1 group D member 1 (NR1D1), American Type Culture Collection (ATCC), fetal bovine serum (FBS), 3-isobutyl-1-methylxanthine (IBMX), dexamethasone (DEX), short hairpin RNA ULK1 (sh-ULK1), wild-type (WT), mutant (MUT), Enzyme-linked immunosorbent assay (ELISA), mitochondrial reactive oxygen species (mtROS), Chromatin immunoprecipitation (ChIP), Quantitative real-time PCR (qRT-PCR), Immunofluorescence (IF), standard deviation (SD).

BMI1 activates WNT signaling in colon cancer by negatively regulating the WNT antagonist IDAX.

Aberrant activation of Wnt signaling plays a critical role in the development of colon cancer. BMI, a component of the polycomb repressive complex (PRC1), is upregulated in various types of cancer and contributes to epigenetic silencing of tumor suppressors. In this study, we showed that BMI1 is upregulated in colon cancer tissues and cell lines. Overexpression of BMI1 in primary epithelial colon cells promotes cellular growth and activates WNT pathway, while BMI1 silencing in colon cancer cells represses these effects. We also found that BMI1 binds to the promoter of IDAX, a Wnt antagonist, and decreases its transcription. Expression of IDAX is downregulated in colon cancer tissues and cell lines and negatively correlated with BMI1 in colon cancer tissues. Furthermore, Silencing of IDAX counteracts the effects of BMI1 suppression, while its overexpression reverses oncogenic effects of BMI1. Together, these findings indicate that BMI1-mediated IDAX epigenetic suppression is crucial for enhancement of colon carcinogenesis, suggesting that BMI1∖IDAX axis as a potential novel diagnostic and therapeutic target of colon cancer.