Rapid and Precise Molecular Nanofiltration Using Ultra-Thin-Film Membranes Derived from 6,6′-Dihydroxy-2,2′-biphenyldiamine

A key challenge in efficient molecular separation is fabricating large-scale, highly selective polymeric membranes with precise pore control at the molecular scale. Herein, a new contorted monomer 6,6′-dihydroxy-2,2′-biphenyldiamine (DHBIPDA) is introduced as a building block to generate cross-linked, ultra-thin microporous nanofilms (sub-10 nm) via interfacial polymerization, enabling rapid, and precise molecular nanofiltration. Using diacyl chloride (TPC) as the cross-linker instead of trimesoyl chloride (TMC) significantly reduces the pore sizes within the membranes and achieves a narrower pore distribution due to a semi-crystalline structure. The film structures are confirmed using comprehensive characterization techniques including wide-angle X-ray scattering (WAXS), X-ray diffraction (XRD), positron annihilation lifetime spectroscopy (PALS), CO2 adsorption analysis, and molecular-scale simulation. The DHBIPDA/TPC and DHBIPDA/TMC membranes achieve methanol permeance values of up to 16.4 and 15.1 LMH bar−1 coupled with molecular weight cutoffs (MWCOs) as low as 283 and 306 Da, respectively. The DHBIPDA/TPC membrane demonstrates both higher permeance and higher selectivity compared to its relatively disordered counterpart DHBIPDA/TMC, consistent with characterization data. The DHBIPDA-derived membrane efficiently separates dye mixtures with similar molecular weights and enables effective recycling of organometallic homogeneous catalysts, suggesting its potential for industrial applications.</p

SP1 transcriptionally regulates UBE2N expression to promote lung adenocarcinoma progression

Abstract Lung adenocarcinoma (LUAD) is the main cause of cancer-related death worldwide. Understanding the mechanisms of LUAD progression may provide insights into targeted therapy approaches for this malignancy. Ubiquitin-conjugating enzyme 2 N (UBE2N) has been demonstrated to play key roles in the progression of various cancers. However, the functions and mechanisms underlying UBE2N expression in LUAD are still unclear. In this study, we found that UBE2N is highly expressed in LUAD and patients with high UBE2N expression in their tumors have poor clinical outcomes. Moreover, we showed that UBE2N interference significantly inhibited LUAD progression in vitro and in vivo. At the molecular level, we demonstrated that the UBE2N is a bona fide target of transcription factor SP1. SP1 directly bound to the promoter of UBE2N and upregulated its expression in LUAD cells, which in turn contributed to the progression of LUAD. Furthermore, we found that there is a strong positive correlation between the expression of SP1 and UBE2N in LUAD samples. Importantly, LUAD patients with concomitantly high expression of SP1 and UBE2N were significantly associated with poor clinical outcomes. In conclusion, our study demonstrated that the SP1-UBE2N signaling axis might play a key role in the malignant progression of LUAD, which provides new targets and strategies for the treatment of LUAD