Electrochemical coalescence of oil-in-water droplets in microchannels of TiO2-x/Ti anode via polarization eliminating electrostatic repulsion and ·OH oxidation destroying oil-water interface film.

Electrochemistry is a sustainable technology for oil-water separation. In the common flat electrode scheme, due to a few centimeters away from the anode, oil droplets have to undergo electromigration to and electrical neutralization at the anodic surface before they coalesce into large oil droplets and rise to water surface, resulting in slow demulsification and easy anode fouling. Herein, a novel strategy is proposed on basis of a TiO2-x/Ti anode with microchannels to overcome these problems. When oil droplets with several microns in diameter flow through channels with tens of microns in diameter, the electromigration distance is shortened by three orders of magnitude, electrical neutralization is replaced by polarization coupling ·OH oxidation. The new strategy was supported by experimental results and theoretical analysis. Taking the suspension containing emulsified oil as targets, COD value dropped from initial 500 mg/L to 117 mg/L after flowing through anodic microchannels in only 58 s of running time, and the COD removal was 21 times higher than that for a plate anode. At similar COD removal, the residence time was 48 times shorter than that of reported flat electrodes. Coalescences of oil droplets in microchannels were observed by a confocal laser scanning microscopy. This new strategy opens a door for using microchannel electrodes to accelerate electrochemical coalescence of oil-in-water droplets.

Matairesinoside, a novel inhibitor of TMEM16A ion channel, loaded with functional hydrogel for lung cancer treatment.

The incidence and mortality rates of lung cancer have remained high for several decades, necessitating the discovery of new drugs and the development of effective treatment strategies. This study identified matairesinoside (MTS) as a potent inhibitor of TMEM16A, a novel drug target for lung cancer. Molecular simulation combined with site-directed mutagenesis experiments confirmed the key binding sites of MTS and TMEM16A. Cell experiments demonstrated that MTS significantly inhibited the growth, migration, and invasion of lung cancer cells, while inducing apoptosis. Gene knockdown and overexpression studies further revealed that TMEM16A is the target for MTS in regulating lung cancer cell growth. Western blot analysis elucidated the signaling transduction network involved in MTS-mediated regulation of lung cancer. Building upon these findings, a biodegradable self-healing functional hydrogel was developed to load MTS, aiming to enhance therapeutic efficacy and minimize side effects in vivo. Animal experiments demonstrated that the hydrogel/MTS formulation exhibited satisfactory inhibitory effects on lung cancer and mitigated the side effects associated with direct MTS injection. This study identified MTS as a potential candidate for anti-lung cancer therapy with well-defined pharmacological mechanisms. Moreover, the targeted drug delivery system utilizing the hydrogel/MTS platform offers a promising approach for lung cancer treatment.

Neochlorogenic Acid Combined with Bone Marrow Mesenchymal Stem Cells Encapsulated into GelMA Hydrogel for Transplantation to Repair Intervertebral Disk Degeneration.

Intervertebral disk degeneration is a common disease with an unknown etiology. Currently, tissue engineering is considered to be an important method for intervertebral disk repair. Although transplanted stem cells may disrupt the repair process because of apoptosis caused by the oxidative microenvironment. Herein, bone marrow mesenchymal stem cell (BMSC) and Neochlorogenic acid (Ncg) were encapsulated into a GelMA hydrogel as a carrier to protect transplanted stem cells. Ncg effectively inhibited the oxidative stress process and reduced the apoptosis rate. A 5% GelMA hydrogel had a large pore size and porosity that provided an enhanced survival space for cells. An in vivo assessment showed that treatment with GelMA + BMSC + Ncg produced greater repair of degenerated intervertebral disks than that found in other model groups. Thus, this study may help contribute to improving stem cell transplantation for treating intervertebral disk degeneration.

TMEM16A ion channel: A novel target for cancer treatment.

Cancer draws attention owing to the high morbidity and mortality. It is urgent to develop safe and effective cancer therapeutics. The calcium-activated chloride channel TMEM16A is widely distributed in various tissues and regulates physiological functions. TMEM16A is abnormally expressed in several cancers and associate with tumorigenesis, metastasis, and prognosis. Knockdown or inhibition of TMEM16A in cancer cells significantly inhibits cancer development. Therefore, TMEM16A is considered as a biomarker and therapeutic target for some cancers. This work reviews the cancers associated with TMEM16A. Then, the molecular mechanism of TMEM16A overexpression in cancer was analyzed, and the possible signal transduction mechanism of TMEM16A regulating cancer development was summarized. Finally, TMEM16A inhibitors with anticancer effect and their anticancer mechanism were concluded. We hope to provide new ideas for pharmacological studies on TMEM16A in cancer.

One novel curcumin derivative ZYX01 induces autophagy of human non-small lung cancer cells A549 through AMPK/ULK1/Beclin-1 signaling pathway.

Presently, curcumin derivatives had been paid more attention in view of their high bioavailability or water solubility, which herein possibly replaced the curcumin for their functional applications in future. Here, one novel chemically synthesized curcumin derivative, ZYX01, was used to identify anti-proliferation activity of human non-small lung cancer cells A549 and its anti-proliferative mechanism. Our study showed that ZYX01 could induce autophagic death of A549 cells by morphological observation, MTT assay, acridine orange staining and MDC assay, which possess a dose-and time-dependent manner. ZYX01-treated A549 cells possessed an increase in LC3-II/LC3-I ratio, upregulation of beclin-1 and downregulation of p62 expression. We further confirmed the cellular AMPK/ULK1/Beclin-1 signaling pathway in A549 cells after ZYX01 treatment. The anti-migration effect of ZYX01 in A549 cells was also explored by wound healing assay and transwell experiment. Current results had confirmed that ZYX01 induced A549 cells autophagy through AMPK/ULK1/Beclin-1 pathway and shed light on the future study on the anti-cancer molecular mechanism.