Ultrafast Laser Ablation, Intrinsic Threshold, and Nanopatterning of Monolayer Molybdenum Disulfide

Laser direct writing is an attractive method for patterning 2D materials without contamination. Literature shows that the femtosecond ablation threshold of graphene across substrates varies by an order of magnitude. Some attribute it to the thermal coupling to the substrates, but it remains by and large an open question. For the first time the effect of substrates on femtosecond ablation of 2D materials is studied using MoS$_{2}$ as an example. We show unambiguously that femtosecond ablation of MoS$_{2}$ is an adiabatic process with negligible heat transfer to the substrates. The observed threshold variation is due to the etalon effect which was not identified before for the laser ablation of 2D materials. Subsequently, an intrinsic ablation threshold is proposed as a true threshold parameter for 2D materials. Additionally, we demonstrate for the first time femtosecond laser patterning of monolayer MoS$_{2}$ with sub-micron resolution and mm/s speed. Moreover, engineered substrates are shown to enhance the ablation efficiency, enabling patterning with low-power femtosecond oscillators. Finally, a zero-thickness approximation is introduced to predict the field enhancement with simple analytical expressions. Our work clarifies the role of substrates on ablation and firmly establishes femtosecond laser ablation as a viable route to pattern 2D materials

Enhanced processing of exhaust gas and power generation by connecting mini-tubular microbial fuel cells in series with a biotrickling filter

Tubular microbial fuel cells (Tube-MFCs) were placed on top of a biotrickling filter-microbial fuel cell (BTF-MFC) to form a tubular biotrickling filter microbial fuel cell (Tube-BTF-MFC) system. Adding Tube-MFCs greatly increased the power output of a Tube-BTF-MFC in treating ethyl acetate (EA). With a progressive water flow pattern generated by circulating water spray, the Tube-MFC can reduce the sharing of electrolyte between anode chambers of MFCs and improve the power output of Tube-BTF-MFC. With 129.8 g/m3·h of EA, the Tube-BTF-MFC exhibited an EA removal efficiency of 93% and a closed circuit voltage (186.5 mV). The maximum elimination capacity of EA by the Tube-BTF-MFC was 1.47 times greater than that of the BTF-MFC, while the highest generated power density was 2.13 times greater. Adding Tube-MFCs to a BTF-MFC system can effectively improve its removal efficiency for EA and increase its power output. The proposed Tube-BTF-MFC can be used to treat industrially emitted gaseous volatile organic compounds while generating electricity

AC-93253 iodide, a novel Src inhibitor, suppresses NSCLC progression by modulating multiple Src-related signaling pathways

Abstract Background The tyrosine kinase Src is involved in the progression of many cancers. Moreover, inhibiting Src activity has been shown to obstruct several signaling pathways regulated by the EGFR. Thus, Src is a valuable target molecule in drug development. The purpose of this study was to identify compounds that directly or indirectly modulate Src to suppress lung cancer cell growth and motility and to investigate the molecular mechanisms underlying the effects of these compounds. Methods Human non-small cell lung cancer (NSCLC) cell lines (PC9, PC9/gef, A549, and H1975) with different EGFR statuses were tested by cytotoxicity and proliferation assays after AC-93253 iodide treatment. Src and Src-related protein expression in AC-93253 iodide-treated PC9, PC9/gef, and A549 cells were assessed by western blotting. The effects of AC-93253 iodide on cancer cell colony formation, invasion, and migration were assessed in PC9 and PC9/gef cells. The synergistic effects of gefitinib and AC-93253 iodide were evaluated by combination index (CI)-isobologram analysis in gefitinib-resistant cell lines. The efficacy of AC-93253 iodide in vivo was determined using nude mice treated with either the compound or the vehicle. Results Among the compounds, AC-93253 iodide exhibited the most potent dose-independent inhibitory effects on the activity of Src as well as on that of the Src-related proteins EGFR, STAT3, and FAK. Furthermore, AC-93253 iodide significantly suppressed cancer cell proliferation, colony formation, invasion, and migration in vitro and tumor growth in vivo. AC-93253 iodide sensitized tumor cells to gefitinib treatment regardless of whether the cells were gefitinib-sensitive (PC9) or resistant (H1975 and PC9/gef), indicating that it may exert synergistic effects when used in combination with established therapeutic agents. Our findings also suggested that the inhibitory effects of AC-93253 iodide on lung cancer progression may be attributable to its ability to modulate multiple proteins, including Src, PI3K, JNK, Paxillin, p130cas, MEK, ERK, and EGFR. Conclusions Our data suggest that AC-93253 iodide inhibits NSCLC cell growth and motility by regulating multiple Src-related pathways. Our findings may facilitate the development of therapeutic strategies and anti-tumor drugs that may be useful for treating lung cancer in the future

Additional file 1: Table S1. of AC-93253 iodide, a novel Src inhibitor, suppresses NSCLC progression by modulating multiple Src-related signaling pathways

The 15 compounds predicted to bind open-form Src by Discovery Studio Client, based on the strengths of their interactions with the protein. Table S2. The combination index (CI) and fractional effect (FE) of combination treatment with AC-93253 iodide and gefitinib (Iressa) in lung cancer A549 cells. Table S3. The CI and FE of combination treatment with AC-93253 iodide and gefitinib (Iressa) in lung cancer PC9/gef cells. Table S4. The CI and FE of combination treatment with AC-93253 iodide and gefitinib (Iressa) in lung cancer H1975 cells. Figure S1. Suppression of Src by candidate compounds in PC9 cell line. Figure S2. Cytotoxic effects of AC-93253 iodide on non-tumour BEAS2B cells, as determined by cell viability assay. Figure S3. Western blotting for the effects of AC-93253 iodide on the expression of Src and its associated proteins in the A549 cell line. Figure S4. AC-93253 iodide-mediated suppression of anchorage-dependent growth in A549 cells. Figure S5. The effects of AC-93253 iodide treatment on CL1-5 cells, as determined by anchorage-independent growth assay. Figure S6. Phosphorylation and expression of Src-related proteins in gefitinib-resistant lung adenocarcinoma cells treated with AC93253 iodide and gefitinib, separately and in combination. Figure S7. Cytotoxic effect of sodium iodide on PC9 and PC9/gef cell lines. Figure S8. Western blotting for the effects of sodium iodide on the phosphorylation and expression of Src and its related proteins in the PC9 and PC9/gef cells. (DOCX 2294 kb

Structural Characteristics and Non-Linear Optical Behaviour of a 2-Hydroxynicotinate-Containing Zinc-Based Metal-Organic Framework

Materials with non-linear optical (NLO) properties play an important role in the construction of electronic devices for optical communications, optical data processing and data storage. With this aim in mind, a Zn(II)-based metal-organic framework {[Zn2(nica)2(bpy)1.5(H2O)]×0.5(bpy)×3H2O}n (1), was synthesized using 4,4ʹ-bipyridine (bpy) and a potentially bidentate ligand, 2-hydroxynicotinic acid (H2nica) with a salicylate binding moiety. A single-crystal X-ray diffraction analysis revealed that compound 1 crystallized in the orthorhombic space group Fdd2 and was composed of a three dimensional porous framework. Since Fdd2 belonged to a class of non-centrosymmetric space groups, we therefore investigated the non-linear optical behaviour of compound 1. Photoluminescence studies revealed that compound 1 exhibited a blue light emission with a maxima at 457 nm

A novel quinoline derivative, DFIQ, sensitizes NSCLC cells to ferroptosis by promoting oxidative stress accompanied by autophagic dysfunction and mitochondrial damage

Abstract Background The development of nonapoptotic programmed cell death inducers as anticancer agents has emerged as a cancer therapy field. Ferroptosis, ferrous ion-driven programmed cell death that is induced by redox imbalance and dysfunctional reactive oxygen species (ROS) clearance, is triggered during sorafenib and PD-1/PD-L1 immunotherapy. DFIQ, a quinoline derivative, promotes apoptosis by disrupting autophagic flux and promoting ROS accumulation. Our pilot experiments suggest that DFIQ participates in ferroptosis sensitization. Thus, in this study, we aimed to reveal the mechanisms of DFIQ in ferroptosis sensitization and evaluate the clinical potential of DFIQ. Methods We treated the non-small cell lung cancer (NSCLC) cell lines H1299, A549, and H460 with the ferroptosis inducer (FI) DFIQ and analyzed viability, protein expression, ROS generation, and fluorescence staining at different time points. Colocalization analysis was performed with ImageJ. Results DFIQ sensitized cells to FIs such as erastin and RSL3, resulting in a decrease in IC50 of at least 0.5-fold. Measurement of ROS accumulation to explore the underlying mechanism indicated that DFIQ and FIs treatment promoted ROS accumulation and SOD1/SOD2 switching. Mitochondria, known ROS sources, produced high ROS levels during DFIQ/FI treatment. RSL3 treatment promoted mitochondrial damage and mitophagy, an autophagy-associated mitochondrial recycling system, and cotreatment with DFIQ induced accumulation of mitochondrial proteins, which indicated disruption of mitophagic flux. Thus, autophagic flux was measured in cells cotreated with DFIQ. DFIQ treatment was found to disrupt autophagic flux, leading to accumulation of damaged mitochondria and eventually inducing ferroptosis. Furthermore, the influence of DFIQ on the effects of clinical FIs, such as sorafenib, was evaluated, and DFIQ was discovered to sensitize NSCLC cells to sorafenib and promote ferroptosis. Conclusions This study indicates that DFIQ not only promotes NSCLC apoptosis but also sensitizes cells to ferroptosis by disrupting autophagic flux, leading to accumulation of dysfunctional mitochondria and thus to ferroptosis. Ferroptosis is a novel therapeutic target in cancer therapy. DFIQ shows the potential to enhance the effects of FIs in NSCLC and act as a potential therapeutic adjuvant in ferroptosis-mediated therapy