In principle, mechanochromic fluorescent (MCF) materials can be classified into two categories: turn-off and turn-on types. The latter is superior to the former as it is more sensitive and less likely to induce false-positive signals. In this study, we report the synthesis and photoluminescence (PL) behaviour of a biplane molecule, 2-amino-3-((E)-((2-hydroxynaphthalen-1-yl)methylene)amino)maleonitrile (AHM), which consists of an electron donor (D) plane and an acceptor (A) plane. AHM undergoes both aggregation-enhanced emission (AEE) and intramolecular charge transfer (ICT) mechanisms. It is weakly emissive in the crystalline phase but shows a remarkable emission enhancement with a large bathochromic-shift (67 nm) upon applying mechanical force. As confirmed by both spectroscopic methods and fluorescence microscopy, MCF arises from crystal defects, where the molecules would twist their conformation to break D–A coupling, inducing strong fluorescence. This defect-induced emission (DIE) endows the material with ultra-high sensitivity toward pressure. The detection limit (DL) of an AHM-based sensing film is as low as 1.1 N (0.62 MPa). Additionally, the DIE phenomenon of AHM further enables a new mechanical printing technique. Handwriting and imprinted letters exhibit a distinct emission change which is readily detected by the naked eyes. We believe that the unique turn-on MCF and high sensitivity make this material well-suited to tackle the challenges faced by conventional MCF materials.

Type 2 diabetic coronary heart disease (T2DM-CHD) is a kind of serious and complex disease. Great attention has been paid to exploring its mechanism; however, the detailed understanding of T2DM-CHD is still limited. Plasma samples from 15 healthy controls, 13 coronary heart disease (CHD) patients, 15 type 2 diabetes mellitus (T2DM) patients and 28 T2DM-CHD patients were analyzed in this research. The potential biomarkers of CHD and T2DM were detected and screened out by¹H NMR-based plasma metabolic profiling and multivariate data analysis. About 11 and 12 representative metabolites of CHD and T2DM were identified respectively, mainly including alanine, arginine, proline, glutamine, creatinine and acetate. Then the diagnostic model was further constructed based on the previous metabolites of CHD and T2DM to detect T2DM-CHD with satisfying sensitivity of 92.9%, specificity of 93.3% and accuracy of 93.2%, validating the robustness of¹H NMR-based plasma metabolic profiling to diagnostic strategy. The results demonstrated that the NMR-based metabolomics approach processed good performance to identify diagnostic plasma biomarkers and most identified metabolites related to T2DM and CHD could be considered as predictors of T2DM-CHD as well as the therapeutic targets for prevention, which provided new insight into diagnosing and forecasting of complex diseases.

Emodin is a natural anthraquinone derivative that is present in various herbal preparations. The pharmacological effects of emodin include anticancer, hepatoprotective, anti-inflammatory, antioxidant and even antimicrobial activities. However, emodin also has been reported to induce hepatotoxicity, nephrotoxicity, genotoxicity and reproductive toxicity. The mechanism of emodin’s adverse effects is complicated and currently not well understood. This study aimed to establish a cell metabonomic method to investigate the toxicity of emodin and explore its potential mechanism and relevant targets. In the present study, metabonomic profiles of cell extracts and cell culture media obtained using the ¹H NMR technique were used to assess emodin toxicity in HepG2 cells. Multivariate statistical analyses such as partial least squares-discriminant analysis (PLS-DA) and orthogonal partial least squares-discriminant analysis (OPLS-DA) were used to characterize the metabolites that differed between the control and emodin groups. The results indicated that emodin resulted in differences in 33 metabolites, including acetate, arginine, aspartate, creatine, isoleucine, leucine and histidine in the cell extract samples and 23 metabolites, including alanine, formate, glutamate, succinate and isoleucine, in the cell culture media samples. Approximately 8 pathways associated with these metabolites were disrupted in the emodin groups. These results demonstrated the potential for using cell metabonomics approaches to clarify the toxicological effects of emodin, the underlying mechanisms and potential biomarkers. Our findings may help with the development of novel strategies to discover targets for drug toxicity, elucidate the changes in regulatory signal networks and explore its potential mechanism of action.