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BackgroundKeratoconus is a diseased corneal dilation of unknown etiology. Studies have shown that inflammation may play a role in keratoconus. Inflammatory enteritis (IBD), including ulcerative colitis (UC), is a chronic, systemic inflammatory disease. We used Mendelian randomization to assess the causal relationship among IBD, UC and keratoconus.MethodsThe instrumental variable of IBD and UC was selected, the information of the instrumental variable in keratoconus outcome was extracted, and the causal relationship was assessed by the inverse variance weighted method by primary analysis, and its relevant sensitivity analysis.ResultsA causal relationship between IBD and keratoconus was observed significantly (P = 0.017, OR = 1.21, 95% CI = 1.03–1.41), and same as to UC and keratoconus (P = 0.038, OR = 1.25, 95% CI = 1.01–1.54).ConclusionIBD may play a causal role in the development of keratoconus, but the mechanism needs to be further elucidated.

Developing a rapid detection method of Cr(VI) and ascorbic acid (AA) is vital in the food and environmental fields. Herein, an anthrylimidazole-based fluorescent ionic liquid (AI-FIL) with the advantageous fluorescent properties was successfully prepared and used to construct a promising “on-off-on” fluoroprobe for rapid/sensitive Cr(VI) and AA detection. Cr(VI) could effectively quench the fluorescence of AI-FIL owing to the inner-filter effect and photoinduced electron-transfer process. However, the decreased fluorescence could be rapidly recovered by AA owing to the redox reaction between AA and Cr(VI). For Cr(VI) detection, a satisfactorily linear response (0.03–300 μM) was achieved with the corresponding detection limit of 9 nM. For AA detection, a good linearity from 1 to 1000 μM was obtained with the resultant detection limit of 0.3 μM. Moreover, the AI-FIL based fluoroprobe was successfully utilized for Cr(VI) and AA detection in food and water samples with satisfactory accuracy and precision.

A novel ratiometric fluorescent probe was constructed for sensitive assay of hydrogen peroxide (H2O2) and glucose, which utilized the synergistically enhanced effects of Ce3+ and Fe2+ on copper nanoclusters (CuNCs) and coumarin. In the CuNCs-Ce3+/Fe2+-coumarin system, Ce3+ triggered the aggregation-induced emission phenomenon of CuNCs, and Fe2+ catalyzed the Fenton reaction to efficiently yield hydroxyl radical (•OH). In the presence of H2O2, the 625-nm red fluorescence of CuNCs was sharply quenched owing to the oxidation of CuNCs to Cu(II) by •OH, but the 460-nm blue fluorescence of 7-hydroxycoumarin from the oxidation of coumarin by •OH dramatically increased. Based on the reversible changes in two fluorescence signals, a satisfactorily ratiometric probe was constructed for H2O2 assay with a detection limit (LOD) of 0.6 μM accompanied by a visual color variation from red to blue. For glucose assay, this ratiometric probe gave a linear range of 3.2–160 μM and LOD of 0.96 μM owing to the oxidization of glucose to yield H2O2 in the presence of glucose oxidase and O2. Overall, the newly developed ratiometric probe shows a great prospect in real applications for visual assay of H2O2 and glucose by our naked eyes.

Despite the wide application of radiotherapy in HCC, radiotherapy efficacy is sometimes limited due to radioresistance. Although radioresistance is reported with high glycolysis, the underlying mechanism between radioresistance and cancer metabolism, as well as the role of cathepsin H (CTSH) within it, remain unclear. In this study, tumor-bearing models and HCC cell lines were used to observe the effect of CTSH on radioresistance. Proteome mass spectrometry, followed by enrichment analysis, were used to investigate the cascades and targets regulated by CTSH. Technologies such as immunofluorescence co-localization flow cytometry and Western blot were used for further detection and verification. Through these methods, we originally found CTSH knockdown (KD) perturbed aerobic glycolysis and enhanced aerobic respiration, and thus promoted apoptosis through up-regulation and the release of proapoptotic factors such as AIFM1, HTRA2, and DIABLO, consequently reducing radioresistance. We also found that CTSH, together with its regulatory targets (such as PFKL, HK2, LDH, and AIFM1), was correlated with tumorigenesis and poor prognosis. In summary, our study found that the cancer metabolic switch and apoptosis were regulated by CTSH signaling, leading to the occurrence of radioresistance in HCC cells and suggesting the potential value of HCC diagnosis and therapy.