Organic solid-state luminescence switching (SLS) materials with the ability to reversibly switch the luminescence by altering the mode of molecular packing without changing the chemical structures of their component molecules have attracted considerable interest in recent years. In this work, we design and synthesize a new class of 2,7diphenylfluorenone derivatives (compounds 1−6) that exhibit prominent aggregation-induced emission (AIE) properties with high solid-state fluorescence quantum yields (29−65%). Among them, 2,7-bis(4-methoxyphenyl)-9H-fluoren-9-one (2) and 2,7-bis(4-ethylphenyl)-9H-fluoren-9-one ( 6) display reversible stimuli-responsive solid-state luminescence switching. Compound 2 transforms between red and yellow crystals (the emission wavelength switches between 601 and 551 nm) under the stimuli of temperature, pressure, or solvent vapor. Similarly, compound 6 exhibits SLS behavior, with luminescence switching between orange (571 nm) and yellow (557 nm). Eight X-ray single-crystal structures, characterization of the photophysical properties, powder X-ray diffraction, and differential scanning calorimetry provide insight into the structure−property relationships of the solid-state fluorescence behavior. The results indicate that the variable solid-state luminescence of the fluorenone derivatives is attributed to the formation of different excimers in different solid phases. Additionally, the stimuli-responsive reversible phase transformations of compounds 2 and 6 involve a structural transition between π−π stacking-directed packing and hydrogen bond-directed packing. The results also demonstrate the feasibility of our design strategy for new solid-state luminescence switching materials: introduction of both π−π stacking and hydrogen bonding into an AIE structure to obtain a metastable solid/crystalline state luminescence system.

Background: Bone marrow mesenchymal stem cells (BMSCs) exhibit the capacity to self-renew and differentiate into multi-lineage cell types, including osteoblasts, which are crucial regulators of fracture healing. Thus, this study aims to investigate the effect of microRNA (miR)-22-3p from BMSC-derived EVs on osteogenic differentiation and its underlying mechanism. Methods: Extracellular vesicles (EVs) were isolated from BMSCs and taken up with BMSCs. Dual-luciferase reporter gene assay was used to verify the binding relationship between miR-22-3p and FTO. Loss-and gain-of-function experiments were performed to determine the roles of EV-delivered miR-22-3p and FTO in osteogenic differentiation as well as their regulatory role in the MYC/PI3K/AKT axis. To determine the osteogenic differentiation, ALP and ARS stainings were conducted, and the levels of RUNX2, OCN, and OPN level were determined. In vivo experiment was conducted to determine the function of EV-delivered miR-22-3p and FTO in osteogenic differentiation, followed by ALP and ARS staining. Results: miR-22-3p expression was repressed, while FTO expression was elevated in the ovariectomized mouse model. Overexpression of miR-22-3p, EV-delivered miR-22-3p, increased ALP activity and matrix mineralization of BMSCs and promoted RUNX2, OCN, and OPN expressions in BMSCs. miR-22-3p negatively targeted FTO expression. FTO silencing rescued the suppressed osteogenic differentiation by EV-delivered miR-22-3p inhibitor. FTO repression inactivated the MYC/PI3K/AKT pathway, thereby enhancing osteogenic differentiation both in vivo and in vitro. Conclusion: In summary, miR-22-3p delivered by BMSC-derived EVs could result in the inhibition of the MYC/PI3K/ AKT pathway, thereby promoting osteogenic differentiation via FTO repression.

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Fungi, especially Candida albicans, were the most common causative organisms. The most common predisposing medical conditions were recent tumor surgery and intravenous administration in rural settings. Most patients with endogenous endophthalmitis who undergo pars plana vitrectomy will have useful vision (counting fingers). Vitreous specimens for culture that were obtained by vitrectomy were more sensitive in detecting the causative organism.

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