Colorimetric and fluorescent dual mode detection methods have gained much attention in recent years; however, it is still desirable to develop new colorimetric and fluorescent dual mode nanosensors with more simple preparation procedures, low cost, and excellent biocompatibility. Herein, a colorimetric and fluorescent nanosensor based on B, N, S-co-doped carbon dots (BNS-CDs) was synthesized by one-step hydrothermal treatment of 2,5-diaminobenzenesulfonic acid and 4-aminophenylboronic acid hydrochloride. Using this nanosensor, a highly sensitive assay of Fe in the range of 0.3-546 μM with a detection limit of 90 nM was provided by quenching the red emission fluorescence. It is more attractive that Fe can also be visualized by this nanosensor via evident color changes of the solution (from red to blue) under sunlight without the aid of an ultraviolet (UV) lamp. Furthermore, the designed nanosensor can be applied for efficient detection of intracellular Fe with excellent biocompatibility and cellular imaging capability, and it holds great promise in biomedical applications.

Recently, the development of new fluorescent probes for the ratiometric detection of target objects inside living cells has received great attention. Normally, the preparation, modification as well as conjugation procedures of these probes are complicated. On this basis, great efforts have been paid to establish convenient method for the preparation of dual emissive nanosensor. In this work, a functional dual emissive carbon dots (dCDs) was prepared by a one-pot hydrothermal carbonization method. The dCDs exhibits two distinctive fluorescence emission peaks at 440 and 624 nm with the excitation at 380 nm. Different from the commonly reported dCDs, this probe exhibited an interesting wavelength dependent dual responsive functionality toward lysine (440 nm) and pH (624 nm), enabling the ratiometric detection of these two targets. The quantitative analysis displayed that a linear range of 0.5-260 μM with a detection limit of 94 nM toward lysine and the differentiation of pH variation from 1.5 to 5.0 could be readily realized in a ratiometric strategy, which was not reported before with other carbon dots (CDs) as the probe. Furthermore, because of the low cytotoxicity, good optical and colloidal stability, and excellent wavelength dependent sensitivity and selectivity toward lysine and pH, this probe was successfully applied to monitor the dynamic variation of lysine and pH in cellular systems, demonstrating the promising applicability for biosensing in the future.

Following spinal cord injury (SCI), immune cell infiltration creates an inflammatory and oxidative microenvironment (known as the secondary injury), which causes neuron death and spinal cord damage, and dramatically hinders neurological functional recovery. Strategies that inhibit the infiltration and/or function of neutrophils offer promises for SCI treatment because they can reduce the secondary injury; however, such strategies remain largely unexplored. Herein, a strategy using neutrophil membrane‐coated nanoparticles (NPs) as decoys (neutrophil decoy, ND) is presented to reduce local neutrophil infiltration and relieve oxidative stress in the injured spinal cord after SCI. Coated with membranes of activated neutrophils, the NDs inherit multiple receptors from the “parent” neutrophils, which can adsorb and neutralize the elevated neutrophil‐related cytokines. In addition, polydopamine NPs with multi‐antioxidative properties (selected as the core for ND) scavenge excessive reactive oxygen and nitrogen species. In a contusion model of SCI, ND treatment significantly reduces neutrophil infiltration and reprograms the inflammatory and oxidative microenvironment in injured spinal cords. Importantly, ND treatment significantly improves neural regeneration and functional recovery in rats. Such a nano‐decoy platform opens up new approaches for efficiently treating SCI.

SUMMARY Stable transmission of genetic material during cell division requires accurate chromosome segregation. PLK1 dynamics at kinetochores control establishment of correct kinetochore-microtubule attachments and subsequent silencing of the spindle checkpoint. However, the regulatory mechanism responsible for PLK1 activity in prometaphase has not yet been affirmatively identified. Here we identify Apolo1, which tunes PLK1 activity for accurate kinetochore-microtubule attachments. Apolo1 localizes to kinetochores during early mitosis, and suppression of Apolo1 results in misaligned chromosomes. Using the fluorescence resonance energy transfer (FRET)-based PLK1 activity reporter, we found that Apolo1 sustains PLK1 kinase activity at kinetochores for accurate attachment during prometaphase. Apolo1 is a cognate substrate of PLK1, and the phosphorylation enables PP1γ to inactivate PLK1 by dephosphorylation. Mechanistically, Apolo1 constitutes a bridge between kinase and phosphatase, which governs PLK1 activity in prometaphase. These findings define a previously uncharacterized feedback loop by which Apolo1 provides fine-tuning for PLK1 to guide chromosome segregation in mitosis.