Hypoxia and hyperoxia, referring to states of biological tissues in which oxygen supply is in sufficient and excessive, respectively, are often pathological conditions. Many luminescent oxygen probes have been developed for imaging intracellular and in vivo hypoxia, but their sensitivity toward hyperoxia becomes very low. Here we report a series of iridium­(III) complexes in which limited internal conversion between two excited states results in dual phosphorescence from two different excited states upon excitation at a single wavelength. Structural manipulation of the complexes allows rational tuning of the dual-phosphorescence properties and the spectral profile response of the complexes toward oxygen. By manipulating the efficiency of internal conversion between the two emissive states, we obtained a complex exhibiting naked-eye distinguishable green, orange, and red emission in aqueous buffer solution under an atmosphere of N2, air, and O2, respectively. This complex is used for intracellular and in vivo oxygen sensing not only in the hypoxic region but also in normoxic and hyperoxic intervals. To the best of our knowledge, this is the first example of using a molecular probe for simultaneous bioimaging of hypoxia and hyperoxia.

Transition metal complexes containing pyrazinium or pyridinium moieties display reversible luminescence changes in response to electrical stimuli, which is useful in the development of erasable information recording electric devices. These complexes are also suitable for temperature-related information protection, since chemically-induced luminescence turn-on is temperature-dependent.

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Phosphorescent iridium(iii) complexes bearing two carbon chains are able to distinguish between endogenous and exogenous analytes when serving as luminescent cellular probes.

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Narrowing the mechanical and electrical mismatch between tissue and implantable microelectronics is essential for reducing immune responses and modulating physioelectrical signals. Nevertheless, the design of such implantable microelectronics remains a...

Gold nanoparticles were synthesized through a continuous UV irradiation method using citric acid as a reducer and protective agent. After a period of continuous UV irradiation, the nanoparticles transformed into two-dimensional (2D) nanonetworks, porous nanoplates and compact nanoplates with hexagonal, triangular or truncated triangular pores through a self-assembly process which was dependent on the citric acid concentration. Selected area electron diffraction (SAED) patterns indicated that both the nanonetworks and the porous nanoplates were single crystalline. The influence of citric acid concentration and irradiation time on the morphological transition of Au nanostructures was investigated. The process of morphological transition was presumably discussed.

Although immune checkpoint inhibitors (ICIs) have been widely applied to treat non‐small cell lung cancer (NSCLC), a significant proportion of patients, especially those with spinal metastasis (NSCLC‐SM), are insensitive to anti‐programmed death 1 (PD‐1)/programmed death ligand 1 (PD‐L1) ICIs. A drug delivery nano‐controller of PD‐L1 that targets NSCLC‐SM can solve this problem, however, none have been developed to date. In this study, it is shown that integrin β3 (β3‐int) is strongly upregulated in NSCLC‐SM. Its inhibitor RGDyK promotes PD‐L1 ubiquitination, indicating the potential application of RGDyK as a new PD‐L1 inhibitor in nano‐controller and a targeting peptide for NSCLC‐SM treatment. According to the synergistic effect of photodynamic therapy and ICIs on T‐cell activation through the release of tumor antigens, RGDyK‐modified and zinc protoporphyrin (ZnPP)‐loaded mesoporous silicon nanoparticles (ZnPP@MSN‐RGDyK) are fabricated. The ZnPP@MSN‐RGDyK nanoparticles precisely target β3‐int to inhibit PD‐L1, exhibiting high photodynamic therapy efficiency, and excellent immunotherapeutic effects in an NSCLC‐SM mouse model. Collectively, the findings indicate that ZnPP@MSN‐RGDyK is a promising immunotherapeutic agent for treating NSCLC‐SM.