Stabilizing Li‐rich layered oxides without capacity/voltage fade upon cycling is a prerequisite for a successful commercialization. Although the inhibition of structural and interfacial changes is identified as an effective strategy, the battery community always seeks for a technologically flexible method to make it really competitive among the cathode. Herein, the gradient W‐doping within Li1.2Mn0.56Ni0.16Co0.08O2 (LLMO) is proposed to relieve crystal disintegration and simultaneously enhance interfacial stability because of the formation of Li2WO4 coating layer on the material surface. This is mainly attributed to the scenario that partial Mn replacement by W can stabilize the LLMO structure and regulate the electrochemical activity of Mn element. The W‐doped LLMO (W@LLMO) possesses improved specific capacity and voltage stability (83.2% capacity retention and voltage retention of 94.9% after 200 cycles at 0.5 C). Besides, a practical pouch cell based on the W@LLMO cathode presents sufficient gravimetric energy density (318 Wh kg−1) and cycling stability (capacity retention of 87.7% after 500 cycles at 1.0 C). This study presents an effective method to design robust Li‐rich layered cathodes for next‐generation Li‐ion batteries.

A nanoparticle (NP) was developed to target choroidal neovascularization (CNV) via topical ocular administration. The NPs were prepared through conjugation of internalizing arginine-glycine-aspartic acid RGD (iRGD; Ac-CCRGDKGPDC) and transactivated transcription (TAT) (RKKRRQRRRC) peptide to polymerized ethylene glycol and lactic-co-glycolic acid. The iRGD sequence can specifically bind with integrin α v β 3 , while TAT facilitates penetration through the ocular barrier. 1 H nuclear magnetic resonance and high-performance liquid chromatography demonstrated that up to 80% of iRGD and TAT were conjugated to poly(ethylene glycol)– poly(lactic-co-glycolic acid). The resulting particle size was 67.0±1.7 nm, and the zeta potential of the particles was −6.63±0.43 mV. The corneal permeation of iRGD and TAT NPs increased by 5.50- and 4.56-fold compared to that of bare and iRGD-modified NPs, respectively. Cellular uptake showed that the red fluorescence intensity of iRGD and TAT NPs was highest among primary NPs and iRGD- or TAT-modified NPs. CNV was fully formed 14 days after photocoagulation in Brown Norway (BN) rats as shown by optical coherence tomography and fundus fluorescein angiography analyses. Choroidal flat mounts in BN rats showed that the red fluorescence intensity of NPs followed the order of iRGD and TAT NPs > TAT-modified NPs > iRGD-modified NPs > primary NPs. iRGD and TAT dual-modified NPs thus displayed significant targeting and penetration ability both in vitro and in vivo, indicating that it is a promising drug delivery system for managing CNV via topical ocular administration.

Dermokine (DMKN) was first identified in relation to skin lesion healing and skin carcinoma. Recently, its expression was associated with pancreatic cancer tumorigenesis, although its involvement remains poorly understood. Herein, we showed that DMKN loss of function in Patu‐8988 and PANC‐1 pancreatic cancer cell lines resulted in reduced phosphorylation of signal transducer and activator of transcription 3, and increased activation of ERK1/2 and AKT serine/threonine kinase. This decreased the proliferation ability of pancreatic ductal adenocarcinoma (PDAC) cells. In addition, DMKN knockdown decreased the invasion and migration of PDAC cells, partially reversed the epithelial–mesenchymal transition, retarded tumor growth in a xenograft animal model by decreasing the density of microvessels, and attenuated the distant metastasis of human PDAC in a mouse model. Taken together, these data suggested that DMKN could be a potential prognostic biomarker and therapeutic target in pancreatic cancer.

Corroles have been previously demonstrated to be a new and promising photosensitizer (PS) in photodynamic therapy (PDT) for cancer cells. This research reported the preparation of an electron-deficient flat gallium(iii) tris(ethoxycarbonyl)corrole (1-Ga). Its in vitro PDT activities towards different cancer cell lines were examined, and the best PDT activity was observed in A549 cell lines. 1-Ga could penetrate the cell membrane rapidly and exhibit remarkable photo-cytotoxicity. 1-Ga can induce A549 cell apoptosis via ROS-mediated mitochondrial pathways, in which p38 and sirt-1 proteins play a key role. A PTD test in vivo showed that 1-Ga can significantly reduce the growth of A549 xenografted tumor cells without an obvious loss of mice weight upon PDT treatment.