Aqueous zinc‐ion batteries with low cost and inherent safety are considered to be the next‐generation energy storage device. However, they suffer from poor cycling stability and low coulombic efficiency caused by the serious zinc dendrites during the cycling. In this work, a porous water‐based filter membrane is first proposed as separator due to its good toughness and uniform pore distribution. The results demonstrate that the symmetrical cell using a filter membrane can cycle over 2600 h with a low voltage hysteresis of 47 mV. Moreover, an aqueous Zn//NaV3O8·1.5H2O cell based on the filter membrane is constructed, which demonstrates a high capacity retention of 83.8% after 5000 cycles at 5 A g−1. The mechanism research results reveal that the excellent dendrites inhibiting the ability of the filter membrane should be attributed to its uniform pore distribution rather than its composition. This work proposes a filter membrane separator and reveals the great influence of separator on the zinc stripping/plating process, which will shed light on the development of high‐performance aqueous zinc‐ion batteries.

A compatible and robust electrode–electrolyte interface is favorable in resolving the severe dendritic growth and side reactions of aqueous Zn‐ion batteries toward commercial‐standard lifespan and charging–discharging rate. Herein, a chemical welding strategy through in situ construction of a gel electrolyte that enables Zn‐ion batteries to achieve ultralong life and reversibility is reported. The gel electrolyte is spontaneously formed on the Zn anode surface by redox polymerization with the initiation of Zn metal. The direct participation of the Zn anode in the chemical synthesis of the gel electrolyte brings a well‐bonded and water‐poor electrode–electrolyte interface, which not only alleviates side reactions but also enables preferential (002) Zn deposition. The in situ symmetric cell thus prepared delivers an ultralong lifespan of 5100 h (>212 days), and a hybrid capacitor with the in situ electrolyte runs smoothly over 40 000 cycles at 20 A g−1. Even at an ultrahigh current density of 40 mA cm−2 and capacity of 40 mAh cm−2, the cell still operates stably for 240 h, alongside a high Zn utilization with 87% depth of discharge. The in situ gel electrolyte integrating robust interface and preparation of all‐in‐one cells demonstrate a commercializable path for aqueous Zn‐storage devices.

Recently, the inflammatory cytokine IL-6 has been reported as a potent inducer of epithelial-mesenchymal transition (EMT) in breast cancer cells with an epithelial phenotype. Furthermore, EMT induces stem cell features in normal and transformed mammary cells. We explored whether IL-6-induced EMT promoted the generation of breast cancer stem-like cells (BrCSCs) in epithelial-like breast cancer cells, and whether the cytokines EGF and bFGF, analogous to IL-6, per se induced epithelial-mesenchymal transition, resulting in the enrichment of BrCSCs in mammosphere cultures. Herein, we provide evidence that IL-6 is capable of generating CD44+ cells with stem-like properties through induction of the EMT in the epithelial-like T47D breast cancer cells. We also show that mammosphere cultures of epithelial-like breast cancer cells, T47D, MCF7, ZR-75-1 and MDA-MB-453 cells, consistently generated stem-like cancer cells solely as a result of the EGF and bFGF cytokines in the mammosphere media mediating EMT. This finding demonstrated the link between the inflammatory cytokine IL-6 and BrCSCs and identified an important mechanism for the enrichment of BrCSCs in mammosphere cultures. Thus, EMT appears to be a critical mechanism for the induction of cancer cells with stem-like properties, and EMT of non-stem cancer cells could be a source of CSCs.

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The objective is to evaluate the association of periodontal disease with the risk of oral cancer. Literature retrieval, selection and assessment, data extraction, and meta-analyses were performed according to the RevMan 5.0 guidelines. In the meta-analysis, we utilized random-effect model to pool the odds ratio (OR) according to the test of heterogeneity. A total of five eligible studies included 1,191 oral cancer patients and 1,992 healthy control subjects were analyzed. By meta-analysis, we found a significant association of periodontal disease with oral cancer [OR = 3.53, 95 % CI (1.52-8.23); P = 0.003]. Patients with periodontal disease have increased susceptibility to oral cancer.

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The renin-angiotensin system (RAS) is a principal determinant of arterial blood pressure and fluid and electrolyte balance. RAS component dysregulation was recently found in some malignancies and correlated with poor patient outcomes. However, the exact mechanism of local RAS activation in tumors is still unclear. Here, we find that the local angiotensin II predominantly exists in the hypoxic regions of tumor formed by nasopharyngeal carcinoma CNE2 cells and breast cancer MDA-MB-231 cells, where these tumor cells autocrinely produce angiotensin II by a chymase-dependent rather than an angiotensin converting enzyme-dependent mechanism. We further demonstrate in nasopharyngeal carcinoma CNE2 and 5–8F cells that this chymase-dependent effect is mediated by increased levels of lactate, a by-product of glycolytic metabolism. Finally, we show that the enhanced angiotensin II plays an important role in the intracellular accumulation of HIF-1α of hypoxic nasopharyngeal carcinoma cells and mediates the radiation-resistant phenotype of these nasopharyngeal carcinoma cells. Thus, our findings reveal the critical role of hypoxia in producing local angiotensin II by a lactate-chymase-dependent mechanism and highlight the importance of local angiotensin II in regulating radioresistance of hypoxic tumor cells.

Radiation therapy has an important role in the treatment of breast cancer. Dysfunction p53 and hypoxia are typical biological characteristics of breast cancer that constitute barriers to the efficacy of radiotherapy. Mitophagy plays a protective role in cellular homeostasis under hypoxic conditions, while mitophagy is inhibited by p53 in normal cells. We explored the effects of a p53 fusion protein, TAT-ODD-p53, on the radiosensitivity of hypoxic breast cancer cells both in vitro and in vivo, as well as investigating the related molecular mechanisms. We found that selective accumulation of TAT-ODD-p53 occurred under hypoxic conditions and significantly increased tumor cell radiosensitivity both in vitro and in vivo. Mitophagy had an important role in maintaining hypoxia-induced radioresistance. Mitophagy was inhibited by TAT-ODD-p53 and this inhibition was suppressed by over-expression of Parkin in hypoxic irradiated breast cancer cells. In addition, mitophagy was induced by deletion of p53, with this effect being weakened by Parkin knockdown at a low oxygen tension. By interacting with Parkin, p53 inhibited the translocation of Parkin to the mitochondria, disrupting the protective mitophagy process. These results suggest that TAT-ODD-p53 has a significant and preferential radiosensitizing effect on hypoxic breast cancer cells by inhibition of Parkin-mediated mitophagy.