We report on what we believe is the first field implementation of a continuous-variable quantum key distribution (CV-QKD) network with point-to-point configuration. Four QKD nodes are deployed on standard communication infrastructures connected with commercial telecom optical fiber. Reliable key exchange is achieved in the wavelength-division-multiplexing CV-QKD network. The impact of a complex and volatile field environment on the excess noise is investigated, since excess noise controlling and reduction is arguably the major issue pertaining to distance and the secure key rate. We confirm the applicability and verify the maturity of the CV-QKD network in a metropolitan area, thus paving the way for a next-generation global secure communication network.

In this study, the anatomical and ultrastructural responses of Capsicum annuum to iron nanoparticles (Fe NPs) were determined. The results showed that the bio-effects of Fe NPs on plants could be positive or negative, depending on the additive concentrations. Low concentrations of Fe NPs were found to promote plant growth. Light and electron microscope analyses showed that the Fe NPs promoted plant growth by altering the leaf organization, and increasing the chloroplast number and grana stacking, as well as regulating the development of vascular bundles. Meanwhile, it was found that the Fe NPs could be absorbed in the roots, and then transported to the central cylinder in bio-available forms, where they were translocated and utilized by the leaves and stems. In contrast, high concentrations of Fe NPs appeared to be harmful to the plants, and the majority of Fe NPs were aggregated into cell walls and transported via the apoplastic pathway in the roots, which may potentially block the transfer of iron nutrients. Taken together, the aforementioned data showed that the rational use of Fe NPs could alleviate iron deficiency, and Fe NPs could be an ideal supply for Fe2+ ions fertilizers in agriculture.

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Research on tumour cell-derived small extracellular vesicles (sEVs) that regulate tumour microenvironment (TME) has provided strategies for targeted therapy of head and neck squamous cell carcinoma (HNSCC). Herein, we demonstrated that sEVs derived from HNSCC cancer cells carried CD73 (sEVs CD73 ), which promoted malignant progression and mediated immune evasion. The sEVs CD73 phagocytosed by tumour-associated macrophages (TAMs) in the TME induced immunosuppression. Higher CD73 high TAMs infiltration levels in the HNSCC microenvironment were correlated with poorer prognosis, while sEVs CD73 activated the NF-κB pathway in TAMs, thereby inhibiting immune function by increasing cytokines secretion such as IL-6, IL-10, TNF-α, and TGF-β1. The absence of sEVs CD73 enhanced the sensitivity of anti-PD-1 therapy through reversed immunosuppression. Moreover, circulating sEVs CD73 increased the risk of lymph node metastasis and worse prognosis. Taken together, our study suggests that sEVs CD73 derived from tumour cells contributes to immunosuppression and is a potential predictor of anti-PD-1 responses for immune checkpoint therapy in HNSCC. K E Y WO R D Santi-PD-1 therapy, CD73, head and heck squamous cell carcinoma, macrophage, small extracellular vesicle

Rationale: Skeletal muscle insulin resistance is detectable before type 2 diabetes is diagnosed. Exposure to di(2-ethylhexyl) phthalate (DEHP), a typical environmental endocrine-disrupting chemical, is a novel risk factor for insulin resistance and type 2 diabetes. This study aimed to explore insulin signaling regulatory pathway in skeletal muscle of the DEHP-induced insulin-resistant mice and to investigate potential therapeutic strategies for treating insulin resistance. Methods: C57BL/6J male mice were exposed to 2 mg/kg/day DEHP for 15 weeks. Whole-body glucose homeostasis, oxidative stress and deregulated miRNA-mediated molecular transduction in skeletal muscle were examined. microRNA (miRNA) interventions based on lentiviruses and adeno-associated viruses 9 (AAV9) were performed. Results: Dnmt3a-dependent promoter methylation and lncRNA Malat1-related sponge functions cooperatively downregulated miR-17 in DEHP-exposed skeletal muscle cells. DEHP suppressed miR-17 to disrupt the Keap1-Nrf2 redox system and to activate oxidative stress-responsive Txnip in skeletal muscle. Oxidative stress upregulated miR-200a, which directly targets the 3'UTR of Insr and Irs1 , leading to hindered insulin signaling and impaired insulin-dependent glucose uptake in skeletal muscle, ultimately promoting the development of insulin resistance. AAV9-induced overexpression of miR-17 and lentivirus-mediated silencing of miR-200a in skeletal muscle ameliorated whole-body insulin resistance in DEHP-exposed mice. Conclusions: The miR-17/Keap1-Nrf2/miR-200a axis contributed to DEHP-induced insulin resistance. miR-17 is a positive regulator, whereas miR-200a is a negative regulator of insulin signaling in skeletal muscle, and both miRNAs have the potential to become therapeutic targets for preventing and treating insulin resistance or type 2 diabetes.

Background: Head and neck squamous cell carcinoma (HNSCC) is an aggressive disease worldwide. Much progress has been made in exploring mechanisms and improving the therapy of HNSCC, but only a few studies have focused on the role of ferroptosis on HNSCC progression. The current study aimed to reveal the underlining mechanisms that caveolin-1 (CAV1)-ROS (reactive oxygen species)-ferroptosis axis affect the process of HNSCC and discover novo therapeutic targets or strategies. Methods:The role of CAV1 in ferroptosis was analyzed by FerrDb, and its clinical significance was examined by TCGA dataset of HNSCC. The expressions of caveolin-1 (CAV1) in HNSCC tissues were measured by immunohistochemistry, western blot, and real-time PCR assay. Three siRNA sequences were designed to silence CAV1 mRNA in HNSCC cells. Cell proliferation, colony formation, wound-healing, and transwell assays were used to examine the proliferation, migration, and invasion of cancer cells.ROS evaluation and intracellular Fe 2+ content assays were performed to examine the levels of ferroptosis.Results: Through the analysis with published data, CAV1 was found to overexpress in HNSCC than normal tissues, and was one of the vital suppressors of ferroptosis pathway. Our study showed that CAV1 was over expressed in HNSCC tissues and the high level of CAV1 predicted poorer prognosis. Further experiments indicated that CAV1 could inhibit the ferroptosis of cancer cells and promote the proliferation, migration and invasion.Conclusions: Overexpression of CAV1 in HNSCC inhibited the process of ferroptosis, leading to aggressive phenotypes, as well as worse prognosis. The regulatory pathway of CAV1 and ferroptosis are potential targets for designing diagnostic and combined therapeutic strategies for HNSCC patients.

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