Secure and Efficient Data Storage and Sharing Scheme Based on Double Blockchain

In the digital era,electronic medical record(EMR)has been a major way for hospitals to store patients’medical data.The traditional centralized medical system and semi-trusted cloud storage are difficult to achieve dynamic balance between privacy protection and data sharing.The storage capacity of blockchain is limited and single blockchain schemes have poor scalability and low throughput.To address these issues,we propose a secure and efficient medical data storage and sharing scheme based on double blockchain.In our scheme,we encrypt the original EMR and store it in the cloud.The storage blockchain stores the index of the complete EMR,and the shared blockchain stores the index of the shared part of the EMR.Users with different attributes can make requests to different blockchains to share different parts according to their own permissions.Through experiments,it was found that cloud storage combined with blockchain not only solved the problem of limited storage capacity of blockchain,but also greatly reduced the risk of leakage of the original EMR.Content Extraction Signature(CES)combined with the double blockchain technology realized the separation of the privacy part and the shared part of the original EMR.The symmetric encryption technology combined with Ciphertext-Policy Attribute-Based Encryption(CP–ABE)not only ensures the safe storage of data in the cloud,but also achieves the consistency and convenience of data update,avoiding redundant backup of data.Safety analysis and performance analysis verified the feasibility and effectiveness of our scheme.

Magnolol and 5-fluorouracil synergy inhibition of metastasis of cervical cancer cells by targeting PI3K/AKT/mTOR and EMT pathways

Objective: This study is designed to investigate the mode of action of the synergistic effect of 5-fluorouracil(5-FU) and magnolol against cervical cancer.Methods: Network pharmacological approach was applied to predict the molecular mechanism of 5-FU combined with magnolol against cervical cancer. CCK-8 assay, colony formation assay, immunofluorescence staining, adhesion assay, wound healing mobility assay, cell migration and invasion assay and Western blot analysis were conducted to validate the results of in silico study.Results: Phosphatidylinositol 3 kinase(PI3K)/protein kinase B(AKT)/mammalian target of rapamycin(mTOR) signaling pathway was identified as the key pathway in silico study. The experimental results showed that 5-FU combined with magnolol strongly inhibited cervical cancer cell proliferation, induced the morphological change of HeLa cells by down-regulating the expression of a-actinin, tensin-2 and vinculin. Moreover, magnolol enhanced inhibitory effect of 5-FU on the cell adhesion, migration and invasion. The phosphorylation of AKT and PI3K and the expression of mTOR were strongly inhibited by the combination of 5-FU and magnolol. Moreover, the expression of E-cadherin and β-catenin was upregulated and the expression of Snail, Slug and vimentin was down-regulated by the 5-FU together with magnolol.Conclusion: Taken together, this study suggests that 5-FU combined with magnolol exerts a synergistic anti-cervical cancer effect by regulating the PI3K/AKT/mTOR and epithelial-mesenchymal transition(EMT) signaling pathways.

Inhibitive effect on phagocytosis of Candida albicans induced by pretreatment with quercetin via actin cytoskeleton interference

OBJECTIVE: To investigate the anti-inflammatory effect of pretreatment with quercetin on macrophages after Candida albicans infection. METHODS: RAW 264.7 macrophages were used as a target cell line. Cell viability after treatment with quercetin at different time points was detected by Carboxyfluorescein diacetate, succinimidyl ester. Phagocytic function of macrophages was determined by a fluorometric assay. Cytokine tumor necrosis factor α(TNF-α) production was measured by enzyme-linked immunosorbent assay. F-actin cytoskeleton of L929 cells was stained by Alexa Fluor 488-phalloidin. RESULTS: Pretreatment with quercetin decreased cell viability only at the highest concentration of 37 μg/mL 2, 24, and 48 h after the treatment. The phagocytic efficiency of macrophages pretreated with quercetin was significantly decreased in a timeand dose-dependent manner. F-actin labeling showed that the actin cytoskeleton of the cells started to break down 2 h after treatment. Moreover, it notably inhibited cytokine TNF-α production after Candida albicans infection. CONCLUSION: Pretreatment with quercetin induced an anti-inflammatory effect against Candida albicans infection in macrophages.