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Electronic health record sharing can help to improve the accuracy of diagnosis, where security and privacy preservation are critical issues in the systems. In recent years, blockchain has been proposed to be a promising solution to achieve personal health information (PHI) sharing with security and privacy preservation due to its advantages of immutability. This work proposes a blockchain-based secure and privacy-preserving PHI sharing (BSPP) scheme for diagnosis improvements in e-Health systems. Firstly, two kinds of blockchains, private blockchain and consortium blockchain, are constructed by devising their data structures, and consensus mechanisms. The private blockchain is responsible for storing the PHI while the consortium blockchain keeps records of the secure indexes of the PHI. In order to achieve data security, access control, privacy preservation and secure search, all the data including the PHI, keywords and the patients' identity are public key encrypted with keyword search. Furthermore, the block generators are required to provide proof of conformance for adding new blocks to the blockchains, which guarantees the system availability. Security analysis demonstrates that the proposed protocol can meet with the security goals. Furthermor, we implement the proposed scheme on JUICE to evaluate the performance.

Our previous study showed that miR-29 attenuates muscle wasting in chronic kidney disease. Other studies found that miR-29 has anti-fibrosis activity. We hypothesized that intramuscular injection of exosome-encapsulated miR-29 would counteract unilateral ureteral obstruction (UUO)-induced muscle wasting and renal fibrosis. We used an engineered exosome vector, which contains an exosomal membrane protein gene Lamp2b that was fused with the targeting peptide RVG (rabies viral glycoprotein peptide). RVG directs exosomes to organs that express the acetylcholine receptor, such as kidney. The intervention of Exo/miR29 increased muscle crosssectional area and decreased UUO-induced upregulation of TRIM63/MuRF1 and FBXO32/atrogin-1. Interestingly, renal fibrosis was partially depressed in the UUO mice with intramuscular injection of Exo/miR29. This was confirmed by decreased TGF-b, alpha-smooth muscle actin, fibronectin, and collagen 1A1 in the kidney of UUO mice. When we used fluorescently labeled Exo/miR29 to trace the Exo/miR route in vivo and found that fluorescence was visible in un-injected muscle and in kidneys. We found that miR-29 directly inhibits YY1 and TGF-b3, which provided a possible mechanism for inhibition of muscle atrophy and renal fibrosis by Exo/miR29. We conclude that Exo/miR29 ameliorates skeletal muscle atrophy and attenuates kidney fibrosis by downregulating YY1 and TGF-b pathway proteins.

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