BDTS: Blockchain-based Data Trading System

Trading data through blockchain platforms is hard to achieve \textit{fair exchange}. Reasons come from two folds: Firstly, guaranteeing fairness between sellers and consumers is a challenging task as the deception of any participating parties is risk-free. This leads to the second issue where judging the behavior of data executors (such as cloud service providers) among distrustful parties is impractical in the context of traditional trading protocols. To fill the gaps, in this paper, we present a \underline{b}lockchain-based \underline{d}ata \underline{t}rading \underline{s}ystem, named BDTS. BDTS implements a fair-exchange protocol in which benign behaviors can get rewarded while dishonest behaviors will be punished. Our scheme requires the seller to provide consumers with the correct encryption keys for proper execution and encourage a rational data executor to behave faithfully for maximum benefits from rewards. We analyze the strategies of consumers, sellers, and dealers in the trading game and point out that everyone should be honest about their interests so that the game will reach Nash equilibrium. Evaluations prove efficiency and practicability.Comment: ICICS 2023 (Best Paper Award

Decentralized Finance (DeFi): A Survey

Decentralized Finance (DeFi) is a new paradigm in the creation, distribution, and utilization of financial services via the integration of blockchain technology. Our research conducts a comprehensive introduction and meticulous classification of various DeFi applications. Beyond that, we thoroughly analyze these risks from both technical and economic perspectives, spanning multiple layers. Lastly, we point out research directions in DeFi, encompassing areas of technological advancements, innovative economics, and privacy optimization

US-guided percutaneous radiofrequency ablation of secondary hyperparathyroidism as a bridge to renal transplantation

AbstractPurpose Secondary hyperparathyroidism (SHPT) is a frequently encountered problem in patients with end-stage renal disease (ESRD) prior to renal transplantation (RTP), and the successful management of SPHP currently is challenging. In this study, we aimed to investigate the effectiveness of radiofrequency ablation (RFA) for SHPT as a bridge to RTP and to evaluate post-transplantation outcomes.Methods Patients with SHPT receiving RFA treatment were retrospectively reviewed, and those underwent RTP after ablation were enrolled. Serum parathyroid hormone (PTH), calcium, and phosphate levels were collected before ablation and at follow-up periods. The primary endpoints are PTH values at time of transplantation and at the final follow-up. The secondary endpoints were RFA-related complications, serum calcium and phosphate concentrations, and allograft function.Results Eleven patients with 43 enlarged parathyroid glands were treated with 16 RFA sessions and enrolled in the study. Complete ablation was achieved in all glands with transient hoarseness and hypocalcemia occurring in two and five of the treatments, respectively. At time of transplantation, serum PTH levels (246.7 ± 182.6 pg/mL) were significantly lower than that before RFA (1666.55 ± 874.48 pg/mL, p < 0.001) and were all within guideline-oriented range. The median follow-up period was 57.2 months. At last visit, all patients were alive, with normal PTH values and functioning grafts.Conclusions Ultrasound-guided RFA is effective for destroying hyperplastic parathyroid tissues in SHPT patients, whose PTH values fall within the guideline-oriented range both pre-and post-transplantation. Percutaneous RFA acts as an effective bridge to RTP and might provide a new management paradigm designed to improve post-transplant outcomes

CD38 deficiency alleviates Ang II-induced vascular remodeling by inhibiting small extracellular vesicle-mediated vascular smooth muscle cell senescence in mice

Abstract CD38 is the main enzyme for nicotinamide adenine dinucleotide (NAD) degradation in mammalian cells. Decreased NAD levels are closely related to metabolic syndromes and aging-related diseases. Our study showed that CD38 deficiency significantly alleviated angiotensin II (Ang II)-induced vascular remodeling in mice, as shown by decreased blood pressures; reduced vascular media thickness, media-to-lumen ratio, and collagen deposition; and restored elastin expression. However, our bone marrow transplantation assay showed that CD38 deficiency in lymphocytes led to lack of protection against Ang II-induced vascular remodeling, suggesting that the effects of CD38 on Ang II-induced vascular remodeling might rely primarily on vascular smooth muscle cells (VSMCs), not lymphocytes. In addition, we observed that CD38 deficiency or NAD supplementation remarkably mitigated Ang II-induced vascular senescence by suppressing the biogenesis, secretion, and internalization of senescence-associated small extracellular vesicles (SA-sEVs), which facilitated the senescence of neighboring non-damaged VSMCs. Furthermore, we found that the protective effects of CD38 deficiency on VSMC senescence were related to restoration of lysosome dysfunction, particularly with respect to the maintenance of sirtuin-mediated mitochondrial homeostasis and activation of the mitochondria–lysosomal axis in VSMCs. In conclusion, our findings demonstrated that CD38 and its associated intracellular NAD decline are critical for Ang II-induced VSMC senescence and vascular remodeling