A Two-Party Hierarchical Deterministic Wallets in Practice

The applications of Hierarchical Deterministic Wallet are rapidly growing in various areas such as cryptocurrency exchanges and hardware wallets. Improving privacy and security is more important than ever. In this study, we proposed a protocol that fully support a two-party computation of BIP32. Our protocol, similar to the distributed key generation, can generate each party’s secret share, the common chain-code, and the public key without revealing a seed and any descendant private keys. We also provided a simulation-based proof of our protocol assuming a rushing, static, and malicious adversary in the hybrid model. Our master key generation protocol produces up to total of two bit leakages from a honest party given the feature that the seeds will be re-selected after each execution. The proposed hardened child key derivation protocol leads up to a one bit leakage in the worst situation of simulation from a honest party and will be accumulated with each execution. Fortunately, in reality, this issue can be largely mitigated by adding some validation criteria of boolean circuits and masking the input shares before each execution. We then implemented the proposed protocol and ran in a single thread on a laptop which turned out with practically acceptable execution time. Lastly, the outputs of our protocol can be easily integrated with many threshold sign protocols

Evaluating Spillover Effects in Network-Based Studies In the Presence of Missing Outcomes

Estimating causal effects in the presence of spillover among individuals embedded within a social network is often challenging with missing information. The spillover effect is the effect of an intervention if a participant is not exposed to the intervention themselves but is connected to intervention recipients in the network. In network-based studies, outcomes may be missing due to the administrative end of a study or participants being lost to follow-up due to study dropout, also known as censoring. We propose an inverse probability censoring weighted (IPCW) estimator, which is an extension of an IPW estimator for network-based observational studies to settings where the outcome is subject to possible censoring. We demonstrated that the proposed estimator was consistent and asymptotically normal. We also derived a closed-form estimator of the asymptotic variance estimator. We used the IPCW estimator to quantify the spillover effects in a network-based study of a nonrandomized intervention with censoring of the outcome. A simulation study was conducted to evaluate the finite-sample performance of the IPCW estimators. The simulation study demonstrated that the estimator performed well in finite samples when the sample size and number of connected subnetworks (components) were fairly large. We then employed the method to evaluate the spillover effects of community alerts on self-reported HIV risk behavior among people who inject drugs and their contacts in the Transmission Reduction Intervention Project (TRIP), 2013 to 2015, Athens, Greece. Community alerts were protective not only for the person who received the alert from the study but also among others in the network likely through information shared between participants. In this study, we found that the risk of HIV behavior was reduced by increasing the proportion of a participant's immediate contacts exposed to community alerts

A novel murine model to deplete hepatic stellate cells uncovers their role in amplifying liver damage in mice

UnlabelledWe have developed a novel model for depleting mouse hepatic stellate cells (HSCs) that has allowed us to clarify their contributions to hepatic injury and fibrosis. Transgenic (Tg) mice expressing the herpes simplex virus thymidine kinase gene (HSV-Tk) driven by the mouse GFAP promoter were used to render proliferating HSCs susceptible to killing in response to ganciclovir (GCV). Effects of GCV were explored in primary HSCs and in vivo. Panlobular damage was provoked to maximize HSC depletion by combining CCl(4) (centrilobular injury) with allyl alcohol (AA) (periportal injury), as well as in a bile duct ligation (BDL) model. Cell depletion in situ was quantified using dual immunofluorescence (IF) for desmin and GFAP. In primary HSCs isolated from both untreated wild-type (WT) and Tg mice, GCV induced cell death in ≈ 50% of HSCs from Tg, but not WT, mice. In TG mice treated with CCl(4) +AA+GCV, there was a significant decrease in GFAP and desmin-positive cells, compared to WT mice (≈ 65% reduction; P < 0.01), which was accompanied by a decrease in the expression of HSC-activation markers (alpha smooth muscle actin, beta platelet-derived growth factor receptor, and collagen I). Similar results were observed after BDL. Associated with HSC depletion in both fibrosis models, there was marked attenuation of fibrosis and liver injury, as indicated by Sirius Red/Fast Green, hematoxylin and eosin quantification, and serum alanine/aspartate aminotransferase. Hepatic expression of interleukin-10 and interferon-gamma was increased after HSC depletion. No toxicity of GCV in either WT or Tg mice accounted for the differences in injury.ConclusionActivated HSCs significantly amplify the response to liver injury, further expanding this cell type's repertoire in orchestrating hepatic injury and repair

Regulation of Embryonic Kidney Branching Morphogenesis and Glomerular Development by KISS1 Receptor (Gpr54) through NFAT2- and Sp1-mediated Bmp7 Expression*

G-protein-coupled receptor 54 (Gpr54, KISS1 receptor) plays critical roles in puberty regulation, tumor metastasis suppression, and vasoconstriction. Bone morphogenetic protein-7 (Bmp7) is required for kidney organogenesis. However, whether Gpr54 is involved in embryonic kidney development and how Bmp7 expression is regulated in the kidney are largely unknown. Here we report that Gpr54 deletion leads to kidney branching morphogenesis and glomerular development retardation in embryonic kidneys in vivo and in explanted kidneys in vitro. Gpr54 inactivation results in a high risk of low glomerular number in adult kidneys. Gpr54 is expressed in condensed mesenchyme at E12.5 and epithelial cells of proximal and distal tubules and collecting ducts at E17.5 and P0 mouse kidney. Deletion of Gpr54 decreases Bmp7 expression and Smad1 phosphorylation in the developing kidney. Using chromatin immunoprecipitation and luciferase assays, we demonstrate that Gpr54 regulates NFAT2- and Sp1-mediated Bmp7 transcription. Furthermore, we show that NFAT2 cooperates with Sp1 to promote Bmp7 transcription activation. Together, these data suggest that Gpr54 regulates Bmp7 expression through NFAT2 and Sp1 and plays an important role in embryonic kidney branching morphogenesis and glomerular development