Global dynamics in a chemotaxis model describing tumor angiogenesis with/without mitosis in any dimensions

In this work, we study the Neumann initial boundary value problem for a three-component chemotaxis model in any dimensional bounded and smooth domains; this model is used to describe the branching of capillary sprouts during angiogenesis. First, we find three qualitatively simple sufficient conditions for qualitative global boundedness, and then, we establish two types of global stability for bounded solutions in qualitative ways. As a consequence of our findings, the underlying system without chemotaxis and the effect of ECs mitosis can not give rise to pattern formations. Our findings quantify and extend significantly previous studies, which are set in lower dimensional convex domains and are with no qualitative information.Comment: 43 pages, under review in a journa

Efficient Online-friendly Two-Party ECDSA Signature

Two-party ECDSA signatures have received much attention due to their widespread deployment in cryptocurrencies. Depending on whether or not the message is required, we could divide two-party signing into two different phases, namely, offline and online. Ideally, the online phase should be made as lightweight as possible. At the same time, the cost of the offline phase should remain similar to that of a normal signature generation. However, the existing two-party protocols of ECDSA are not optimal: either their online phase requires decryption of a ciphertext, or their offline phase needs at least two executions of multiplicative-to-additive conversion which dominates the overall complexity. This paper proposes an online-friendly two-party ECDSA with a lightweight online phase and a single multiplicative-to-additive function in the offline phase. It is constructed by a novel design of a re-sharing of the secret key and a linear sharing of the nonce. Our scheme significantly improves previous protocols based on either oblivious transfer or homomorphic encryption. We implement our scheme and show that it outperforms prior online-friendly schemes (i.e., those have lightweight online cost) by a factor of roughly 2 to 9 in both communication and computation. Furthermore, our two-party scheme could be easily extended to the $2$-out-of-$n$ threshold ECDSA

Efficient Multiplicative-to-Additive Function from Joye-Libert Cryptosystem and Its Application to Threshold ECDSA

Threshold ECDSA receives interest lately due to its widespread adoption in blockchain applications. A common building block of all leading constructions involves a secure conversion of multiplicative shares into additive ones, which is called the multiplicative-to-additive (MtA) function. MtA dominates the overall complexity of all existing threshold ECDSA constructions. Specifically, $O(n^2)$ invocations of MtA are required in the case of $n$ active signers. Hence, improvement of MtA leads directly to significant improvements for all state-of-the-art threshold ECDSA schemes. In this paper, we design a novel MtA by revisiting the Joye-Libert (JL) cryptosystem. Specifically, we revisit JL encryption and propose a JL-based commitment, then give efficient zero-knowledge proofs for JL cryptosystem which are the first to have standard soundness. Our new MtA offers the best time-space complexity trade-off among all existing MtA constructions. It outperforms state-of-the-art constructions from Paillier by a factor of $1.85$ to $2$ in bandwidth and $1.2$ to $1.7$ in computation. It is $7\times$ faster than those based on Castagnos-Laguillaumie encryption only at the cost of $2\times$ more bandwidth. While our MtA is slower than OT-based constructions, it saves $18.7\times$ in bandwidth requirement. In addition, we also design a batch version of MtA to further reduce the amotised time and space cost by another $25$%

UHRF1 is required for basal stem cell proliferation in response to airway injury

Cellular senescence is a cell fate characterized by an irreversible cell cycle arrest, but the molecular mechanism underlying this senescence hallmark remains poorly understood. Through an unbiased search for novel senescence regulators in airway basal cells, we discovered that the epigenetic regulator ubiquitin-like with PHD and ring finger domain-containing protein 1 (UHRF1) is critical for regulating cell cycle progression. Upon injury, basal cells in the mouse airway rapidly induce the expression of UHRF1 in order to stimulate stem cell proliferation and tissue repair. Targeted depletion of Uhrf1 specifically in airway basal cells causes a profound defect in cell cycle progression. Consistently, cultured primary human basal cells lacking UHRF1 do not exhibit cell death or differentiation phenotypes but undergo a spontaneous program of senescence. Mechanistically, UHRF1 loss induces G1 cell cycle arrest by abrogating DNA replication factory formation as evidenced by loss of proliferating cell nuclear antigen (PCNA) puncta and an inability to enter the first cell cycle. This proliferation defect is partially mediated by the p15 pathway. Overall, our study provides the first evidence of an indispensable role of UHRF1 in somatic stem cells proliferation during the process of airway regeneration

Small extracellular vesicles derived from four dimensional-culture of mesenchymal stem cells induce alternatively activated macrophages by upregulating IGFBP2/EGFR to attenuate inflammation in the spinal cord injury of rats

Effectively reducing the inflammatory response after spinal cord injury (SCI) is a challenging clinical problem and the subject of active investigation. This study employed a porous scaffold-based three dimensional long-term culture technique to obtain human umbilical cord mesenchymal stem cell (hUC-MSC)-derived Small Extracellular Vesicles (sEVs) (three dimensional culture over time, the “4D-sEVs”). Moreover, the vesicle size, number, and inner protein concentrations of the MSC 4D-sEVs contained altered protein profiles compared with those derived from 2D culture conditions. A proteomics analysis suggested broad changes, especially significant upregulation of Epidermal Growth Factors Receptor (EGFR) and Insulin-like Growth Factor Binding Protein 2 (IGFBP2) in 4D-sEVs compared with 2D-sEVs. The endocytosis of 4D-sEVs allowed for the binding of EGFR and IGFBP2, leading to downstream STAT3 phosphorylation and IL-10 secretion and effective induction of macrophages/microglia polarization from the pro-inflammatory M1 to anti-inflammatory M2 phenotype, both in vitro and in the injured areas of rats with compressive/contusive SCI. The reduction in neuroinflammation after 4D-sEVs delivery to the injury site epicenter led to significant neuroprotection, as evidenced by the number of surviving spinal neurons. Therefore, applying this novel 4D culture-derived Small Extracellular Vesicles could effectively curb the inflammatory response and increase tissue repair after SCI