RESUMEN
In the era of the interconnection of all things, the security of the Internet of Things (IoT) has become a new challenge. The theoretical basis of unconditional security can be guaranteed by using quantum keys, which can form a QKD network-based security protection system of quantum Internet of Things (Q-IoT). However, due to the low generation rate of the quantum keys, the lack of a reasonable key allocation scheme can reduce the overall service quality. Therefore, this paper proposes a dynamic on-demand key allocation scheme, named DDKA-QKDN, to better meet the requirements of lightweight in the application scenario of Q-IoT and make efficient use of quantum key resources. Taking the two processes of the quantum key pool (QKP) key allocation and the QKP key supplement into account, the scheme dynamically allocates quantum keys and supplements the QKP on demand, which quantitatively weighs the quantum key quantity and security requirements of key requests in proportion. The simulation results show that the system efficiency and the ability of QKP to provide key request services are significantly improved by this scheme.
RESUMEN
Transgenic mouse models are powerful for understanding the critical genes controlling osteoclast differentiation and activity, and for studying mechanisms and pharmaceutical treatments of osteoporosis. Cathepsin K (Ctsk)-Cre mice have been widely used for functional studies of osteoclasts. The signal transducer and activator of transcription 3 (STAT3) is relevant in bone homeostasis, but its role in osteoclasts in vivo remains poorly defined. To provide the in vivo evidence that STAT3 participates in osteoclast differentiation and bone metabolism, we generated an osteoclast-specific Stat3 deletion mouse model (Stat3 fl/fl; Ctsk-Cre) and analyzed its skeletal phenotype. Micro-CT scanning and 3D reconstruction implied increased bone mass in the conditional knockout mice. H&E staining, calcein and alizarin red double staining, and tartrate-resistant acid phosphatase (TRAP) staining were performed to detect bone metabolism. In short, this protocol describes some canonical methods and techniques to analyze skeletal phenotype and to study the critical genes controlling osteoclast activity in vivo.