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Vehicle Ad-hoc network (VANET) can provide technical support and solutions for the construction of intelligent and efficient transportation systems, and the routing protocol directly affects the efficiency of VANET. The rapid movement of nodes and uneven density distribution affect the routing stability and data transmission efficiency in VANET. To improve the local optimality and routing loops of the path-aware greedy perimeter stateless routing protocol (PA-GPSR) in urban sparse networks, a weight-based path-aware greedy perimeter stateless routing protocol (W-PAGPSR) is proposed. The protocol is divided into two stages. Firstly, in the routing establishment stage, the node distance, reliable node density, cumulative communication duration, and node movement direction are integrated to indicate the communication reliability of the node, and the next hop node is selected using the weight greedy forwarding strategy to achieve reliable transmission of data packets. Secondly, in the routing maintenance stage, based on the data packet delivery angle and reliable node density, the next hop node is selected for forwarding using the weight perimeter forwarding strategy to achieve routing repair. The simulation results show that compared to the greedy peripheral stateless routing protocol (GPSR), for the maximum distance–minimum angle greedy peripheral stateless routing (MM-GPSR) and PA-GPSR protocols, the packet loss rate of the protocol is reduced by an average of 24.47%, 25.02%, and 14.12%, respectively; the average end-to-end delay is reduced by an average of 48.34%, 79.96%, and 21.45%, respectively; and the network throughput is increased by an average of 47.68%, 58.39%, and 20.33%, respectively. This protocol improves network throughput while reducing the average end-to-end delay and packet loss rate.

Aging is a complex process of impaired physiological integrity and function, and is associated with increased risk of cardiovascular disease, diabetes, neurodegeneration, and cancer. The cellular environment of the aging brain exhibits perturbed bioenergetics, impaired adaptive neuroplasticity and flexibility, abnormal neuronal network activity, dysregulated neuronal Ca2+ homeostasis, accumulation of oxidatively modified molecules and organelles, and clear signs of inflammation. These changes make the aging brain susceptible to age-related diseases, such as Alzheimer’s and Parkinson’s diseases. In recent years, unprecedented advances have been made in the study of aging, especially the effects of herbal/natural compounds on evolutionarily conserved genetic pathways and biological processes. Here, we provide a comprehensive review of the aging process and age-related diseases, and we discuss the molecular mechanisms underlying the therapeutic properties of herbal/natural compounds against the hallmarks of brain aging.

Cervical cancer is a common gynecological malignancy afflicting women all over the world. Ginsenoside Rh2 (GRh2), especially 20(S)-GRh2, is a biologically active component in the natural plant ginseng, which can exhibit anticancer effects. Here, we aimed to investigate the effect of 20(S)-GRh2 on cervical cancer and elucidate the underlying mechanism through RNA-seq. In this study, the CCK-8 assay showed that 20(S)-GRh2 inhibited HeLa cell viability in a time- and dose-dependent manner. Caspase 3 activity and Annexin V staining results showed that 20(S)-GRh2 induced apoptosis of HeLa cells. Gene function enrichment analysis revealed that the biological process gene ontology (GO) terms were associated with the apoptotic signaling pathway. Biological process GO terms’ similarity network indicated that apoptosis might be from endoplasmic reticulum stress (ERs). Kyoto Encyclopedia of Genes and Genomes enrichment analysis revealed that 20(S)-GRh2 primarily modulates apoptosis pathway genes. Combined protein–protein interaction network, hub gene screening, and qPCR validation data showed that ERs-related genes (ATF4 and DDIT3) and the downstream apoptotic genes (JUN, FOS, BBC3, and PMAIP1) were potential novel targets of 20(S)-GRh2-inducing cervical cancer cell apoptosis. Differential transcript usage analysis indicated that DDIT3 is also a differential transcript and its usage of the isoform (ENST00000552740.5) was reduced by 20(S)-GRh2. Molecular docking suggested that 20(S)-GRh2 binds to the targets (ATF4, DDIT3, JUN, FOS, BBC3, and PMAIP1) with high affinity. In conclusion, our findings indicated that 20(S)-GRh2 might promote ERs-related apoptosis of cervical cancer cells by regulating the DDIT3-based targets’ signal pathway. The role of 20(S)-GRh2 at the transcriptome level provides novel targets and evidence for the treatment of cervical cancer.