Wireless sensor networks (WSNs) play a crucial role in the Internet of Things (IoT) for ubiquitous data acquisition and tracking. However, the limited battery life of sensor nodes poses significant challenges to the long-term scalability and sustainability of these networks. Wireless power transfer technology offers a promising solution by enabling the recharging of energy-depleted nodes through a wireless portable charging device (WPCD). While this approach can extend node lifespan, it also introduces the challenge of bottleneck nodes—nodes whose remaining energy falls below a critical value of the threshold. The paper addresses this issue by formulating an optimization problem that aims to identify the optimal traveling path for the WPCD based on ant colony optimization (WPCD-ACO), with a focus on minimizing energy consumption and enhancing network stability. To achieve it, we propose an objective function by incorporating a time-varying z phase that is managed through linear programming to efficiently address the bottleneck nodes. Additionally, a gateway node continually updates the remaining energy levels of all nodes and relays this information to the IoT cloud. Our findings indicate that the outage-optimal distance achieved by WPCD-ACO is 6092 m, compared to 7225 m for the shortest path and 6142 m for Dijkstra’s algorithm. Furthermore, the WPCD-ACO minimizes energy consumption to 1.543 KJ, significantly outperforming other methods: single-hop at 4.8643 KJ, GR-Protocol at 3.165 KJ, grid clustering at 2.4839 KJ, and C-SARSA at 2.5869 KJ, respectively. Monte Carlo simulations validate that WPCD-ACO is outshining the existing methods in terms of the network lifetime, stability, survival rate of sensor nodes, and energy consumption.

Cryptosporidium, a protozoan parasite affecting the gastrointestinal system, is primarily known for causing diarrhea, especially in those with weakened immune systems. However, there is increasingly persuasive evidence that it may be directly involved in tumorigenesis. This review examines some of the potential mechanisms through which Cryptosporidium infections can induce cancer, specifically chronic inflammation, manipulation of the immune system, and alteration of cell signaling pathways. Persistent inflammation with immune system changes due to chronic infection, particularly among immunocompromised hosts, leads to a microenvironment that facilitates tumorigenesis. Cryptosporidium manipulates important cellular pathways such as PI3K, NF-κB, Wnt, and p38/MAPK to promote cell survival, regulate immune responses, and foster tissue remodeling, all of which contribute to a tumor-friendly microenvironment. Moreover, Cryptosporidium virulence factors such as ROP1, sPLA2, and microRNAs disrupt host cellular stability and significantly alter host cellular gene expression, which also exacerbates inflammation and tissue damage. Epidemiological data have indicated higher rates of Cryptosporidium infection in cancer patients, especially patients with gastrointestinal cancers. This, among other observations, raises the possibility that the infection may be connected to cancer progression. In animal models, especially studies with C. parvum-challenged rodents, chronic inflammation, immune repression, and genetic mutations related to neoplasia have been reported. While this has provided us with valuable information, we still have a long way to go to fully understand the long-term ramifications of Cryptosporidium infection. These cover aspects such as the contribution of latent infections and the genetic diversity of Cryptosporidium strains in cancer. Further investigation is urgently needed to understand the molecular processes by which Cryptosporidium might contribute to carcinogenesis and explore potential strategies for therapy and prevention especially among immunocompromised populations.