Clustering sensor nodes is an effective method in designing routing algorithms for Wireless Sensor Networks (WSNs), which improves network lifetime and energy efficiency. In clustered WSNs, cluster heads are the key nodes, they need to perform more tasks, so they consume more energy. Therefore, it is an important problem to select the optimal cluster heads. In this paper, we propose a clustering algorithm that selects cluster heads using an improved artificial bee colony (ABC) algorithm. Based on the standard ABC algorithm, an efficient improved ABC algorithm is proposed, and then the network cluster head energy, cluster head density, cluster head location and other similar factors are introduced into the improved ABC algorithm theory to solve the clustering problem in WSNs. In the network initialization period, all nodes have the same energy level, the improved ABC algorithm is used to optimize fuzzy C-means clustering to find the optimal clustering method. We also propose an energy-efficient routing algorithm based on an improved ant colony optimization for routing between the cluster heads and the base station. In order to improve energy efficiency and further improve network throughput, in the stable transmission phase, we introduce a polling control mechanism based on busy/idle nodes into intra-cluster communication. The performance of the proposed protocol is evaluated in several different scenarios. The simulation results show that the proposed protocol has a better performance compared to a number of recent similar protocols. INDEX TERMS WSN, clustering, energy efficiency, network lifetime, high throughput, polling, routing algorithm, artificial bee colony
Psoriasis is a chronic inflammatory skin disorder. The aim of this study was to determine a potential role of microRNA (miR)-130a in psoriasis, and underlying mechanism. Expression levels of miR-130a in psoriasis specimens and normal skin tissues were analyzed. MiR-130a mimic, inhibitor, miR-control, small interfering RNA (siRNA) specific serine/threonine kinase 40 (STK40), or sex-determining region Y chromosome-box 9 (SOX9) were transfected to human keratinocyte HaCaT cells, respectively. After transfection, the cell viability, apoptosis, and migration were determined. Luciferase reporter assay, quantitative reverse transcription-polymerase chain reaction, and western blot were performed to explore whether STK40 was a target of miR-130a. The effects of aberrant expressions of miR-130a, STK40, or SOX9 on key proteins of NF-κB and c-Jun N-terminal kinase (JNK)/mitogen-activated protein kinase (MAPK) pathway were assessed. The miR-130a levels were significantly higher in patients with psoriasis compared to the healthy controls (p < 0.01). Overexpressing miR-130a strikingly promoted HaCaT cell viability and migration and inhibited apoptosis (p < 0.01 or p < 0.05). We confirmed that STK40 was a direct target of miR-130a, and STK40 was involved in miR-130a-induced cell functions. Overexpressing miR-130a significantly upregulated NF-κB p65, SOX9, p-c-Jun, p-JNK, and p-p38MAPK proteins and silencing miR-130a downregulated them. In addition, silencing STK40 alleviated the effects of anti-miR-130a on SOX9 expression. Furthermore, silencing SOX9 also decreased levels of p-c-Jun, p-JNK, and p-p38MAPK proteins. MiR-130a regulates human keratinocyte HaCaT viability, migration and apoptosis might be by direct regulation of STK40-mediated NF-κB pathway and by indirect regulation of SOX9-mediated downstream JNK/MAPK signaling pathway.
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