SPS and DPS: Two New Grid-Based Source Location Privacy Protection Schemes in Wireless Sensor Networks.

Wireless Sensor Networks (WSNs) have been widely deployed to monitor valuable objects. In these applications, the sensor node senses the existence of objects and transmitting data packets to the sink node (SN) in a multi hop fashion. The SN is a powerful node with high performance and is used to collect all the information sensed by the sensor nodes. Due to the open nature of the wireless medium, it is easy for an adversary to trace back along the routing path of the packets and get the location of the source node. Once adversaries have got the source node location, they can capture the monitored targets. Thus, it is important to protect the source node location privacy in WSNs. Many methods have been proposed to deal with this source location privacy protection problem, and most of them provide routing path diversity by using phantom node (PN) which is a fake source node used to entice the adversaries away from the actual source node. But in the existing schemes, the PN is determined by the source node via flooding, which not only consumes a lot of communication overhead, but also shortens the safety period of the source node. In view of the above problems, we propose two new grid-based source location privacy protection schemes in WSNs called grid-based single phantom node source location privacy protection scheme (SPS) and grid-based dual phantom node source location privacy protection scheme (DPS) in this paper. Different from the idea of determining the phantom node by the source node in the existing schemes, we propose to use powerful sink node to help the source node to determine the phantom node candidate set (PNCS), from which the source node randomly selects a phantom node acting as a fake source node. We evaluate our schemes through theoretical analysis and experiments. Experimental results show that compared with other schemes, our proposed schemes are more efficient and achieves higher security, as well as keeping lower total energy consumption. Our proposed schemes can protect the location privacy of the source node even in resource-constrained wireless network environments.

[Inhibitory effect of polydatin on expression of toll-like receptor 4 in ischemia-reperfusion injured NRK-52E cells].

Polydatin is a monocrystaline compound isolated from Polygonum cuspidatum Sieb. et Zucc. (Polygonaceae) with biological properties, such as anti-inflammation, anti-oxidative and nephroprotective effects. Increasing number of studies have demonstrated the protective effect of polydatin on renal ischemia reperfusion injury. However, the possible mechanisms of this protection are not fully elucidated. This study aimed to investigate the effect of polydatin on ischemia-reperfusion induced expression of toll-like receptor4 (TLR4) in rat renal tubular epithelia cells (NRK-52E), and analyze the mechanism of polydatin on TLR4 signal pathway. The cultured NRK-52E cells were incubated in three gas incubators for a period of 6 h at hypoxia and 24h at reoxygenation to simulate the ischemia-reperfusion injury in vitro. TLR4 mRNA level was analyzed by real-time-PCR, and the protein expression of TLR4 and NF-κB by Western blotting, while TNF-α and IL-1ß proteins expressions were detected by ELISA. Polydatin downregulated I/R induced mRNA and protein expressions of TLR4, and decreased the protein expression of NF-κB, TNF-α and IL-1ß. The TLR4 blocker partially antagonized the effect of I/R on NF-κB signaling, and such inhibitory effect was markedly enhanced by polydatin. In the present study, polydatin protects NRK-52E cells from I/R injury possibly by relieving the inflammatory response through regulation of TLR4/NF-κB signaling pathway.

Identification of Immune-Related Seven-Long Non-Coding RNA Signature for Overall Survival and Validation of the Effect of LINC01270 in Malignant Phenotypes of Clear Cell Renal Carcinoma.

Introduction: The overall survival of patients with high-stage clear cell renal carcinoma (ccRCC) is poor. However, promising molecular-level prognostic marker is still lacking to date. Methods: We systematically evaluated the prognostic potential of immune-related long non-coding RNAs (lncRNAs) in ccRCC. The expressions of lncRNAs were validated in clinical tissues of ccRCC. Functional experiments were performed to investigate the role of lncRNAs in ccRCC. Results: Eight hundred and ninety-three lncRNAs were differentially expressed in ccRCC and compared with normal controls and were screened out using three independent cohorts. Among them, 290 immune-related lncRNAs were identified. We identified a seven-lncRNA signature (LINC01270, FIRRE, RP11-37B2.1, RP11-253I19.3, RP11-438L19.1, RP11-504P24.9, and CTB-41I6.1) associated with the overall survival of late-stage ccRCC patients. Further multivariate Cox analysis using clinical factors as covariates showed that our lncRNA signature was an independent biomarker in training (P < 0.001, Log rank test) and validation cohorts (P = 0.003). The seven lncRNAs were closely related to the major targets (PD-1, PD-L1, and CTLA4) of immune checkpoint blockade drugs, implying that they may have potential value in predicting immunotherapy response. The seven lncRNAs may play an important role in tumor-infiltrating immune cells (eg, T/B cells) and tumor progression through regulating the binding of protein receptors/complexes, as revealed by functional analysis. qRT-PCR showed that LINC01270 was upregulated in ccRCC tissues (n=20) compared with paired normal samples. Functional experiments showed that LINC01270 silencing inhibited the proliferation, invasion, and migration of ccRCC cells. Discussion: In summary, the seven-lncRNA signature has great potential in prognosis for patients with late-stage ccRCC, which could be a novel clinical biomarker. LINC01270 could be a novel therapeutic target of ccRCC.

Attenuation of Inflammation by Emodin in Lipopolysaccharide-induced Acute Kidney Injury via Inhibition of Toll-like Receptor 2 Signal Pathway.

INTRODUCTION: Emodin, an anthraquinone derivative from the Chinese herb Radix et Rhizoma Rhe, has been reported to possess anti-inflammatory property in vivo and in vitro. However, the effect of emodin on inflammation in lipopolysaccharide (LPS)-induced acute kidney injury as an immunomodulator has yet to be determined. This study aimed to investigate whether emodin had protective effects against LPS-induced acute kidney injury by inhibiting toll-like receptor 2 (TLR2) signal pathway in normal rat kidney epithelial cells (NRK-52E). MATERIALS AND METHODS: The NRK-52E cells were incubated with LPS with and without the indicated concentrations of emodin for 24 hours. The TLR2 and NF-κB protein level was detected by Western blot method. Tumor necrosis factor (TNF)-α, interleukin (IL)-1ß, and IL-6 protein levels were measured using an enzyme-linked immunosorbent assay. The mRNA expression of TLR2, NF-κB, TNF-α, IL-1ß, and IL-6 was detected using a real-time polymersase chain reaction. RESULTS: A concentration of 102 ng/mL of LPS significantly upregulated mRNA and protein levels of TLR2 and NF-κB and increased TNF-α, IL-1ß, and IL-6 mRNA and protein levels. At doses of 20 µM and 40 µM, emodin was able to inhibit LPS-induced TLR2, NF-κB, TNF-α, IL-1ß and IL-6 mRNA and protein expressions in cultured NRK-52E cells. CONCLUSIONS: These results demonstrate that an elevated expression of inflammatory cytokines and TLR2 in cells stimulated by LPS were simultaneously inhibited by emodin. Therefore, emodin attenuates the inflammation by inhibiting TLR2-mediated NF-κB signal pathway, which may contribute to the immune inflammation regulation of emodin in LPS-induced acute kidney injury.