On the Security of a PUF-Based Authentication and Key Exchange Protocol for IoT Devices.

Recently, Roy et al. proposed a physically unclonable function (PUF)-based authentication and key exchange protocol for Internet of Things (IoT) devices. The PUF protocol is efficient, because it integrates both the Node-to-Node (N2N) authentication and the Node-to-Server (N2S) authentication into a standalone protocol. In this paper, we therefore examine the security of the PUF protocol under the assumption of an insider attack. Our cryptanalysis findings are the following. (1) A legitimate but malicious IoT node can monitor the secure communication among the server and any other IoT nodes in both N2N authentication and N2S authentication. (2) A legitimate but malicious IoT node is able to impersonate a target IoT node to cheat the server and any other IoT nodes in N2N authentication and the server in N2S authentication, respectively. (3) A legitimate but malicious IoT node can masquerade as the server to cheat any other target IoT nodes in both N2N authentication and N2S authentication. To the best of our knowledge, our work gives the first non-trivial concrete security analysis for the PUF protocol. In addition, we employ the automatic verification tool of security protocols, i.e., Scyther, to confirm the weaknesses found in the PUF protocol. We finally consider how to prevent weaknesses in the PUF protocol.

Dysbiosis of the Gut Microbiome in Lung Cancer.

Lung cancer (LC) is one of the most serious malignant tumors, which has the fastest growing morbidity and mortality worldwide. A role of the lung microbiota in LC pathogenesis has been analyzed, but a comparable role of the gut microbiota has not yet been investigated. In this study, the gut microbiota of 30 LC patients and 30 healthy controls were examined via next-generation sequencing of 16S rRNA and analyzed for diversity and biomarkers. We found that there was no decrease in significant microbial diversity (alpha diversity) in LC patients compared to controls (P observed = 0.1422), while the composition (beta diversity) differed significantly between patients and controls (phylum [stress = 0.153], class [stress = 0.16], order [stress = 0.146], family [stress = 0.153]). Controls had a higher abundance of the bacterial phylum Actinobacteria and genus Bifidobacterium, while patients with LC showed elevated levels of Enterococcus. These bacteria were found as possible biomarkers for LC. A decline of normal function of the gut microbiome in LC patients was also observed. These results provide the basic guidance for a systematic, multilayered assessment of the role of the gut microbiome in LC, which has a promising potential for early prevention and targeted intervention.

MCM2 is a therapeutic target of lovastatin in human non-small cell lung carcinomas.

Human non-small cell lung carcinoma (NSCLC) is one of the most common cancer worldwide. In previous studies, lovastatin, acting as an inhibitor of 3-hydroxy-3-methylglutaryl Co A (HMG-CoA) reductase, exhibited significant antitumor activity during tumorigenesis. However, whether or not this effect is mediated through changes in minichromosome maintenance (MCM) 2 expression remains unclear. The present study investigated whether lovastatin inhibits proliferation due to MCM2 in NSCLCs. We first assessed the effects of lovastatin on cell anti-proliferation, cell cycle progression and apoptosis in NSCLC cells. We found, by quantitative RT-PCR and western blot analysis, that lovastatin treatment markedly and consistently inhibited the expression of MCM2. Then, to further explore the anticancer mechanism of lovastatin involving MCM2, we silenced MCM2 by siRNA in two cell lines (A549 and GLC-82). Silencing of MCM2 triggered G1/S arrest. Following further examination of cell cycle-related factors, MCM2 knockdown inhibited protein retinoblastoma (Rb), cyclin D1 and CDK4 expression, but increased p21 and p53 expression, suggesting that siMCM2 indeed triggered cell cycle arrest. In addition, siMCM2 induced apoptosis. Finally, lovastatin treatment increased p-JNK, which is involved in the downregulation of MCM2. In conclusion, our data suggest that MCM2 may be a novel therapeutic target of lovastatin treatment in NSCLCs.