Web service locating unit in RFID-centric anti-counterfeit system

Abstract-The problem of piracy has disturbed people's daily life for hundreds of years and has not been relieved until now, though many existing anti-counterfeit solutions have been applied. However, due to the emergences of Radio Frequency IDentification (RFID) technologies, there is a more reliable alternative solution to construct authentication system. On the other hand, there arises another issue of how to simplify the deployment of RFID-centric anti-counterfeit system over the Internet. In this article, we propose an approach, Web Service Locating Unit (WSLU), to achieve this goal to manage numbers of RFID-centric authentication services (relied on web services)

The Fermi level effect in III-V intermixing: The final nail in the coffin?

Copyright 1997 American Institute of Physics. This article may be downloaded for personal use only. Any other use requires prior permission of the author and the American Institute of Physics. This article appeared in Journal of Applied Physics 81, 2179 (1997) and may be found at

ZIKV infection activates the IRE1-XBP1 and ATF6 pathways of unfolded protein response in neural cells.

BACKGROUND: Many viruses depend on the extensive membranous network of the endoplasmic reticulum (ER) for their translation, replication, and packaging. Certain membrane modifications of the ER can be a trigger for ER stress, as well as the accumulation of viral protein in the ER by viral infection. Then, unfolded protein response (UPR) is activated to alleviate the stress. Zika virus (ZIKV) is a mosquito-borne flavivirus and its infection causes microcephaly in newborns and serious neurological complications in adults. Here, we investigated ER stress and the regulating model of UPR in ZIKV-infected neural cells in vitro and in vivo. METHODS: Mice deficient in type I and II IFN receptors were infected with ZIKV via intraperitoneal injection and the nervous tissues of the mice were assayed at 5 days post-infection. The expression of phospho-IRE1, XBP1, and ATF6 which were the key markers of ER stress were analyzed by immunohistochemistry assay in vivo. Additionally, the nuclear localization of XBP1s and ATF6n were analyzed by immunohistofluorescence. Furthermore, two representative neural cells, neuroblastoma cell line (SK-N-SH) and astrocytoma cell line (CCF-STTG1), were selected to verify the ER stress in vitro. The expression of BIP, phospho-elF2α, phospho-IRE1, and ATF6 were analyzed through western blot and the nuclear localization of XBP1s was performed by confocal immunofluorescence microscopy. RT-qPCR was also used to quantify the mRNA level of the UPR downstream genes in vitro and in vivo. RESULTS: ZIKV infection significantly upregulated the expression of ER stress markers in vitro and in vivo. Phospho-IRE1 and XBP1 expression significantly increased in the cerebellum and mesocephalon, while ATF6 expression significantly increased in the mesocephalon. ATF6n and XBP1s were translocated into the cell nucleus. The levels of BIP, ATF6, phospho-elf2α, and spliced xbp1 also significantly increased in vitro. Furthermore, the downstream genes of UPR were detected to investigate the regulating model of the UPR during ZIKV infection in vitro and in vivo. The transcriptional levels of atf4, gadd34, chop, and edem-1 in vivo and that of gadd34 and chop in vitro significantly increased. CONCLUSION: Findings in this study demonstrated that ZIKV infection activates ER stress in neural cells. The results offer clues to further study the mechanism of neuropathogenesis caused by ZIKV infection

Noisy pre-processing facilitating a photonic realisation of device-independent quantum key distribution

Device-independent quantum key distribution provides security even when the equipment used to communicate over the quantum channel is largely uncharacterized. An experimental demonstration of device-independent quantum key distribution is however challenging. A central obstacle in photonic implementations is that the global detection efficiency, i.e., the probability that the signals sent over the quantum channel are successfully received, must be above a certain threshold. We here propose a method to significantly relax this threshold, while maintaining provable device-independent security. This is achieved with a protocol that adds artificial noise, which cannot be known or controlled by an adversary, to the initial measurement data (the raw key). Focusing on a realistic photonic setup using a source based on spontaneous parametric down conversion, we give explicit bounds on the minimal required global detection efficiency.Comment: 5+16 pages, 4 figure

Zika virus promotes CCN1 expression via the CaMKIIα-CREB pathway in astrocytes.

Zika virus (ZIKV) infection in the human central nervous system (CNS) causes Guillain-Barre syndrome, cerebellum deformity, and other diseases. Astrocytes are immune response cells in the CNS and an important component of the blood-brain barrier. Consequently, any damage to astrocytes facilitates the spread of ZIKV in the CNS. Connective tissue growth factor/Nephroblastoma overexpressed gene family 1 (CCN1), an important inflammatory factor secreted by astrocytes, is reported to regulate innate immunity and viral infection. However, the mechanism by which astrocyte viral infection affects CCN1 expression remains undefined. In this study, we demonstrate that ZIKV infection up-regulates CCN1 expression in astrocytes, thus promoting intracellular viral replication. Other studies revealed that the cAMP response element (CRE) in the CCN1 promoter is activated by the ZIKV NS3 protein. The cAMP-responsive element-binding protein (CREB), a transacting factor of the CRE, is also activated by NS3 or ZIKV. Furthermore,a specific inhibitor of CREB, i.e. SGC-CBP30, reduced ZIKV-induced CCN1 up-regulation and ZIKV replication. Moreover, co-immunoprecipitation, overexpression, and knockdown studies confirmed that the interaction between NS3 and the regulatory domain of CaMKIIα could activate the CREB pathway, thus resulting in the up-regulation of CCN1 expression and enhancement of virus replication. In conclusion, the findings of our investigations on the NS3-CaMKIIα-CREB-CCN1 pathway provide a foundation for understanding the infection mechanism of ZIKV in the CNS

Network intrusion detection based on LDA for payload feature selection

Anomaly Intrusion Detection System (IDS) is a statistical based network IDS which can detect attack variants and novel attacks without a priori knowledge. Current anomaly IDSs are inefficient for real-time detection because of their complex computation. This paper proposes a novel approach to reduce the heavy computational cost of an anomaly IDS. Linear Discriminant Analysis (LDA) and difference distance map are used for selection of significant features. This approach is able to transform high-dimensional feature vectors into a low-dimensional domain. The similarity between new incoming packets and a normal profile is determined using Euclidean distance on the simple, low-dimensional feature domain. The final decision will be made according to a pre-calculated threshold to differentiate normal and abnormal network packets. The proposed approach is evaluated using DARPA 1999 IDS dataset. ©2010 IEEE

A stateful mechanism for the tree-rule firewall

© 2014 IEEE. In this paper, we propose a novel connection tracking mechanism for Tree-rule firewall which essentially organizes firewall rules in a designated Tree structure. A new firewall model based on the proposed connection tracking mechanism is then developed and extended from the basic model of Net filter's Conn Track module, which has been used by many early generation commercial and open source firewalls including IPTABLES, the most popular firewall. To reduce the consumption of memory space and processing time, our proposed model uses one node per connection instead of using two nodes as appeared in Net filter model. This can reduce memory space and processing time. In addition, we introduce an extended hash table with more hashing bits in our firewall model in order to accommodate more concurrent connections. Moreover, our model also applies sophisticated techniques (such as using static information nodes, and avoiding timer objects and memory management tasks) to improve its processing speed. Finally, we implement this model on Linux Cent OS 6.3 and evaluate its speed. The experimental results show that our model performs more efficiently in comparison with the Net filter/IPTABLES