Wireless sensor networks (WSNs) consist of sensors, gateways and users. Sensors are widely distributed to monitor various conditions, such as temperature, sound, speed and pressure but they have limited computational ability and energy. To reduce the resource use of sensors and enhance the security of WSNs, various user authentication protocols have been proposed. In 2011, Yeh et al. first proposed a user authentication protocol based on elliptic curve cryptography (ECC) for WSNs. However, it turned out that Yeh et al.'s protocol does not provide mutual authentication, perfect forward secrecy, and key agreement between the user and sensor. Later in 2013, Shi et al. proposed a new user authentication protocol that improves both security and efficiency of Yeh et al.'s protocol. However, Shi et al.'s improvement introduces other security weaknesses. In this paper, we show that Shi et al.'s improved protocol is vulnerable to session key attack, stolen smart card attack, and sensor energy exhausting attack. In addition, we propose a new, security-enhanced user authentication protocol using ECC for WSNs.

MMP1-1,607 dupG and MMP9-1,562 C homozygotes demonstrated an increased risk of colorectal cancer regardless of ethnic differences, whereas other MMP and PAI1 polymorphisms did not. Nevertheless, specific MMP haplotypes on 11q22.1-23.3 and 20q12-13 seem to be implicated in susceptibility to colorectal cancer.

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A smart-card-based user authentication scheme for wireless sensor networks (in short, a SUA-WSN scheme) is designed to restrict access to the sensor data only to users who are in possession of both a smart card and the corresponding password. While a significant number of SUA-WSN schemes have been suggested in recent years, their intended security properties lack formal definitions and proofs in a widely-accepted model. One consequence is that SUA-WSN schemes insecure against various attacks have proliferated. In this paper, we devise a security model for the analysis of SUA-WSN schemes by extending the widely-accepted model of Bellare, Pointcheval and Rogaway (2000). Our model provides formal definitions of authenticated key exchange and user anonymity while capturing side-channel attacks, as well as other common attacks. We also propose a new SUA-WSN scheme based on elliptic curve cryptography (ECC), and prove its security properties in our extended model. To the best of our knowledge, our proposed scheme is the first SUA-WSN scheme that provably achieves both authenticated key exchange and user anonymity. Our scheme is also computationally competitive with other ECC-based (non-provably secure) schemes.

The nonclassical human leukocyte antigen (HLA)-E and -G molecules have previously been shown to inhibit natural killer-and cytotoxic T-lymphocytemediated cell lysis and have also been shown to prevent the proliferation of CD4 T cells and secrete cytokines that appear to be important in the modulation of the BehcetÕs disease (BD) immune systems. Polymorphisms in the HLA-E and HLA-G genes have been associated with differential expression and function. Thus, we conducted an analysis of the HLA-E and HLA-G alleles using Amplification Refractory Mutation System-polymerase chain reaction (PCR) and PCRrestriction fragment length polymorphism techniques in a study comprising 312 patients with BD and 486 controls. The HLA-E*0101 and HLA-G*010101 alleles were associated with a reduced risk of BD (P ¼ 0.0002, odds ratio (OR) ¼ 0.7 and P ¼ 0.002, OR ¼ 0.7, respectively). By way of contrast, the variants HLA-E*010302, HLA-G*010102, G*0105N alleles and 3741_3754ins14bp were all associated with an increased risk of BD (P < 0.0001, OR ¼ 1.6; P ¼ 0.002, OR ¼ 1.8; P ¼ 0.024, OR ¼ 2.0 and P ¼ 0.003, OR ¼ 1.4, respectively). Individuals carrying both the HLA-E*0101 and the HLA-G*010101 alleles evidenced significantly lower frequency in the patients than in the controls (35.6% vs 49.6%; P < 0.0001, OR ¼ 0.6). These results indicate that variant HLA-E and HLA-G molecules appear to function independently and synergistically, increasing the risk of BD, and may result in an imbalance of lymphocytic functions, which may culminate in the development of BD.

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