A Secured Authentication Protocol for Wireless Sensor Networks Using Elliptic Curves Cryptography

User authentication is a crucial service in wireless sensor networks (WSNs) that is becoming increasingly common in WSNs because wireless sensor nodes are typically deployed in an unattended environment, leaving them open to possible hostile network attack. Because wireless sensor nodes are limited in computing power, data storage and communication capabilities, any user authentication protocol must be designed to operate efficiently in a resource constrained environment. In this paper, we review several proposed WSN user authentication protocols, with a detailed review of the M.L Das protocol and a cryptanalysis of Das’ protocol that shows several security weaknesses. Furthermore, this paper proposes an ECC-based user authentication protocol that resolves these weaknesses. According to our analysis of security of the ECC-based protocol, it is suitable for applications with higher security requirements. Finally, we present a comparison of security, computation, and communication costs and performances for the proposed protocols. The ECC-based protocol is shown to be suitable for higher security WSNs

CloudBook: Implementing an E-book reader on a cloud platform by an optimized vector graphic library

[[abstract]]Problems of the E-book application include different file formats, performance inefficiency and image distortion; those may cause a slow development of E-book marketing in the industry of information technology. This paper proposes an innovative E-book system called CloudBook, which utilizes an embedded Graphics Processing Unit (GPU) and a data locality aware Hadoop system to resolve the problems. The results of the experiments show that the CloudBook system can increase the performance of the OpenVG library by 73%, reduce the execution time of file conversion by 50%–75%, and improve the data hit ratio in cloud platform by 10%.[[notice]]補正完

The Monitoring System Based on Nagios for Data Grid Environment

[[abstract]]The amount of digital data in today’s society is already enormous and it will continue to grow exponentially. Therefore, it is necessary to devise new ways to preserve and manage the data effectively and efficiently. SRB (Storage Resource Broker), and its extension iRODS (the Integrated Rule-Oriented Data System), are data grid technologies for managing colossal amounts of data. In a distributed environment, monitoring systems oversee the operation of computing systems. The monitoring service is crucial because it must ensure a high-quality computing environment and provide reliable services. In this paper, we introduce a monitoring system called SIAM, which is based on Nagios. SIAM supports full monitoring services for SRB/iRODS-based systems, including fault-tolerance and notification functions. This study focuses on extending existing components and notification functions to satisfy clients’ needs and improve our system’s failover scheme. The results of experiments show that the proposed system is feasible for cloud storage services, and it is adaptable robust, and responsive in the face of system failures. Overall, SIAM enhances the reliability of SRB/iRODS based systems significantly.[[conferencetype]]國際[[conferencedate]]20110717~20110721[[booktype]]紙本[[iscallforpapers]]Y[[conferencelocation]]Las Vegas, US

Interplay of Epidermal Growth Factor Receptor and Signal Transducer and Activator of Transcription 3 in Prostate Cancer: Beyond Androgen Receptor Transactivation

Prostate cancer (PCa) is one of the most common cancers in the world and causes thousands of deaths every year. Conventional therapy for PCa includes surgery and androgen deprivation therapy (ADT). However, about 10–20% of all PCa cases relapse; there is also the further development of castration resistant adenocarcinoma (CRPC-Adeno) or neuroendocrine (NE) PCa (CRPC-NE). Due to their androgen-insensitive properties, both CRPC-Adeno and CRPC-NE have limited therapeutic options. Accordingly, this study reveals the inductive mechanisms of CRPC (for both CRPC-Adeno and CRPC-NE) and fulfils an urgent need for the treatment of PCa patients. Although previous studies have illustrated the emerging roles of epidermal growth factor receptors (EGFR), signal transducer, and activator of transcription 3 (STAT3) signaling in the development of CRPC, the regulatory mechanisms of this interaction between EGFR and STAT3 is still unclear. Our recent studies have shown that crosstalk between EGFR and STAT3 is critical for NE differentiation of PCa. In this review, we have collected recent findings with regard to the involvement of EGFR and STAT3 in malignancy progression and discussed their interactions during the development of therapeutic resistance for PCa

Disruption of ETV6 leads to TWIST1-dependent progression and resistance to epidermal growth factor receptor tyrosine kinase inhibitors in prostate cancer

Abstract Background ETS variant gene 6 (ETV6) is a putative tumor suppressor and repressed by epidermal growth factor receptor (EGFR) signaling in prostate cancer. Since EGFR antagonists seem ineffective in castration-resistant prostate cancer (CRPC), we aim to study the role of ETV6 in the development of drug resistance. Methods Etv6 target gene was validated by ChIP and promoter reporter assays. Correlation of ETV6 and TWIST1 was analyzed in human clinical datasets and tissue samples. Migration, invasion, and metastasis assays were used to measure the cellular responses after perturbation of ETV6 -TWIST1 axis. Proliferation and tumor growth in xenograft model were performed to evaluate the drug sensitivities of EGFR-tyrosine kinase inhibitors (TKIs). Results ETV6 inhibits TWIST1 expression and disruption of ETV6 promotes TWIST1-dependent malignant phenotypes. Importantly, ETV6 is required to the anti-proliferation effects of EGFR-TKIs, partly due to the inhibitory function of ETV6 on TWIST1. We also found that EGFR-RAS signaling is tightly controlled by ETV6, supporting its role in TKI sensitivity. Conclusions Our study demonstrates that disruption of ETV6 contributes to EGFR-TKI resistance, which is likely due to derepression of TWIST1 and activation of EGFR-RAS signaling. Our results implicate ETV6 as a potential marker for predicting efficacy of an EGFR-targeted anticancer approach. Combination treatment of TWIST1 inhibitors could sensitize the anti-proliferation effects of EGFR-TKIs

CHRM4/AKT/MYCN upregulates interferon alpha-17 in the tumor microenvironment to promote neuroendocrine differentiation of prostate cancer

Abstract Current treatment options for prostate cancer focus on targeting androgen receptor (AR) signaling. Inhibiting effects of AR may activate neuroendocrine differentiation and lineage plasticity pathways, thereby promoting the development of neuroendocrine prostate cancer (NEPC). Understanding the regulatory mechanisms of AR has important clinical implications for this most aggressive type of prostate cancer. Here, we demonstrated the tumor-suppressive role of the AR and found that activated AR could directly bind to the regulatory sequence of muscarinic acetylcholine receptor 4 (CHRM4) and downregulate its expression. CHRM4 was highly expressed in prostate cancer cells after androgen-deprivation therapy (ADT). CHRM4 overexpression may drive neuroendocrine differentiation of prostate cancer cells and is associated with immunosuppressive cytokine responses in the tumor microenvironment (TME) of prostate cancer. Mechanistically, CHRM4-driven AKT/MYCN signaling upregulated the interferon alpha 17 (IFNA17) cytokine in the prostate cancer TME after ADT. IFNA17 mediates a feedback mechanism in the TME by activating the CHRM4/AKT/MYCN signaling-driven immune checkpoint pathway and neuroendocrine differentiation of prostate cancer cells. We explored the therapeutic efficacy of targeting CHRM4 as a potential treatment for NEPC and evaluated IFNA17 secretion in the TME as a possible predictive prognostic biomarker for NEPC

Additional file 1: of Disruption of ETV6 leads to TWIST1-dependent progression and resistance to epidermal growth factor receptor tyrosine kinase inhibitors in prostate cancer

Figure Legends and Tables. (ZIP 1350 kb

Involvement of a BH3-only apoptosis sensitizer gene Blm-s in hippocampus-mediated mood control

Mood disorders are an important public health issue and recent advances in genomic studies have indicated that molecules involved in neurodevelopment are causally related to mood disorders. BLM-s (BCL-2-like molecule, small transcript isoform), a BH3-only proapoptotic BCL-2 family member, mediates apoptosis of postmitotic immature neurons during embryonic cortical development, but its role in the adult brain is unknown. To better understand the physiological role of Blm-s gene in vivo, we generated a Blm-s-knockout (Blm-s-/-) mouse. The Blm-s-/- mice breed normally and exhibit grossly normal development. However, global depletion of Blm-s is highly associated with depression- and anxiety-related behaviors in adult mutant mice with intact learning and memory capacity. Functional magnetic resonance imaging of adult Blm-s-/- mice reveals reduced connectivity mainly in the ventral dentate gyrus (vDG) of the hippocampus with no alteration in the dorsal DG connectivity and in total hippocampal volume. At the cellular level, BLM-s is expressed in DG granule cells (GCs), and Blm-s-/- mice show reduced dendritic complexity and decreased spine density in mature GCs. Electrophysiology study uncovers that mature vGCs in adult Blm-s-/- DG are intrinsically more excitable. Interestingly, certain genetic variants of the human Blm homologue gene (VPS50) are significantly associated with depression traits from publicly resourced UK Biobank data. Taken together, BLM-s is required for the hippocampal mood control function. Loss of BLM-s causes abnormality in the electrophysiology and morphology of GCs and a disrupted vDG neural network, which could underlie Blm-s-null-associated anxiety and depression