• Journal of Advanced Navigation Technology
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• v.14 no.5
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• pp.625-631
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• 2010

In this paper, robustness performance of SNUR message is compared with those of existing ones, RTCM(Radio Technical Commission for Maritime Services) v2 MT(Message Type) 18/19 and MT 20/21 under a poor broadcast condition such as temporary data loss or disconnection We defined the temp oral data loss as 2 second delay and reconnection after disconnection as 7 second latency, and then evaluated its robustness for each latency case by double differentiating the observables. Our result shows that SNUR protocol method can reduce the latency error of the existing RTCM messages by 30~60%. Moreover, a rover using SNUR message, whose latency error is bounded within 1/4 L1 wave length, can figure out its own fixed position continuously in spite of 7 second disconnection, while the other using RTCM message, whose error is larger than half wave length, cannot keep its previous fixed solution.

• Experimental and Molecular Medicine
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• v.50 no.11
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• pp.7.1-7.12
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• 2018

Recent findings from The Cancer Genome Atlas project have provided a comprehensive map of genomic alterations that occur in hepatocellular carcinoma (HCC), including unexpected mutations in apolipoprotein B (APOB). We aimed to determine the clinical significance of this non-oncogenetic mutation in HCC. An Apob gene signature was derived from genes that differed between control mice and mice treated with siRNA specific for Apob (1.5-fold difference; P < 0.005). Human gene expression data were collected from four independent HCC cohorts (n = 941). A prediction model was constructed using Bayesian compound covariate prediction, and the robustness of the APOB gene signature was validated in HCC cohorts. The correlation of the APOB signature with previously validated gene signatures was performed, and network analysis was conducted using ingenuity pathway analysis. APOB inactivation was associated with poor prognosis when the APOB gene signature was applied in all human HCC cohorts. Poor prognosis with APOB inactivation was consistently observed through cross-validation with previously reported gene signatures (NCIP A, HS, high-recurrence SNUR, and high RS subtypes). Knowledge-based gene network analysis using genes that differed between low-APOB and high-APOB groups in all four cohorts revealed that low-APOB activity was associated with upregulation of oncogenic and metastatic regulators, such as HGF, MTIF, ERBB2, FOXM1, and CD44, and inhibition of tumor suppressors, such as TP53 and PTEN. In conclusion, APOB inactivation is associated with poor outcome in patients with HCC, and APOB may play a role in regulating multiple genes involved in HCC development.