• 한국항행학회논문지
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• 제14권5호
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• pp.625-631
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• 2010

본 논문에서는 대표적인 측정치 기반형 보정정보인 RTCM v2 18/19 메시지와 보정치 기반형 보정정보인 RTCM v2 20/21 메시지, 그리고 저속통신매체용으로 제안된 바 있는 SNUR 메시지에 대하여 난수신 환경에서의 강전성 비교를 수행하였다. 일시적은 데이터 손실 경우와 단절 인지 후 재접속의 경우를 난수신 환경으로 가정하여, 각각 2초와 7초 동안 모든 메시지가 지연된 경우에 대하여 이중 차분된 측정치 비교를 통해 성능을 평가하였다. 수행 결과 7초 통신 단절의 경우 SNUR방식이 기존 RTCM 메시지에 비해 오차의 양을 30~60% 줄일 수 있음을 확인하였다. 뿐만 아니라, RTCM 메시지의 경우 7초의 지연시 L1반파장 이상의 오차가 발생하여 기추정된 미지정수를 사용할 수 없는 경우가 발생하였으나, SNUR 메시지 적용시 오차가 모두 1/4 파장이내에 포함됨을 확인하였다.

• Experimental and Molecular Medicine
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• 제50권11호
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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.