Taiwan Centres for Disease Control.

No abstract

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This paper introduces a novel deep network for estimating depth maps from a light field image. For utilizing the views more effectively and reducing redundancy within views, we propose a view selection module that generates an attention map indicating the importance of each view and its potential for contributing to accurate depth estimation. By exploring the symmetric property of light field views, we enforce symmetry in the attention map and further improve accuracy. With the attention map, our architecture utilizes all views more effectively and efficiently. Experiments show that the proposed method achieves state-of-the-art performance in terms of accuracy and ranks the first on a popular benchmark for disparity estimation for light field images.

Diagnostic systematic review is a vital step in the evaluation of diagnostic technologies. In many applications, it involves pooling pairs of sensitivity and specificity of a dichotomized diagnostic test from multiple studies. We propose a composite likelihood method for bivariate meta-analysis in diagnostic systematic reviews. This method provides an alternative way to make inference on diagnostic measures such as sensitivity, specificity, likelihood ratios and diagnostic odds ratio. Its main advantages over the standard likelihood method are the avoidance of the non-convergence problem, which is non-trivial when the number of studies are relatively small, the computational simplicity and some robustness to model mis-specifications. Simulation studies show that the composite likelihood method maintains high relative efficiency compared to that of the standard likelihood method. We illustrate our method in a diagnostic review of the performance of contemporary diagnostic imaging technologies for detecting metastases in patients with melanoma.

Purpose: We herein examine whether macrophage inflammatory protein-3a (MIP-3a) is a biomarker for nasopharyngeal carcinoma (NPC) and whether it is involved in modulating NPC cell functions. Experimental Design: The study population comprises 275 NPC patients and 250 controls. MIP-3a levels in tissues and sera were examined by immunohistochemistry and ELISA, respectively. EBV DNA load and EBV viral capsid antigen IgA were measured by quantitative real-time PCR and immunofluorescence assay, respectively. Effects of MIP-3a on NPC cell motility were investigated byTranswell migration/invasion assays and RNA interference. Results: MIP-3a was overexpressed in NPC tumor cells. Serum MIP-3a levels were significantly higher in untreated patients, recurrent patients and patients with distant metastases versus non-NPC controls, patients with complete remission, and long-term disease-free patients. In the prospective cohort, serum MIP-3a levels were significantly higher in untreated NPC patients with advanced tumor-node-metastasis stage versus early stage and also correlated with EBV DNA load. Measurement of MIP-3a, EBV DNA, and viral capsid antigen IgA levels in serial serum/plasma samples from treated patients at 6-month intervals revealed a high association between MIP3a level, EBV DNA load, and disease status. Among 155 consecutive NPC patients, subjects with pretreated MIP-3a serum levels over 65 pg/mL had worse prognoses for overall survival and distant metastasis-free survival in univariate and multivariate analysis. Additionally, cell functional assays showed that MIP-3a contributed to migration and invasion of NPC cells, which could be effectively inhibited by MIP-3a knockdown. Conclusions: MIP-3a may be a novel biomarker and prognosticator for NPC and is involved in migration and invasion of NPC cells.

Dysregulated expression of zinc transporters is involved in the progression of gliomas. Our results suggest that ZIP4 may serve as a potential diagnostic and prognostic marker for gliomas.

Purpose: Little is known about the genetic alterations characteristic of small bowel adenocarcinoma (SBA). Our purpose was to identify targetable alterations and develop experimental models of this disease. Experimental Design: Whole-exome sequencing (WES) was completed on 17 SBA patient samples and targeted-exome sequencing (TES) on 27 samples to confirm relevant driver mutations. Two SBA models with ERBB2 kinase activating mutations were tested for sensitivity to anti-ERBB2 agents in vivo and in vitro. Biochemical changes were measured by reverse-phase protein arrays. Results: WES identified somatic mutations in 4 canonical pathways (WNT, ERBB2, STAT3, and chromatin remodeling), which were validated in the TES cohort. Although APC mutations were present in only 23% of samples, additional WNT-related alterations were seen in 12%. ERBB2 mutations and amplifications were present in 23% of samples. Patients with alterations in the ERBB2 signaling cascade (64%) demonstrated worse clinical outcomes (median survival 70.3 months vs. 109 months; log-rank HR ¼ 2.4, P ¼ 0.03). Two ERBB2-mutated (V842I and Y803H) cell lines were generated from SBA patient samples. Both demonstrated high sensitivity to ERBB2 inhibitor dacomitinib (IC 50 < 2.5 nmol/L). In xenografts derived from these samples, treatment with dacomitinib reduced tumor growth by 39% and 59%, respectively, whereas it had no effect in an SBA wild-type ERBB2 model. Conclusions: The in vitro and in vivo models of SBA developed here provide a valuable resource for understanding targetable mutations in this disease. Our findings support clinical efforts to target activating ERBB2 mutations in patients with SBA that harbor these alterations.