Fast and Accurate Dual-Way Streaming PARAFAC2 for Irregular Tensors -- Algorithm and Application

How can we efficiently and accurately analyze an irregular tensor in a dual-way streaming setting where the sizes of two dimensions of the tensor increase over time? What types of anomalies are there in the dual-way streaming setting? An irregular tensor is a collection of matrices whose column lengths are the same while their row lengths are different. In a dual-way streaming setting, both new rows of existing matrices and new matrices arrive over time. PARAFAC2 decomposition is a crucial tool for analyzing irregular tensors. Although real-time analysis is necessary in the dual-way streaming, static PARAFAC2 decomposition methods fail to efficiently work in this setting since they perform PARAFAC2 decomposition for accumulated tensors whenever new data arrive. Existing streaming PARAFAC2 decomposition methods work in a limited setting and fail to handle new rows of matrices efficiently. In this paper, we propose Dash, an efficient and accurate PARAFAC2 decomposition method working in the dual-way streaming setting. When new data are given, Dash efficiently performs PARAFAC2 decomposition by carefully dividing the terms related to old and new data and avoiding naive computations involved with old data. Furthermore, applying a forgetting factor makes Dash follow recent movements. Extensive experiments show that Dash achieves up to 14.0x faster speed than existing PARAFAC2 decomposition methods for newly arrived data. We also provide discoveries for detecting anomalies in real-world datasets, including Subprime Mortgage Crisis and COVID-19.Comment: 12 pages, accept to The 29th ACM SIGKDD International Conference on Knowledge Discovery and Data Mining (KDD) 202

The Mechanical\u27s Bull-Session 1930

https://ir.uiowa.edu/mechanicals-bull-session/1000/thumbnail.jp

Graphene Photonics and Optoelectronics

The richness of optical and electronic properties of graphene attracts enormous interest. Graphene has high mobility and optical transparency, in addition to flexibility, robustness and environmental stability. So far, the main focus has been on fundamental physics and electronic devices. However, we believe its true potential to be in photonics and optoelectronics, where the combination of its unique optical and electronic properties can be fully exploited, even in the absence of a bandgap, and the linear dispersion of the Dirac electrons enables ultra-wide-band tunability. The rise of graphene in photonics and optoelectronics is shown by several recent results, ranging from solar cells and light emitting devices, to touch screens, photodetectors and ultrafast lasers. Here we review the state of the art in this emerging field.Comment: Review Nature Photonics, in pres

Expression of Aquaporin 5 (AQP5) Promotes Tumor Invasion in Human Non Small Cell Lung Cancer

The aquaporins (AQP) are water channel proteins playing a major role in transcellular and transepithelial water movement. Recently, the role of AQPs in human carcinogenesis has become an area of great interest. Here, by immunohistochemistry (IHC), we have found an expression of AQP5 protein in 35.3% (IHC-score: ≥1, 144/408) of the resected NSCLC tissue samples. Cases with AQP5-positive status (IHC-score: ≥2) displayed a higher rate of tumor recurrence than negative ones in NSCLC (54.7% vs. 35.1%, p = 0.005) and worse disease-free survival (p = 0.033; OR = 1.52; 95%CI:1.04−2.23). Further in vitro invasion assay using BEAS-2B and NIH3T3 cells stably transfected with overexpression constructs for full length wild-type AQP5 (AQP5) and its two mutants, N185D which blocks membrane trafficking and S156A which blocks phosphorylation on Ser156, showed that AQP5 induced cell invasions while both mutants did not. In BEAS-2B cells, the expression of AQP5 caused a spindle-like and fibroblastic morphologic change and losses of cell-cell contacts and cell polarity. Only cells with AQP5, not either of two mutants, exhibited a loss of epithelial cell markers and a gain of mesenchymal cell markers. In a human SH3-domains protein array, cellular extracts from BEAS-2B with AQP5 showed a robust binding activity to SH3-domains of the c-Src, Lyn, and Grap2 C-terminal. Furthermore, in immunoprecipitation assay, activated c-Src, phosphorylated on Tyr416, showed a stronger binding activity to cellular extracts from BEAS-2B with AQP5 compared with N185D or S156A mutant. Fluorescence in situ hybridization (FISH) analysis failed to show evidence of genomic amplification, suggesting AQP5 expression as a secondary event. Based on these clinical and molecular observations, we conclude that AQP5, through its phosphorylation on Ser156 and subsequent interaction with c-Src, plays an important role in NSCLC invasion and, therefore, may provide a unique opportunity for developing a novel therapeutic target as well as a prognostic marker in NSCLC