Recently, deep Convolutional Neural Networks (CNNs) can achieve human-level performance in edge detection with the rich and abstract edge representation capacities. However, the high performance of CNN based edge detection is achieved with a large pretrained CNN backbone, which is memory and energy consuming. In addition, it is surprising that the previous wisdom from the traditional edge detectors, such as Canny, Sobel, and LBP are rarely investigated in the rapid-developing deep learning era. To address these issues, we propose a simple, lightweight yet effective architecture named Pixel Difference Network (PiDiNet) for efficient edge detection. PiDiNet adopts novel pixel difference convolutions that integrate the traditional edge detection operators into the popular convolutional operations in modern CNNs for enhanced performance on the task, which enjoys the best of both worlds. Extensive experiments on BSDS500, NYUD, and Multicue are provided to demonstrate its effectiveness, and its high training and inference efficiency. Surprisingly, when training from scratch with only the BSDS500 and VOC datasets, PiDiNet can surpass the recorded result of human perception (0.807 vs. 0.803 in ODS F-measure) on the BSDS500 dataset with 100 FPS and less than 1M parameters. A faster version of PiDiNet with less than 0.1M parameters can still achieve comparable performance among state of the arts with 200 FPS. Results on the NYUD and Multicue datasets show similar observations. The codes are available at https://github.com/zhuoinoulu/pidinet.

Purpose: The expression of LIM and SH3 protein 1 (LASP1) was upregulated in colorectal cancer cases, thereby contributing to the aggressive phenotypes of colorectal cancer cells. However, we still cannot decipher the underlying molecular mechanism associated with colorectal cancer metastasis.Experimental Design: In this study, IHC was performed to investigate the expression of proteins in human colorectal cancer tissues. Western blot analysis was used to assess the LASP1-induced signal pathway. Two-dimensional difference gel electrophoresis was performed to screen LASP1-modulated proteins and uncover the molecular mechanism of LASP1. TGFb was used to induce an epithelial-mesenchymal transition (EMT).Results: LASP1 expression was correlated with the mesenchymal marker vimentin and was inversely correlated with epithelial markers, namely, E-cadherin and b-catenin, in clinical colorectal cancer samples. The gain-and loss-of-function assay showed that LASP1 induces EMT-like phenotypes in vitro and in vivo. S100A4, identified as a LASP1-modulated protein, was upregulated by LASP1. Moreover, it is frequently coexpressed with LASP1 in colorectal cancer. S100A4 was required for EMT, and an increased cell invasiveness of colorectal cancer cell is induced by LASP1. Furthermore, the stimulation of TGFb resulted in an activated Smad pathway that increased the expression of LASP1 and S100A4. The depletion of LASP1 or S100A4 expression inhibited the TGFb signaling pathway. Moreover, it significantly weakened the proinvasive effects of TGFb on colorectal cancer cells.Conclusion: These findings elucidate the central role of LASP1 in the TGFb-mediated EMT process and suggest a potential target for the clinical intervention in patients with advanced colorectal cancer. Clin Cancer Res; 20(22); 5835-47. Ó2014 AACR.

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In bacteria, Zur is a key regulator for zinc homeostasis. Our previous work has shown that, in the phytopathogen Xanthomonas campestris pv. campestris, in addition to regulating zinc homeostasis, Zur is essential for full virulence. Here, we demonstrate that the X. campestris pv. campestris Zur is involved in hypersensitive response (HR) and positively regulates the transcription of hrpA to hrpF operons and hrpX but not hrpG. Constitutively expressing hrpX but not hrpG in the zur mutant could bypass the requirement of Zur for the expression of hrpA to hrpF operons and the induction of wild-type HR, indicating that Zur controls the expression of hrp cluster via hrpX. Promoter-gusA reporter and semiquantitative reverse-transcription polymerase chain reaction analyses revealed that HrpG controls the expression of hrpX and HrpX regulates the expression of all the six hrp operons (hrpA to hrpF) in X. campestris pv. campestris.

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