Cascade Residual Learning: A Two-stage Convolutional Neural Network for Stereo Matching

Leveraging on the recent developments in convolutional neural networks (CNNs), matching dense correspondence from a stereo pair has been cast as a learning problem, with performance exceeding traditional approaches. However, it remains challenging to generate high-quality disparities for the inherently ill-posed regions. To tackle this problem, we propose a novel cascade CNN architecture composing of two stages. The first stage advances the recently proposed DispNet by equipping it with extra up-convolution modules, leading to disparity images with more details. The second stage explicitly rectifies the disparity initialized by the first stage; it couples with the first-stage and generates residual signals across multiple scales. The summation of the outputs from the two stages gives the final disparity. As opposed to directly learning the disparity at the second stage, we show that residual learning provides more effective refinement. Moreover, it also benefits the training of the overall cascade network. Experimentation shows that our cascade residual learning scheme provides state-of-the-art performance for matching stereo correspondence. By the time of the submission of this paper, our method ranks first in the KITTI 2015 stereo benchmark, surpassing the prior works by a noteworthy margin.Comment: Accepted at ICCVW 2017. The first two authors contributed equally to this pape

Frequent Heterogeneous Missense Mutations of GGAP2 in Prostate Cancer: Implications for Tumor Biology, Clonality and Mutation Analysis

Prostate cancer is the most common visceral malignancy in Western men and a major cause of cancer deaths. Increased activation of the AKT and NFkB pathways have been identified as critical steps in prostate cancer initiation and progression. GGAP2 (GTP-binding and GTPase activating protein 2) is a multidomain protein that contains an N-terminal Ras homology domain (GTPase), followed by a PH domain, a C-terminal GAP domain and an ankyrin repeat domain. GGAP2 can directly activate signaling via both the AKT and NFkB pathways and acts as a node of crosstalk between these pathways. Increased GGAP2 expression is present in three quarters of prostate cancers. Mutations of GGAP2 have been reported in cell lines from other malignancies. We therefore analyzed 84 prostate cancer tissues and 43 benign prostate tissues for somatic mutations in GGAP2 by direct sequencing of individual clones derived from the GAP and GTPase domains of normal and tumor tissue. Overall, half of cancers contained mutant GAP domain clones and in 20% of cancers, 30% or more of clones were mutant in the GAP domain. Surprisingly, the mutations were heterogeneous and nonclonal, with multiple different mutations being present in many tumors. Similar findings were observed in the analysis of the GTPase domain. Mutant GGAP2 proteins had significantly higher transcriptional activity using AP-1 responsive reporter constructs when compared to wild-type protein. Furthermore, the presence of these mutations was associated with aggressive clinical behavior. The presence of high frequency nonclonal mutations of a single gene is novel and represents a new mode of genetic alteration that can promote tumor progression. Analysis of mutations in cancer has been used to predict outcome and guide therapeutic target identification but such analysis has focused on clonal mutations. Our studies indicate that in some cases high frequency nonclonal mutations may need to be assessed as well

17β-Estradiol Enhances Breast Cancer Cell Motility and Invasion via Extra-Nuclear Activation of Actin-Binding Protein Ezrin

Estrogen promotes breast cancer metastasis. However, the detailed mechanism remains largely unknown. The actin binding protein ezrin is a key component in tumor metastasis and its over-expression is positively correlated to the poor outcome of breast cancer. In this study, we investigate the effects of 17β-estradiol (E2) on the activation of ezrin and its role in estrogen-dependent breast cancer cell movement. In T47-D breast cancer cells, E2 rapidly enhances ezrin phosphorylation at Thr567 in a time- and concentration-dependent manner. The signalling cascade implicated in this action involves estrogen receptor (ER) interaction with the non-receptor tyrosine kinase c-Src, which activates the phosphatidylinositol-3 kinase/Akt pathway and the small GTPase RhoA/Rho-associated kinase (ROCK-2) complex. E2 enhances the horizontal cell migration and invasion of T47-D breast cancer cells in three-dimensional matrices, which is reversed by transfection of cells with specific ezrin siRNAs. In conclusion, E2 promotes breast cancer cell movement and invasion by the activation of ezrin. These results provide novel insights into the effects of estrogen on breast cancer progression and highlight potential targets to treat endocrine-sensitive breast cancers

DNA methylation and aberrant expression of Sprouty1 in human prostate cancer

Sprouty1 is a negative regulator of fibroblast growth factor signaling with a potential tumor suppressor function in prostate cancer (PCa). Sprouty1 is downregulated in human PCa and Sprouty1 expression can markedly inhibit PCa proliferation in vitro. The aim of this study was to investigate the role of DNA methylation in Sprouty1 expression in human prostate tumors. We used pyrosequencing to quantitatively measure the methylation status of the Sprouty1 promoter region in prostate tissues and cell lines and assessed Sprouty1 mRNA expression by quantitative RT-PCR. Our data demonstrates significantly higher % methylation of Sprouty1 promoter in the PCa tissues when compared to matched normal tissues. Hypermethylation of Sprouty1 promoter was detected in PCa cell lines compared to the normal prostate epithelial cells. The increased % methylation was associated with reduced Sprouty1 mRNA expression in the PCa tissues and cell lines. Methylation modification of the Sprouty1 promoter using Sss1 methylase abolished promoter activity whereas global demethylation with 5′-Aza-2′-Deoxycytidine treatment induced Sprouty1 expression. Our data demonstrates that DNA methylation in the Sprouty1 promoter region is responsible for downregulating Sprouty1 expression in prostate cancer. © 2009 Landes Bioscience

DiffSinger: Singing Voice Synthesis via Shallow Diffusion Mechanism

Singing voice synthesis (SVS) systems are built to synthesize high-quality and expressive singing voice, in which the acoustic model generates the acoustic features (e.g., mel-spectrogram) given a music score. Previous singing acoustic models adopt a simple loss (e.g., L1 and L2) or generative adversarial network (GAN) to reconstruct the acoustic features, while they suffer from over-smoothing and unstable training issues respectively, which hinder the naturalness of synthesized singing. In this work, we propose DiffSinger, an acoustic model for SVS based on the diffusion probabilistic model. DiffSinger is a parameterized Markov chain that iteratively converts the noise into mel-spectrogram conditioned on the music score. By implicitly optimizing variational bound, DiffSinger can be stably trained and generate realistic outputs. To further improve the voice quality and speed up inference, we introduce a shallow diffusion mechanism to make better use of the prior knowledge learned by the simple loss. Specifically, DiffSinger starts generation at a shallow step smaller than the total number of diffusion steps, according to the intersection of the diffusion trajectories of the ground-truth mel-spectrogram and the one predicted by a simple mel-spectrogram decoder. Besides, we propose boundary prediction methods to locate the intersection and determine the shallow step adaptively. The evaluations conducted on a Chinese singing dataset demonstrate that DiffSinger outperforms state-of-the-art SVS work. Extensional experiments also prove the generalization of our methods on text-to-speech task (DiffSpeech). Audio samples: https://diffsinger.github.io. Codes: https://github.com/MoonInTheRiver/DiffSinger

Altered Fibroblast Growth Factor Receptor 4 Stability Promotes Prostate Cancer Progression1

Fibroblast growth factor receptor 4 (FGFR-4) is expressed at significant levels in almost all human prostate cancers, and expression of its ligands is ubiquitous. A common polymorphism of FGFR-4 in which arginine (Arg388) replaces glycine (Gly388) at amino acid 388 is associated with progression in human prostate cancer. We show that the FGFR-4 Arg388 polymorphism, which is present in most prostate cancer patients, results in increased receptor stability and sustained receptor activation. In patients bearing the FGFR-4 Gly388 variant, expression of Huntingtin-interacting protein 1 (HIP1), which occurs in more than half of human prostate cancers, also results in FGFR-4 stabilization. This is associated with enhanced proliferation and anchorage-independent growth in vitro. Our findings indicate that increased receptor stability and sustained FGFR-4 signaling occur in most human prostate cancers due to either the presence of a common genetic polymorphism or the expression of a protein that stabilizes FGFR-4. Both of these alterations are associated with clinical progression in patients with prostate cancer. Thus, FGFR-4 signaling and receptor turnover are important potential therapeutic targets in prostate cancer

Adjacent seam pressure-relief gas drainage technique based on ground movement for initial mining phase of longwall face

Disallowed gas concentration (DGC), i.e., a cease in production due to gas concentration exceeding the allowable limits, occurs frequently during the initial mining phase of longwall faces in Yangquan Coalfield, and seriously affects safety. The mechanism of DGC during the initial mining phase of longwall face is determined by analyzing the outflow behavior of methane. The results show that mining can induce ground movement and lead to pressure relief, leading to desorption and migration of the gas in the adjacent seams. Gas drainage from the high-level gas drainage roadway is unsuccessful because it is normally located too high to connect to vertical broken crevices of overlying strata in a timely manner during the initial mining phase, subsequently, the released methane from adjacent seams flows into the goaf. This results in the occurrence of DGC at the longwall face. Thus, based on the analysis of overlying strata movement and the flow characteristics of gas from adjacent seams, we propose an adjacent seams gas drainage technique of a large-diameter blind shaft joined to the high-level gas drainage roadway (LDBS-HGDR) for the initial mining phase. A computational fluid dynamics simulation was conducted to obtain the optimal design of the layout parameters for the LDBS-HGDR at Panel 15201. Compared with the conventional rear high-level gas drainage roadway technique, the gas drainage technique of the LDBS-HGDR is advantageous in terms of ease of construction, low cost, and sufficiently long drainage hours. Moreover, the outflow of gas from adjacent seams can be effectively decreased with this technique, thereby eliminating the hazards originating from the frequent occurrence of DGC

GGAP2 mutations result in enhanced transcription from AP-1 reporter constructs.

<p>Asterisks indicate statistically significant increase relative to wild-type (WT) GGAP2 by ANOVA (p<.05). Mean +/−SEM. Mutation and number of transfections are shown.</p