Analyzing Hidden Representations in End-to-End Automatic Speech Recognition Systems

Neural models have become ubiquitous in automatic speech recognition systems. While neural networks are typically used as acoustic models in more complex systems, recent studies have explored end-to-end speech recognition systems based on neural networks, which can be trained to directly predict text from input acoustic features. Although such systems are conceptually elegant and simpler than traditional systems, it is less obvious how to interpret the trained models. In this work, we analyze the speech representations learned by a deep end-to-end model that is based on convolutional and recurrent layers, and trained with a connectionist temporal classification (CTC) loss. We use a pre-trained model to generate frame-level features which are given to a classifier that is trained on frame classification into phones. We evaluate representations from different layers of the deep model and compare their quality for predicting phone labels. Our experiments shed light on important aspects of the end-to-end model such as layer depth, model complexity, and other design choices.Comment: NIPS 201

Additional file 5: Table S4. of Oncogenic miR-210-3p promotes prostate cancer cell EMT and bone metastasis via NF-ÎşB signaling pathway

The relationship between miR-210-3p and clinicopathological characteristics in 149 patients with prostate cancer. (PDF 58 kb

Additional file 9: Figure S5. of Oncogenic miR-210-3p promotes prostate cancer cell EMT and bone metastasis via NF-κB signaling pathway

miR-210-3p expression levels was markedly elevated in metastatic bone tissues compared with that in primary PCa tissues with bone metastasis (BM, n = 6; Bone, n = 7). *P < 0.05. (PDF 28 kb

Additional file 6: Figure S2. of Oncogenic miR-210-3p promotes prostate cancer cell EMT and bone metastasis via NF-κB signaling pathway

Silencing miR-210-3p repressed EMT, invasion and migration in PC-3 cells in vitro. Real-time PCR analysis of miR-210-3p expression in PC-3 cells transduced with antagomiR-210-3p compared to controls. Transcript levels were normalized by U6 expression. Error bars represent the mean ± s.d. of three independent experiments. *P < 0.05

The expression of PTOV1 protein in archived NPC tissues from patients at different clinical stages.

<p>The expression of PTOV1 protein in archived NPC tissues from patients at different clinical stages.</p

Bmi-1 Promotes Glioma Angiogenesis by Activating NF-κB Signaling

<div><p>Angiogenesis in glioma is associated with the poor prognosis of the disease and closely correlates with the highly invasive phenotype of glioma cells, which represents the most challenging impediment against the currently glioma treatments. Bmi-1, an onco-protein, has been implicated in the progression of various human cancers, including gliomas, whereas its role in glioma angiogenesis remains unclear. Our current study examined the effects of Bmi-1 on glioma angiogenesis in vitro as well as in vivo. We found that overexpression of Bmi-1 enhanced, whereas knockdown of Bmi-1 diminished, the capability of glioma cells to induce tubule formation and migration of endothelial cells and neovascularization in chicken chorioallantoic membrane. <em>In vivo</em>, Bmi-1 overexpression and knockdown, respectively, promoted and inhibited angiogenesis in orthotopically transplanted human gliomas. Furthermore, NF-κB activity and VEGF-C expression was induced by Bmi-1 overexpression, whereas Bmi-1 knockdown attenuated NF-κB signaling and decreased VEGF-C expression. Additionally suppression of NF-κB activity using a specific chemical inhibitor abrogated the NF-κB activation and the pro-angiogenic activities of glioma cells. Together, our data suggest that Bmi-1 plays an important role in glioma angiogenesis and therefore could represent a potential target for anti-angiogenic therapy against the disease.</p> </div

The effects of dysregulation of SPHK1 expression on epirubicin induced-apoptosis <i>in vivo</i>.

<p>(A) Tumor volumes were measured on the indicated days. Left panel, indicated cells (2×10⁶) were injected in the flank of nude mice. When the mean tumor volume reached approximately 50 mm³, the mice were injected i.p. with epirubicin (5 mg/kg), every 3 days, up to 15 days. Right panel, U87MG-vector cells (2×10⁶) were injected in the flank of nude mice. When the mean tumor volume reached approximately 50 mm³, the mice were randomized into two groups (n = 5) and injected intraperitoneally either with epirubicin (Epi, 5 mg/kg) or epirubicin (Epi, 5 mg/kg) plus SK1-I (50 mg/kg) every 3 days, up to 15days. (B) Mean tumor weights were measured. Immunofluorescent images (C) and quantification (D) of TUNEL positive cells. For (B) and (D), error bars represent mean ± SD from three independent experiments with similar results *, <i>p</i><0.05.</p

Multivariate analysis of prognostic factors for NPC patients.

<p>Abbreviations: CI = confident interval; HR = hazard ratio; OS = overall survival; PFS = progression-free survival</p><p>Multivariate analysis of prognostic factors for NPC patients.</p