A Unified Optimization Approach for Sparse Tensor Operations on GPUs

Sparse tensors appear in many large-scale applications with multidimensional and sparse data. While multidimensional sparse data often need to be processed on manycore processors, attempts to develop highly-optimized GPU-based implementations of sparse tensor operations are rare. The irregular computation patterns and sparsity structures as well as the large memory footprints of sparse tensor operations make such implementations challenging. We leverage the fact that sparse tensor operations share similar computation patterns to propose a unified tensor representation called F-COO. Combined with GPU-specific optimizations, F-COO provides highly-optimized implementations of sparse tensor computations on GPUs. The performance of the proposed unified approach is demonstrated for tensor-based kernels such as the Sparse Matricized Tensor- Times-Khatri-Rao Product (SpMTTKRP) and the Sparse Tensor- Times-Matrix Multiply (SpTTM) and is used in tensor decomposition algorithms. Compared to state-of-the-art work we improve the performance of SpTTM and SpMTTKRP up to 3.7 and 30.6 times respectively on NVIDIA Titan-X GPUs. We implement a CANDECOMP/PARAFAC (CP) decomposition and achieve up to 14.9 times speedup using the unified method over state-of-the-art libraries on NVIDIA Titan-X GPUs

Fast acquisition method using modified PCA with a sparse factor for burst DS spread-spectrum transmission

To improve the acquisition speed and inbound capacity of the ground station in a burst direct-sequence (DS) spread-spectrum transmission system, an acquisition method based on a modified parallel code-phase acquisition (PCA) scheme is proposed. By taking advantage of the sparsity of the acquisition result with PCA in the time domain, we introduce the sparse factor to handle the signals via sparsification and apply the sparse recovery algorithm to search and estimate the acquisition result. The computational complexity, mean acquisition time, and relationship between the inbound capacity and acquisition performance are provided. We theoretically analyse the effect of the sparse factor on the acquisition performance. The estimation errors verify our analysis, and simulations show that the acquisition time of our proposed method outperforms that of advanced PCA by 1.2–4.0 times; additionally, the inbound capacity increases by 6.2–36.7%

Identification of miR-320 family members as potential diagnostic and prognostic biomarkers in myelodysplastic syndromes

Abstract Myelodysplastic syndromes (MDS) are characterized by ineffective hematopoiesis and the abnormal differentiation of hematopoietic stem cells. An increasing number of researches have demonstrated that microRNAs play crucial roles in the pathogenesis of myelodysplastic syndromes. Herein, we aimed to identify novel potential microRNAs bound up with the diagnosis and prognosis of MDS. MiRNA microarray analysis was used to screen deregulated microRNAs in the bone marrow of MDS patients. qRT-PCR was employed to confirm the microarray results. All members of miR-320 family (miR-320a, miR-320b, miR-320c, miR-320d, and miR-320e) were significantly increased in MDS patients compared to normal control. Although we found no correlation between miR-320 family and most clinical characteristics, high miR-320c and miR-320d expression seemed to be associated with high numbers of bone marrow (BM) blasts and worse karyotype. High expression of all the members of the miR-320 family seemed to be associated with a high prognostic score based on International Prognostic Scoring System (IPSS). The areas under the miR-320 family member ROC curves were 0.9037 (P < 0.0001), 0.7515 (P = 0.0002), 0.9647 (P < 0.0001), 0.8064 (P < 0.0001) and 0.9019 (P < 0.0001). Regarding Kaplan–Meier analysis, high miR-320c and miR-320d expression were related to shorter overall survival (OS). Moreover, multivariate analysis revealed the independent prognostic value of miR-320d for OS in MDS. The expression of miR-320 family members was up-regulated in MDS, and miR-320 family members could serve as candidate diagnostic biomarkers for MDS. High expression of miR-320d was an independent prognostic factor for OS in MDS

Doxycycline Inducible Kruppel-Like Factor 4 Lentiviral Vector Mediates Mesenchymal to Epithelial Transition in Ovarian Cancer Cells

<div><p>Ovarian cancer presents therapeutic challenges due to its typically late detection, aggressive metastasis, and therapeutic resistance. The transcription factor Krüppel-like factor 4 (KLF4) has been implicated in human cancers as a tumor suppressor or oncogene, although its role depends greatly on the cellular context. The role of KLF4 in ovarian cancer has not been elucidated in mechanistic detail. In this study, we investigated the role of KLF4 in ovarian cancer cells by transducing the ovarian cancer cell lines SKOV3 and OVCAR3 with a doxycycline-inducible KLF4 lentiviral vector. Overexpression of KLF4 reduced cell proliferation, migration, and invasion. The epithelial cell marker gene E-cadherin was significantly upregulated, whereas the mesenchymal cell marker genes vimentin, twist1and snail2 (slug) were downregulated in both KLF4-expressing SKOV3 and OVCAR3 cells. KLF4 inhibited the transforming growth factor β (TGFβ)-induced epithelial to mesenchymal transition (EMT) in ovarian cancer cells. Taken together, our data demonstrate that KLF4 functions as a tumor suppressor gene in ovarian cancer cells by inhibiting TGFβ-induced EMT.</p></div

KLF4 reduces ovarian cancer cell invasion.

<p><b>A, B</b>. Cell invasion assay was performed using Matrigel-coated transwell plates for SKOV3 (<b>A</b>) and OVCAR3 cells (<b>B</b>). The invasion rate was significantly reduced in KLF4-overexpressing cells compared to that in Dox-treated control cells from both SKOV3 and OVCAR3 cells (**<i>p</i><0.01). Data were collected from three separate experiments and analyzed using Student <i>t</i>-tests.</p

KLF4 inhibits TGFβ-induced EMT in ovarian cancer cells.

<p>Ovarian cancer cell lines SKOV3 (<b>A</b>) and OVCAR3 (<b>B</b>) transduced with lentiviral KLF4 overexpression and control vector were treated with TGFβ for 48 h, and the protein expressions of EMT-associated marker genes E-cadherin, snail2 and vimentin were examined using Western blot. Significant differences were compared between KLF4 expressing and control group (**p<0.05, ***p<0.001).</p

KLF4 promotes mesenchymal-epithelial cell transition.

<p><b>A. B</b>. Western blots were performed in KLF4- and EGFP-transduced SKOV3 (<b>A</b>) and OVCAR3 cells (<b>B</b>) with or without Dox induction. E-cadherin expression was significantly upregulated (***<i>p</i><0.001), whereas vimentin (**<i>p</i><0.01) and snail2 (***<i>p</i><0.001) were downregulated in KLF4- overexpressing SKOV3 cells compared to control cells (<b>A</b>). E-cadherin (**<i>p</i><0.01) was upregulated, whereas vimentin (*<i>p</i><0.05) and snail2 (***<i>p</i><0.001) were downregulated in KLF4-overexpressing OVCAR3 cells compared to Dox-treated control cells (<b>B</b>). E-cadherin (<b>C</b>) and vimentin (<b>D</b>) were immunostained in cellular membranes in KLF4-expressing and control SKOV3 cells. <b>E</b>. Snail2 was stained in cell nuclei in KLF4-expressing and control SKOV3 cells. <b>F</b>. KLF4 binding to the promoter of E-cadherin in SKOV3 cells was examined by chromatin immunoprecipitation using KLF4 antibody and detected by real-time PCR using E-cadherin-specific primers. The ChIP-enriched DNA levels were normalized to input DNA, followed by subtraction of non-specific binding determined by control IgG (***<i>p</i><0.001).</p

KLF4 inhibits cell proliferation and colony formation.

<p><b>A</b>. Cell proliferation of SKOV3 cells transduced with either EGFP or KLF4 was examined by MTT assay at different time points following Dox treatment. Overexpression of KLF4 significantly reduced cell proliferation compared to that in Dox-treated control cells (*<i>p</i><0.05). <b>B</b>. 200 SKOV3 cells transduced with lentiviral KLF4 or EGFP control vectors were seeded into each well of a 6-well plate and cultured for 14 d. Cell colonies were counted following crystal violet staining. The number of colonies in KLF4-overexpressing cells was significantly reduced compared to that in Dox-treated control cells (***<i>p</i><0.001). <b>C</b>. The number of colonies in KLF4-overexpressing OVCAR3 cells was significantly reduced compared to that in Dox-treated control cells (**<i>p</i><0.01). <b>D</b>. Soft agar colony formation assay was performed in triplicate using SKOV3 cells. Colonies were photographed and counted after 3 weeks. The number of colonies in KLF4-overexpressing cells was significantly reduced compared to that in Dox-treated control cells (***<i>p</i><0.001).</p

KLF4 reduces cell migration in ovarian cancer cells.

<p><b>A</b>. Wound-healing assay was performed to examine the migration rate of SKOV3 cells transduced with KLF4 and EGFP lentiviral vectors. Photographs were taken at 0 and 24 h following the initial scratch. Migration rates were quantified by measuring three different wound areas. Three separate experiments were performed. Migration rate was significantly reduced in KLF4-overexpressing cells compared to that in Dox-treated controls (**<i>p</i><0.01). <b>B, C</b>. Transwell migration assay was performed in SKOV3 and OVCAR3 cells. Overexpression of KLF4 significantly reduced cell migration in SKOV3 (<b>B</b>) and OVCAR3 (<b>C</b>) cells compared with that in Dox-treated controls (***<i>p</i><0.001).</p