Image operator learning coupled with CNN classification and its application to staff line removal

Many image transformations can be modeled by image operators that are characterized by pixel-wise local functions defined on a finite support window. In image operator learning, these functions are estimated from training data using machine learning techniques. Input size is usually a critical issue when using learning algorithms, and it limits the size of practicable windows. We propose the use of convolutional neural networks (CNNs) to overcome this limitation. The problem of removing staff-lines in music score images is chosen to evaluate the effects of window and convolutional mask sizes on the learned image operator performance. Results show that the CNN based solution outperforms previous ones obtained using conventional learning algorithms or heuristic algorithms, indicating the potential of CNNs as base classifiers in image operator learning. The implementations will be made available on the TRIOSlib project site.Comment: To appear in ICDAR 201

STAT3 siRNA suppressed IL-6/sIL-6R-induced VEGF-C expression in SV-LECs.

<p>(A) Cells were transiently transfected with negative control siRNA or STAT3 siRNA for 48 h. After transfection, cells were treated with IL-6 plus sIL6R (20 ng/ml) for another 6 h. The extent of VEGF-C mRNA was analyzed by RT-PCR as described in the “Materials and Methods” section. Each column represents the mean ± S.E.M. of five independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R. (B) Cells were transiently transfected with negative control siRNA or STAT3 siRNA for 48 h. After transfection, cells were treated with IL-6 plus sIL6R (20 ng/ml) for another 24 h. The VEGF-C protein level was then determined by immunoblotting. Each column represents the mean ± S.E.M. of four independent experiments. * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R. (C) Cells were pretreated with the vehicle, PP2 (1 μM) or NSC 667249 (0.3 μM) for 30 min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 4 h. The ChIP assay was performed as described in the ‘‘Materials and methods” section. Typical traces representative of three independent experiments with similar results are shown. The VEGF-C promoter region (-367/-198) was detected in the cross-linked chromatin sample before immunoprecipitation (bottom panels of the chart, Input, positive control).</p

Src-FAK signaling blockade reduced IL-6/sIL-6R-induced SV-LEC migration.

<p>SV-LECs were starved in DMEM medium without FBS for 16 h. After starvation, cells were pretreated with PP2 (A) or NSC 667249 (B) at indicated concentrations followed by the stimulation with IL-6 plus sIL6R (20 ng/ml) for another 24 h. Cell migration was determined as described in the ‘‘Materials and methods” section. Each column represents the mean ± S.E.M. of five independent experiments * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

FAK mediated IL-6/sIL-6R-induced ERK1/2 and p38MAPK phosphorylation in SV-LECs.

<p>Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 30 min. The extent of ERK1/2 (A), p38MAPK (B) or Src (C) phosphorylation was then determined by immunoblotting. Each column represents the mean ± S.E.M. of five independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

Schematic summary of IL-6-induced VEGF-C expression in SV-LECs.

<p>IL-6/sIL-6R activates the Src-FAK signaling cascade, leading to STAT3, C/EBPβ or NF-κB activation and subsequent VEGF-C expression SV-LECs.</p

Src-FAK signaling blockade suppressed IL-6/sIL-6R-induced tube formation of SV-LECs.

<p>(A) SV-LECs were seeded on Matrigel in the presence of VEGF-C (50 ng/ml) or IL-6 plus sIL6R (20 ng/ml) with or without PP2. Cells were then photographed under phase-contrast after 3 h. A representative microscopic phenotype of the formed tubes is shown (N = 3). (B) Total tube length of the formed capillary-like tube under different treatments as described in (A) was also measured using pen type digital meter. Each column represents the mean ± S.E.M. of three independent experiments. (C) SV-LECs were seeded on Matrigel in the presence of IL-6 plus sIL6R (20 ng/ml) with or without NSC 667249. Cells were then photographed under phase-contrast after 3 h. Total tube length of the formed capillary-like tube under different treatments was measured using pen type digital meter. Each column represents the mean ± S.E.M. of three independent experiments. * p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

FAK contributed to IL-6/sIL-6R-induced C/EBPß, NF-κB and STAT3 activation in SV-LECs.

<p>Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 30 min. The extent of C/EBPß (A), p65 (B) or STAT3 (C) phosphorylation was then determined by immunoblotting. Each column represents the mean ± S.E.M. of five independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R. Cells were transfected with C/EBPß (D), NF-κB-luc (E) or VEGF-C promoter-luc-370 (F) plus renilla-luc for 48 h. After transfection, SV-LECs were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 24 h. The luciferase activity was then determined. Each column represents the mean ± S.E.M. of at least four independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

FAK contributed to IL-6/sIL-6R-induced VEGF-C expression in SV-LECs.

<p>(A) Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30 min before treatment with IL-6 plus sIL6R (20 ng/ml) for another 24 h. The VEGF-C level and was then determined by immunoblotting. Each column represents the mean ± S.E.M. of eight independent experiments. (B) After treatment as described in (A), cell culture media were collected and VEGF-C in the media was quantified using a ELISA kit. Each column represents the mean ± S.E.M. of four independent experiments. (C) Cells were transiently transfected with VEGF-C promoter-luc-370 and renilla-luc for 48 h. After transfection, cells were treated with vehicle or NSC 667249 (0.3 μM) for 30 min, followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 24 h. Luciferase activity was then determined as described in the “Materials and Methods” section. Data represent the mean ± S.E.M. of three independent experiments performed in duplicate. (D). Cells were pretreated with the vehicle or NSC 667249 (0.3 μM) for 30min followed by treatment with IL-6 plus sIL6R (20 ng/ml) for another 30 min. The extent of FAK phosphorylation was then determined by immunoblotting. Each column represents the mean ± S.E.M. of four independent experiments. *p<0.05, compared to the control group; ^# p<0.05, compared to the vehicle-treated group in the presence of IL-6 plus sIL6R.</p

Genes that are co-regulated with TAZ-AXL-CTGF expression in GSE14333 colon cancer patient cohort.

<p>Genes that are co-regulated with TAZ-AXL-CTGF expression in GSE14333 colon cancer patient cohort.</p

The prognostic significance of <i>ANO1</i> and <i>SQLE</i> mRNA expression in colon cancer patients stratified by their TAZ-AXL-CTGF mRNA expression.

<p>Kaplan-Meier analyses for <i>ANO1</i> mRNA expression in patients overexpressing (A) none, (B) one, (C) two and (D) three of the three genes (TAZ, <i>AXL</i> and <i>CTGF</i>) in the GSE14333 colon cancer patient datasets. Kaplan-Meier analyses for <i>SQLE</i> mRNA expression in patients overexpressing (E) none, (F) one, (G) two and (H) three of the three genes in the GSE14333 colon cancer patient datasets. Kaplan-Meier analyses for <i>ANO1</i> mRNA expression in patients overexpressing (I) none, (J) one, (K) two and (L) three of the three genes in the GSE17538 colon cancer patient datasets. Kaplan-Meier analyses for <i>SQLE</i> mRNA expression in patients overexpressed in the GSE17538 colon cancer patient datasets.</p