33 research outputs found
FPM-WSI: Fourier ptychographic whole slide imaging via feature-domain backdiffraction
Fourier ptychographic microscopy (FPM), characterized by high-throughput computational imaging, theoretically provides a cunning solution to the trade-off between spatial resolution and field of view (FOV), which has a promising prospect in the application of digital pathology. However, block reconstruction and then stitching has currently become an unavoidable procedure due to vignetting effects. The stitched image tends to present color inconsistency in different image segments, or even stitching artifacts. In response, we reported a computational framework based on feature-domain backdiffraction to realize full-FOV, stitching-free FPM reconstruction. Different from conventional algorithms that establish the loss function in the image domain, our method formulates it in the feature domain, where effective information of images is extracted by a feature extractor to bypass the vignetting effect. The feature-domain error between predicted images based on estimation of model parameters and practically captured images is then digitally diffracted back through the optical system for complex amplitude reconstruction and aberration compensation. Through massive simulations and experiments, the method presents effective elimination of vignetting artifacts, and reduces the requirement of precise knowledge of illumination positions. We also found its great potential to recover the data with a lower overlapping rate of spectrum and to realize automatic blind-digital refocusing without a prior defocus distance
Additional file 3 of Enhancing medical education in respiratory diseases: efficacy of a 3D printing, problem-based, and case-based learning approach
Supplementary Material 3. Main examinatio
Additional file 1 of Enhancing medical education in respiratory diseases: efficacy of a 3D printing, problem-based, and case-based learning approach
Supplementary Material 1. Pre-class qui
MicroRNA-7 Inhibits Tumor Metastasis and Reverses Epithelial-Mesenchymal Transition through AKT/ERK1/2 Inactivation by Targeting EGFR in Epithelial Ovarian Cancer
<div><p>Epidermal growth factor receptor (EGFR) overexpression and activation result in increased proliferation and migration of solid tumors including ovarian cancer. In recent years, mounting evidence indicates that EGFR is a direct and functional target of miR-7. In this study, we found that miR-7 expression was significantly downregulated in highly metastatic epithelial ovarian cancer (EOC) cell lines and metastatic tissues, whereas the expression of, EGFR correlated positively with metastasis in both EOC patients and cell lines. Overexpression of miR-7 markedly suppressed the capacities of cell invasion and migration and resulted in morphological changes from a mesenchymal phenotype to an epithelial-like phenotype in EOC. In addition, overexpression of miR-7 upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, accompanied with EGFR inhibition and AKT/ERK1/2 inactivation. Similar to miR-7 transfection, silencing of EGFR with this siRNA in EOC cells also upregulated CK-18 and β-catenin expression and downregulated Vimentin expression, and decreased phosphorylation of both Akt and ERK1/2, confirming that EGFR is a target of miR-7 in reversing EMT. The pharmacological inhibition of PI3K-AKT and ERK1/2 both significantly enhanced CK-18 and β-catenin expression and suppressed vimentin expression, indicating that AKT and ERK1/2 pathways are required for miR-7 mediating EMT. Finally, the expression of miR-7 and EGFR in primary EOC with matched metastasis tissues was explored. It was showed that miR-7 is inversely correlated with EGFR. Taken together, our results suggested that miR-7 inhibited tumor metastasis and reversed EMT through AKT and ERK1/2 pathway inactivation by reducing EGFR expression in EOC cell lines. Thus, miR-7 might be a potential prognostic marker and therapeutic target for ovarian cancer metastasis intervention.</p></div
Additional file 4 of Enhancing medical education in respiratory diseases: efficacy of a 3D printing, problem-based, and case-based learning approach
Supplementary Material 4. Questionnaire surve
Additional file 2 of Enhancing medical education in respiratory diseases: efficacy of a 3D printing, problem-based, and case-based learning approach
Supplementary Material 2. Post-class qui
Up regulated expression of citrate synthase (CS) in human ovarian tumors and human ovarian tumor cell lines.
<p>(<b>A</b>) <i>CS</i> mRNA and (<b>B</b>) protein expression was assessed in normal human ovarian surface epithelium (HOSE), ovarian cancer cell lines, benign (n = 11) and malignant ovarian tumors (n = 21) using real-time PCR and western blot, respectively (B =  ovarian benign tumor, M =  ovarian malignant tumor). Mean ± SEM. **<i>P</i><0.01 and ***<i>P</i><0.001.</p
Citrate Synthase Expression Affects Tumor Phenotype and Drug Resistance in Human Ovarian Carcinoma
<div><p>Citrate synthase (CS), one of the key enzymes in the tricarboxylic acid (TCA) cycle, catalyzes the reaction between oxaloacetic acid and acetyl coenzyme A to generate citrate. Increased CS has been observed in pancreatic cancer. In this study, we found higher CS expression in malignant ovarian tumors and ovarian cancer cell lines compared to benign ovarian tumors and normal human ovarian surface epithelium, respectively. <i>CS</i> knockdown by RNAi could result in the reduction of cell proliferation, and inhibition of invasion and migration of ovarian cancer cells in vitro. The drug resistance was also inhibited possibly through an excision repair cross complementing 1 (ERCC1)-dependent mechanism. Finally, upon <i>CS</i> knockdown we observed significant increase expression of multiple genes, including <i>ISG15</i>, <i>IRF7</i>, <i>CASP7</i>, and <i>DDX58</i> in SKOV3 and A2780 cells by microarray analysis and real-time PCR. Taken together, these results suggested that CS might represent a potential therapeutic target for ovarian carcinoma.</p></div
EGFR expression in EOC tissues and matched metastases.
<p>H-score =  proportion score×intensity score. A total score of 0–12 was calculated and graded as negative (−, score:0), weak (+, score:1–4), moderate (++, score:5–8) or strong (+++, score:9–12).</p
miR-7 expression is inversely correlated with EOC metastasis.
<p>(A) The relative expression of miR-7 in 17-paired EOC tissues from omentum or peritoneum metastases and primary EOC tissues was detected by qRT-PCR. The U6 small nuclear RNA was used as an internal control and the fold change was calculated by the ΔΔCt method (B) The expression level of miR-7 in one pair of low and high metastatic EOC cell lines. (C) The expression level of miR-7 in seven EOC cell lines. (*P<0.05. **P<0.01).</p