Electrochemical double-layer capacitor performance of novel carbons derived from SAPO zeolite templates

Mesoporous carbons have been synthesized using template method by polymerizing and then carbonizing carbon precursor of sucrose accommodated in novel templates of SAPO-11 and SAPO-34 after the removal of templates with NaOH solution (50 vol.% ethanol-50 vol.% H2O). High surface areas and excellent eletrochemical properties of the mesoporous carbons were identified by the Brunauer-Emmett-Teller method, cyclic voltammetry, electrochemical impedance spectroscopy and constant current charge-discharge tests. The surface areas of the sample carbons are the range of 950-975 m2/g, with a narrow pore size between 3.8 and 11.0 nm. The sample carbon derived from SAPO-11 exhibits better electrochemical performance over the one from SAPO-34, with the specific capacitance of 154.8, 113.5 F/g them, respectively, measured in 1 M KOH aqueous solution at the loading current density of 0.25 A/g

Decision tree analysis of traditional risk factors of carotid atherosclerosis and a cutpoint-based prevention strategy.

BACKGROUND: Reducing the exposure to risk factors for the prevention of cardio-cerebral vascular disease is a crucial issue. Few reports have described practical interventions for preventing cardiovascular disease in different genders and age groups, particularly detailed and specific cutpoint-based prevention strategies. METHODS: We collected the health examination data of 5822 subjects between 20 and 80 years of age. The administration of medical questionnaires and physical examinations and the measurement of blood pressure, fasting plasma glucose (FPG) and blood lipids [total cholesterol (TC), triglycerides (TG), high density lipoprotein-cholesterol (HDL-C), and low density lipoprotein-cholesterol (LDL-C)] were performed by physicians. Carotid ultrasound was performed to examine the carotid intima-media thickness (CIMT), which was defined as carotid atherosclerosis when CIMT ≥0.9 mm. Decision tree analysis was used to screen for the most important risk factors for carotid atherosclerosis and to identify the relevant cutpoints. RESULTS: In the study population, the incidence of carotid atherosclerosis was 12.20% (men: 14.10%, women: 9.20%). The statistical analysis showed significant differences in carotid atherosclerosis incidence between different genders (P<0.0001) and age groups (P<0.001). The decision tree analysis showed that in men, the most important traditional risk factors for carotid atherosclerosis were TC (cutpoint [CP]: 6.31 mmol/L) between the ages of 20-40 and FPG (CP: 5.79 mmol/L) between the ages of 41-59. By comparison, LDL-C (CP: 4.27 mmol/L) became the major risk factor when FPG ≤5.79 mmol/L. FPG (CP: 5.52 mmol/L) and TG (CP: 1.51 mmol/L) were the most important traditional risk factors for women between 20-40 and 41-59 years of age, respectively. CONCLUSION: Traditional risk factors and relevant cutpoints were not identical in different genders and age groups. A specific gender and age group-based cutpoint strategy might contribute to preventing cardiovascular disease

The assessment of traditional risk factors for carotid atherosclerosis in women in different age groups using decision tree analysis.

<p>The assessment of traditional risk factors for carotid atherosclerosis in women in different age groups using decision tree analysis.</p

Normal Fibroblasts Induce E-Cadherin Loss and Increase Lymph Node Metastasis in Gastric Cancer

<div><p>Background</p><p>A tumor is considered a heterogeneous complex in a three-dimensional environment that is flush with pathophysiological and biomechanical signals. Cell-stroma interactions guide the development and generation of tumors. Here, we evaluate the contributions of normal fibroblasts to gastric cancer.</p><p>Methodology/Principal Findings</p><p>By coculturing normal fibroblasts in monolayers of BGC-823 gastric cancer cells, tumor cells sporadically developed short, spindle-like morphological characteristics and demonstrated enhanced proliferation and invasive potential. Furthermore, the transformed tumor cells demonstrated decreased tumor formation and increased lymphomatic and intestinal metastatic potential. Non-transformed BGC-823 cells, in contrast, demonstrated primary tumor formation and delayed intestinal and lymph node invasion. We also observed E-cadherin loss and the upregulation of vimentin expression in the transformed tumor cells, which suggested that the increase in metastasis was induced by epithelial-to-mesenchymal transition.</p><p>Conclusion</p><p>Collectively, our data indicated that normal fibroblasts sufficiently induce epithelial-to-mesenchymal transition in cancer cells, thereby leading to metastasis.</p></div

TBGCs exhibited cisplatin resistance.

<p><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g003" target="_blank"><b>Figure 3</b></a><b>.1.</b> Twenty-four-hour line plot of the cisplatin-inhibition test. **p<0.01. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g003" target="_blank"><b>Figure 3</b></a><b>.2.</b> Twenty-four-hour line plot of the 5-FU inhibition test. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g003" target="_blank"><b>Figure 3</b></a><b>.3.</b> Flow cytometry was used to assess apoptosis in BGC and TBGC cells after exposure to different concentrations of cisplatin (20, 40 µM) for 24 hours. Cells were stained with Annexin V-FITC (marker of apoptosis) and propidium iodide (PI) (marker of dead cells). <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g003" target="_blank"><b>Figure 3</b></a><b>.4.</b> Bar plot of cisplatin-induced apoptosis in BGC-823 cells and TBGCs. Bar graph showing the percentage of apoptotic cells according to flow cytometry. **p<0.01 vs cells in the dimethyl sulfoxide (DMSO) control wells.</p

Proliferation, invasion, and mobility of TBGCs.

<p><b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g002" target="_blank">Figure 2</a>.1.</b>Line plot of the proliferation assay. Vertical lines denote standard differences. **p<0.01. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g002" target="_blank"><b>Figure 2</b></a><b>.2.</b> Line plot of the scratching assay. Vertical lines denote standard differences. **p<0.01. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g002" target="_blank"><b>Figure 2</b></a><b>.3.</b> Scratching assay of BGC-823 cells (above) and TBGCs (below) under a phase-contrast microscope. (A–D, E–H) Time from initial to 72 hours. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g002" target="_blank"><b>Figure 2</b></a><b>.4.</b> Box plot of the invasive and migration assays. Differences between BGC-823 cells and TGBCs are significant (p<0.01). <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g002" target="_blank"><b>Figure 2</b></a><b>.5.</b> The top 2 photos show the results of the invasive modified transwell assay with Matrigel. Representative images of the transwell invasion assays for (A) BGC and (B) TBGC. Cells invading the underside of the transwell insert are shown. The bottom 2 photos are representative images of the transwell migration assays for (C) BGC and (D) TBGC. Cells migrating to the underside of the transwell insert are shown.</p

Morphological changes in BGC-823 cells were associated with the epithelial-mesenchymal-transition.

<p><b><a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank">Figure 1</a>.1.</b> Schematic of the experimental protocol. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.2.</b> Origin of the supernatant cells. (A) GFP-labeled BGC-823 cells (green). (B) BGC-823 cells that were cocultured with fibroblasts (red). (C) BGC-823 cells grew into clumps and demonstrated round shapes in suspension. (D) TBGCs were induced by coculturing. Magnification 100×. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.3.</b> Transformation from BGC-823 cells to TBGCs under a phase-contrast microscope. (A–D) BGC-823 cells in a dense culture system can form clusters and shed off cells into the suspension. (E–H) Passage of suspended tumor cells. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.4.</b> Immunofluorescent staining of pan-CK (red), E-cadherin (red), vimentin (red) and N-cadherin (red). BGC-823 cells (above) and TBGCs (below) were labeled with GFP (green). The nucleus was stained with DAPI (blue). <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.5.</b> Heat plot of gene expression profiles analyzed using fluorescence quantitative RT-PCR. The depth of the color indicates relative gene expression. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.6.</b> Western blots of proteins. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0097306#pone-0097306-g001" target="_blank"><b>Figure 1</b></a><b>.7.</b> Bar plot of protein expression determined using Western blot analysis. Bars denote the relative expression levels measured using IOD. Vertical lines denote standard differences. **p<0.01.</p