11 research outputs found

    Ni<sub>12</sub>P<sub>5</sub> Nanoparticles as an Efficient Catalyst for Hydrogen Generation <i>via</i> Electrolysis and Photoelectrolysis

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    The exploitation of a low-cost catalyst is desirable for hydrogen generation from electrolysis or photoelectrolysis. In this study we have demonstrated that nickel phosphide (Ni<sub>12</sub>P<sub>5</sub>) nanoparticles have efficient and stable catalytic activity for the hydrogen evolution reaction. The catalytic performance of Ni<sub>12</sub>P<sub>5</sub> nanoparticles is favorably comparable to those of recently reported efficient nonprecious catalysts. The optimal overpotential required for 20 mA/cm<sup>2</sup> current density is 143 ± 3 mV in acidic solution (H<sub>2</sub>SO<sub>4</sub>, 0.5 M). The catalytic activity of Ni<sub>12</sub>P<sub>5</sub> is likely to be correlated with the charged natures of Ni and P. Ni<sub>12</sub>P<sub>5</sub> nanoparticles were introduced to silicon nanowires, and the power conversion efficiency of the resulting composite is larger than that of silicon nanowires decorated with platinum particles. This result demonstrates the promising application potential of metal phosphide in photoelectrochemical hydrogen generation

    Tungsten Sulfide Enhancing Solar-Driven Hydrogen Production from Silicon Nanowires

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    Tungsten sulfides, including WS<sub>2</sub> (crystalline) and WS<sub>3</sub> (amorphous), were introduced to silicon nanowires, and both can promote the photoelectrochemical hydrogen production of silicon nanowires. In addition, more enhancement of energy conversion efficiency can be achieved by the loading of WS<sub>3</sub>, in comparison with loading of WS<sub>2</sub>. Polarization curves of WS<sub>3</sub> and WS<sub>2</sub> suggest that WS<sub>3</sub> has higher catalytic activity in the hydrogen evolution reaction than WS<sub>2</sub>, affording higher energy conversion efficiency in silicon nanowires decorated with WS<sub>3</sub>. The higher electrocatalytic activity of WS<sub>3</sub> correlates with the amorphous structure of WS<sub>3</sub> and larger surface area of WS<sub>3</sub>, which result in more active sites in comparison with crystalline WS<sub>2</sub>

    Age at Menarche and Risk of Colorectal Cancer: A Meta-Analysis

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    <div><p>Background</p><p>Various observational studies have focused on the relationship between menarcheal age and the risk of colorectal cancer (CRC). However, the association is still controversial because of inconsistent results. Therefore, we performed a meta-analysis to assess this issue from epidemiological studies.</p><p>Methods</p><p>After a literature search in MEDLINE, EMBASE, and Web of Science for studies of menarcheal age and CRC risk published through the end of January 2013, we pooled the relative risks (RRs) from included studies using a fixed- or random-effects model and performed heterogeneity and publication bias analyses. All statistical tests were two-sided.</p><p>Results</p><p>Eleven case-control and 11 cohort studies were eligible for inclusion in our analysis. The random-effects pooled RR for oldest versus youngest menarcheal age was 0.95 [95% confidence intervals (CIs) = 0.85–1.06], with significant heterogeneity (<i>Q</i> = 61.03, <i>P</i><0.001, <i>I</i><sup>2</sup> = 65.6%). When separately analyzed, case-control (RR = 0.95, 95% CI = 0.75–1.21) and cohort studies (RR = 0.97, 95% CI = 0.90–1.04) yielded similar results. Moreover, similar results were also observed among the subgroup analyses by study quality, population, exposure assessment, anatomic cancer site, subsite of colon cancer, and several potential important confounders and risk factors. There was no evidence of publication bias and significant heterogeneity between subgroups detected by meta-regression analyses.</p><p>Conclusions</p><p>Findings from this meta-analysis demonstrated that menarcheal age was not associated with the risk of CRC in humans. Further studies are warranted to stratify results by the subsite of colon cancer and menopause status in the future.</p></div

    Summary risk estimates of the association between menarcheal age and colorectal cancer risk.

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    <p>RR: relative risk; CI: confidence interval; CRC: colorectal cancer; OC: oral contraceptive.</p>*<p><i>P</i> value for heterogeneity within each subgroup.</p>**<p><i>P</i> value for heterogeneity between subgroups with meta-regression analysis.</p

    Forest plot (random effects model) of menarcheal age and colorectal cancer risk in overall studies.

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    <p>Squares indicate study-specific relative risks (size of the square reflects the study-specific statistical weight); horizontal lines indicate 95% CIs; diamond indicates the summary relative risk estimate with its 95% CI. CI: confidence interval; RR: relative risk.</p

    Increase of ADAM10 Level in Coronary Artery In-Stent Restenosis Segments in Diabetic Minipigs: High ADAM10 Expression Promoting Growth and Migration in Human Vascular Smooth Muscle Cells via Notch 1 and 3

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    <div><p>Background</p><p>This study aimed to identify major proteins in the pathogenesis of coronary artery in-stent restenosis (ISR) in diabetic minipigs with sirolimus-eluting stenting, and to investigate the roles of key candidate molecules, particularly ADAM10, in human arterial smooth muscle cells (HASMCs).</p> <p>Methods and Results</p><p>The stents were implanted in the coronary arteries of 15 diabetic and 26 non-diabetic minipigs, and angiography was repeated at six months. The intima of one vascular segment with significant ISR and one with non-ISR in diabetic minipigs were isolated and cultured in conditioned medium (CM). The CM was analyzed by LC-MS/MS to uncover proteins whose levels were significantly increased (≥1.5-fold) in ISR than in non-ISR tissues. After literature searching, we focused on the identified proteins, whose biological functions were most potentially related to ISR pathophysiology. Among them, ADAM10 was significantly increased in diabetic and non-diabetic ISR tissues as compared with non-ISR controls. In cell experiments, retrovirus-mediated overexpression of ADAM10 promoted growth and migration of HASMCs. The effects of ADAM10 were more remarkable in high-glucose culture than in low-glucose culture. Using shRNA and an inhibitor of γ-secretase (GSI), we found that the influences of ADAM10 were in part mediated by Notch1 and notch 3 pathway, which up-regulated Notch downstream genes and enhanced nuclear translocation of the small intracellular component of Notch1 and Notch3.</p> <p>Conclusions</p><p>This study has identified significantly increased expression of ADAM10 in the ISR versus non-ISR segment in diabetic minipigs and implicates ADAM10 in the enhanced neointimal formation observed in diabetes after vascular injury. </p> </div

    ADAM10 induced proliferation and migration of HASMCs in part through activation of Notch1 and Notch3.

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    <p><b>A</b>, MTT assay were done to measure proliferation ability in HASMCs of pLXSN-vector and pLXSN-ADAM10 overexpression with transfection of control, Notch1 and Notch3 siRNA, in the presence or absence of γ-secretase inhibitor treatment (10 uM). *P<0.05, vs. vector-transduced HASMCs; #P<0.05, vs. ADAM10-overexpressing HASMCs; $P<0.05, vs. HASMCs of vector- and ADAM10-overexpression with Notch1 siRNA transfection; @ P<0.05, vs. HASMCs of vector- and ADAM10-overexpression with Notch3 siRNA transfection. <b>B</b>, BrdU proliferation assay was performed in the HASMCs as in A. The symbols of comparison were same as in A. C and D, wound healing and transwell assay were performed in the HASMCs as in A. In wound healing assay, the images were taken before and 24 h after scratch. In transwell assay, the cells were added to the upper chamber, and the chamber was incubated at 37°C in a CO<sub>2</sub> incubator for 8 h. Then, the migrated cells were stained and the image was taken, followed by quantification by OD 560 nm measurement. <b>E</b> and <b>F</b>, quantification of wound healing and transwell assay results, respectively. The symbols of comparison were same as in A. G, real-time-PCR analysis was done to examine the mRNA levels of Notch downstream genes in these cells. The symbols of comparison were same as in A. <b>H</b>, the protein levels of Notch1, and Notch3 by Notch1 and Notch 3 siRNA transfection versus mock siRNA.</p

    Notch 1 IC and Notch 3 IC levels were significantly increased in ISR versus non-ISR intima of diabetic minipigs.

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    <p><b>A</b>, <b>B</b>, <b>C</b>, <b>D</b>, the protein levels of Notch 1, Notch2, Notch3 and Notch4, and their IC domains were compared by Western blot assay between ISR and non-ISR intima, with quantification (ISR samples, n=6; non-ISR samples, n=24; for each sample, 3 replicates were performed). §P<0.05, vs. non-ISR intima. </p

    ADAM10 mediates activation of Notch signaling pathway.

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    <p>ADAM10-overexpressing, ADAM10 shRNA-expressing and vector-transduced HASMCs were generated by retrovirus-mediated gene transfer and selection. <b>A</b>, the protein levels of ADAM10, Notch 1 IC, Notch 1, Notch 3 IC and Notch 3 were detected in these HASMCs by Western blot, and β-actin was served as internal control. <b>B</b>, quantification of the data in <b>A</b>, *P<0.05, vs. vector-transduced HASMCs. <b>C</b>, cytoplasm and nuclear distribution of Notch 1 IC and Notch 3 IC in these HASMCs were displayed by immuno-fluorescence assay. <b>D</b>, the mRNA levels of Notch downstream genes, HES1, HEY2 and myc, were detected by real-time PCR assay, *P<0.05, vs. vector-transduced HASMCs.</p
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