11 research outputs found
Pressure-Stabilized Semiconducting Electrides in Alkaline-Earth-Metal Subnitrides
High pressure is able to modify profoundly
the chemical bonding
and generate new phase structures of materials with chemical and physical
properties not accessible at ambient conditions. We here report an
unprecedented phenomenon on the pressure-induced formation of semiconducting
electrides via compression of layered alkaline-earth subnitrides Ca<sub>2</sub>N, Sr<sub>2</sub>N, and Ba<sub>2</sub>N that are conducting
electrides with loosely confined electrons in the interlayer voids
at ambient pressure. Our extensive first-principles swarm structure
searches identified the high-pressure semiconducting electride phases
of a tetragonal <i>I</i>4Ì…2<i>d</i> structure
for Ca<sub>2</sub>N and a monoclinic <i>Cc</i> structure
shared by Sr<sub>2</sub>N and Ba<sub>2</sub>N, both of which contain
atomic-size cavities with paring electrons distributed within. These
electride structures are validated by the excellent agreement between
the simulated X-ray diffraction patterns and the experimental data
available. We attribute the emergence of the semiconducting electride
phases to the p<i>–</i>d hybridization on alkaline-earth-metal
atoms under compression as well as the filling of the p<i>–</i>d hybridized band due to the interaction between Ca and N. Our work
provides a unique example of pressure-induced metal-to-semiconductor
transition in compound materials and reveals unambiguously the electron-confinement
topology change between different types of electrides
MOESM1 of Sodium ferulate and n-butylidenephthalate combined with bone marrow stromal cells (BMSCs) improve the therapeutic effects of angiogenesis and neurogenesis after rat focal cerebral ischemia
Additional file 1: Figure S1. Different dosages of BP combined with SF and BMSC enhanced VEGF and DCX expressions post-stroke. Representative western blot results for VEGF and DCX in ischemic hemisphere of each group (n = 6) were shown and quantitative analysis was presented. It indicated that SF + BP (10 mg/kg) + BMSC group significantly enhanced VEGF and DCX expressions in comparison with other groups. Data are expressed as means ± SD. *p < 0.05, vs. Simvastatin + BMSC group; #p < 0.05, vs. SF + BMSC group. Figure S2. Neurological functional outcomes post-surgery. Garcia JH neurological score evaluation was performed at 1 and 7 days in each group (n = 6). Both of SF (60 mg/kg) + BP + BMSC and Simvastatin + BMSC group could dramatically improve neurological functional recovery compared with other four groups on 7th day. Data are expressed as means ± SD. *p < 0.05, vs. BMSC; #p < 0.05, vs. SF (120 mg/kg) + BP + BMSC; &p < 0.05, vs. SF (30 mg/kg) + BP + BMSC
Effect of GW4869 on Ox-LDL-induced apoptosis in cultured VSMCs (n = 3).
<p>Cells were incubated in control medium (in DMSO), 50 µg/ml Ox-LDL alone (in DMSO), 50 µg/ml Ox-LDL in the presence of 20 µM GW4869 (in DMSO) or 50 µg/ml Ox-LDL in the presence of 20 µM GW4869 and 5 µM C2-ceramide (in DMSO) for 24 hours. (<b>A</b>) The percentage of apoptotic cells was then assessed. (<b>B</b>) Caspase-3 activity was measured and results are shown as percentage of control. (<b>C</b>) p-Bcl2 and p-Bad protein levels were detected by immunoblot analysis. (<b>D</b>) p-Bcl2 and p-Bad protein levels were quantified and normalized to total Bcl2 and Bad levels. (<b>E</b>) Cells were treated with/without 20 µM GW4869 and 5 µM C2-ceramide in the presence of Ox-LDL for 7 days. The calcium content was quantified using ocresolphthalein complexone method. *p<0.01.</p
Effect of GW4869 on Ox-LDL-induced VSMC calcification.
<p>Cells were treated with 50 µg/ml Ox-LDL (in DMSO) for 14 days. N-SMase inhibitor, GW4869 (20 µM in DMSO) was used to treat cells in the presence of Ox-LDL (n = 3). (<b>A</b>) Alizarin red was used to assess mineralization (bar = 200 µm). (<b>B</b>) Quantification of mineral deposition was performed. (<b>C</b>) ALP activity was measured by spectrophotometry. (<b>D&E</b>) Msx2 and Osterix mRNA levels were determined by quantitative real-time PCR. *p<0.01.</p
Ox-LDL-induced VSMC calcification was enhanced by ceramide treatment.
<p>Cells were treated with 50 µg/ml Ox-LDL alone or 50 µg/ml Ox-LDL in the presence of 5 µM C2-ceramide for 7 days (n = 3). (<b>A</b>) Cells were stained with alizarin red (bar = 200 µm). (<b>B</b>) Quantification of mineral deposition was performed. (<b>C</b>) The calcium content was measured using ocresolphthalein complexone method. (<b>D</b>) ALP activity was measured by spectrophotometry. *p<0.01.</p
Effect of Ox-LDL on ceramide level and neutral sphingomyelinase (N-SMase) activity in VSMCs.
<p>Cells were incubated with 50 µg/ml Ox-LDL and harvested at indicated time points (n = 3). (<b>A</b>) Ceramide levels were determined using diacylglycerol kinase assay. (<b>B</b>) The activity of N-SMase was measured using <sup>14</sup>C sphingomyelin as substrate. *p<0.01, **p<0.001 vs. control.</p
Effect of ZVAD-fmk on Ox-LDL-induced mineralization in cultured VSMCs (n = 3).
<p>Cells were treated with 5 µM ZVAD-fmk (a caspase inhibitor) in the presence of Ox-LDL for 7 days. (<b>A</b>) Cells were stained with alizarin red and quantification of mineral deposition was performed at indicated times. (<b>B</b>) The calcium content was measured using ocresolphthalein complexone method. (<b>C</b>) ALP activity was measured by spectrophotometry. (<b>D</b>) Msx2 mRNA levels were determined by quantitative real-time PCR after cells were treated with/without ZVAD-fmk. *p<0.01.</p
Effect SB203580 of on Ox-LDL-induced mineralization in cultured VSMCs (n = 3).
<p>Cells were grown in control medium (in DMSO), 50 µg/ml Ox-LDL alone (in DMSO), 50 µg/ml Ox-LDL supplemented with 5 µM SB203580 (in DMSO), 5 µM C2-ceramide alone (in DMSO) or 5 µM C2-ceramide supplemented with 5 µM SB203580 (in DMSO) for 24 hours. (<b>A</b>) p-p38 MAPK protein levels were detected by immunoblot analysis. (<b>B</b>) The percentage of apoptotic cells was then assessed. (<b>C</b>) Caspase-3 activity was measured in a parallel experiment. Cells were treated with SB203580 in the presence of Ox-LDL for 7 days. (<b>D</b>) The calcium content was measured using ocresolphthalein complexone method. (<b>E</b>) Msx2 mRNA expression was determined by quantitative real-time PCR after cells were treated with/without SB203580. *p<0.01.</p
Effect of C2-ceramide on VSMC calcification.
<p>Human VSMCs were incubated in the presence of 1 µM, 5 µM, 10 µM of C2-ceramide (C2-Cer) for 14 days (n = 3). (<b>A</b>) Alizarin red was used to visualize VSMC mineralization (bar = 200 µm). (<b>B</b>) Quantification of mineral deposition was performed. *p<0.05. **p<0.001.</p
Dose-response analysis of the effect of Ox-LDL treatment on human VSMC calcification.
<p>Confluent human VSMCs were cultured in osteogenic medium in the presence of native LDL (control) or Ox-LDL (10 µg/ml, 30 µg/ml, 50 µg/ml) for 14 days (n = 3). (<b>A</b>) VSMCs were stained with alizarin red to assess mineralization. (<b>B</b>) Mineralization was quantified and shown as optical density units and normalized to protein content. (<b>C</b>) Msx2 mRNA levels were determined by quantitative real-time PCR. *P<0.001. Scale bar = 200 µm.</p