| 1. |
- Bai, Sai, et al.
(författare)
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Ethanedithiol Treatment of Solution-Processed ZnO Thin Films: Controlling the Intragap States of Electron Transporting Interlayers for Efficient and Stable Inverted Organic Photovoltaics
- 2015
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Ingår i: Advanced Energy Materials. - : Wiley-VCH Verlag. - 1614-6832 .- 1614-6840. ; 5:5, s. 1401606-
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Tidskriftsartikel (refereegranskat)abstract
- The surface defects of solution-processed ZnO films lead to various intragap states. When the solution-processed ZnO films are used as electron transport interlayers (ETLs) in inverted organic solar cells, the intragap states act as interfacial recombination centers for photogenerated charges and thereby degrade the device performance. Here, a simple passivation method based on ethanedithiol (EDT) treatment is demonstrated, which effectively removes the surface defects of the ZnO nanocrystal films by forming zinc ethanedithiolates. The passivation by EDT treatment modulates the intragap states of the ZnO films and introduces a new intragap band. When the EDT-treated ZnO nanocrystal films are used as ETLs in inverted organic solar cells, both the power conversion efficiency and stability of the devices are improved. The control studies show that the solar cells with EDT-treated ZnO films exhibit reduced charge recombination rates and enhanced charge extraction properties. These features are consistent with the fact that the modulation of the intragap states results in reduction of interfacial recombination as well as the improved charge selectivity and electron transport properties of the ETLs. It is further demonstrated that the EDT treatment-based passivation method can be extended to ZnO films deposited from sol-gel precursors.
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| 2. |
- Wang, Jianpu, et al.
(författare)
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Administration of aerosolized terbutaline and budesonide reduces chlorine gas-induced acute lung injury
- 2004
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Ingår i: Journal of Trauma. - 0022-5282 .- 1529-8809. ; 56:4, s. 850-862
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Tidskriftsartikel (refereegranskat)abstract
- Background: The pathophysiology and treatment of chlorine gas-induced acute lung injury is poorly characterized and based on anecdotal data. This study aimed to assess the effects of aerosolized beta-2 adrenergic agonist and corticosteroid therapy on chlorine gas-induced lung injury.Methods: Anesthetized, ventilated pigs were exposed to chlorine gas (400 parts per million for 20 minutes), then assigned randomly 30 minutes later to receive aerosolized terbutaline, budesonide, terbutaline followed by budesonide or placebo (6 pigs in each group). Hemodynamics, gas exchange, and lung mechanics were evaluated for another 5 hours.Results: All the animals demonstrated an immediate increase in airway and pulmonary artery pressure as well as sharp drops in arterial oxygen tension (PaO2) and lung compliance (C L). Recovery of PaO2 and CL was greatest in the terbutaline plus budesonide group, but therapy with terbutaline and budesonide alone also was associated with significant improvement in PaO2 and CL, as compared with placebo.Conclusions. Treatment of acute chlorine gas lung injury with aerosolized terbutaline followed by aerosolized budesonide improved lung function. Combined treatment was more effective than treatment with either drug alone.
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| 3. |
- Xu, Cang-Bao, et al.
(författare)
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Lipid soluble smoke particles up-regulate vascular smooth muscle ETB receptors via activation of mitogen activating protein kinases and NF-kappaB pathways.
- 2008
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Ingår i: Toxicological Sciences. - : Oxford University Press (OUP). - 1096-0929 .- 1096-6080. ; 106:2, s. 546-555
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Tidskriftsartikel (refereegranskat)abstract
- Cigarette smoke is a strong risk factor for cardiovascular disease. However, the underlying molecular mechanisms that lead to cigarette smoke-associated cardiovascular disease remain elusive. With functional and molecular methods, we demonstrate for the first time that lipid soluble cigarette smoke particles (DSP) increased the expression of endothelin type B (ET(B)) receptors in arterial smooth muscle cells. The increased ET(B) receptors in arterial smooth muscle cells was documented as enhanced contractility (sensitive myograph technique), elevated levels of ET(B) receptor mRNA (quantitative real-time PCR) and protein expressions (immunohistochemistry and Western blotting). Intracellular signalling was studied with Western blotting and phosphoELISA; this revealed that DSP induced extracellular-regulated protein kinase 1 and 2 (ERK1/2), p38 and nuclear factor-kappaB (NF-kappaB) phosphorylation within 3 hours. Blocking ERK1/2, p38 or NF-kappaB activation by their specific inhibitors significantly attenuated the DSP-induced up-regulation of ET(B) receptor-mediated contraction and both ET(B) receptor mRNA and protein expression. In addition, dexamethasone abolished the DSP-induced up-regulation of ET(B) receptor-mediated contraction. In conclusion, up-regulation of ET(B) receptors by DSP in arterial smooth muscle cells involves activation of mitogen activating protein kinases (ERK1/2 and p38) and the downstream transcriptional factor NF-kappaB pathways.
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| 4. |
- Xu, Cang-Bao, et al.
(författare)
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Low density lipoprotein induces upregulation of vasoconstrictive endothelin type B receptor expression.
- 2014
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Ingår i: Vascular Pharmacology. - : Elsevier BV. - 1537-1891. ; 60:1, s. 42-48
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Tidskriftsartikel (refereegranskat)abstract
- Vasoconstrictive endothelin type B (ETB) receptors promote vasospasm and ischemic cerebro- and cardiovascular diseases. The present study was designed to examine if low density lipoprotein (LDL) induces upregulation of vasoconstrictive ETB receptor expression and if extracellular signal-regulated kinases 1 and 2 (ERK1/2) and p38 mitogen-activated protein kinase (MAPK) signal pathways are involved in this process. Rat mesenteric artery segments were organ cultured in the presence and absence of LDL with or without inhibitors for MAPK kinase 1 and 2 (MEK1/2), p38 and transcription. The upregulation of vasoconstrictive ETB receptor expression was studied using a sensitive myograph, real-time PCR and Western blot. LDL (11, 22 and 44mg protein/L) concentration-dependently induced upregulation of vasoconstrictive ETB receptor expression with increase in the receptor-mediated vasoconstriction, elevated levels of the ETB receptor mRNA and protein expressions, and activation of ERK1/2 and p38 MAPK. Blockage of ERK1/2 and p38 MAPK signal pathways using MEK1/2 inhibitors (PD98059 and U0126) or p38 inhibitors (SB203580 and SB239063) significantly abolished the LDL-induced upregulation of vasoconstrictive ETB receptor expression. Actinomycin D (general transcriptional inhibitor) almost completely inhibited the LDL effects. In conclusion, LDL induces upregulation of vasoconstrictive ETB receptor expression through activation of ERK1/2 and p38 MAPK signal pathway-dependent transcriptional mechanisms.
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| 5. |
- Yu, Hongling, et al.
(författare)
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Color-Stable Blue Light-Emitting Diodes Enabled by Effective Passivation of Mixed Halide Perovskites
- 2021
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Ingår i: The Journal of Physical Chemistry Letters. - : American Chemical Society (ACS). - 1948-7185. ; 12:26, s. 6041-6047
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Tidskriftsartikel (refereegranskat)abstract
- Bandgap tuning through mixing halide anions is one of the most attractive features for metal halide perovskites. However, mixed halide perovskites usually suffer from phase segregation under electrical biases. Herein, we obtain high-performance and color-stable blue perovskite LEDs (PeLEDs) based on mixed bromide/ chloride three-dimensional (3D) structures. We demonstrate that the color instability of CsPb(Br1-xClx)(3) PeLEDs results from surface defects at perovskite grain boundaries. By effective defect passivation, we achieve color-stable blue electroluminescence from CsPb(Br1-xClx)(3) PeLEDs, with maximum external quantum efficiencies of up to 4.5% and high luminance of up to 5351 cd m(-2) in the sky-blue region (489 nm). Our work provides new insights into the color instability issue of mixed halide perovskites and can spur new development of high-performance and color-stable blue PeLEDs.
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| 6. |
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| 7. |
- Zheng, Jianpu, et al.
(författare)
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Vasodilation effect of atropine on rat mesenteric artery
- 2005
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Ingår i: Yao Xue Xue Bao. - 0513-4870. ; 40:5, s. 402-405
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Tidskriftsartikel (refereegranskat)abstract
- AIM: To study the vasodilation effect of atropine and its mechanism. METHODS: Isometric tension was recorded in isolated rat super mesenteric arteries precontracted by noradrenaline (NE) to study the vasodilation effect of atropine, and to investigate the role of endothelial cell and vascular smooth muscle cell on vasodilation. RESULTS: Atropine was shown to significantly dilate the endothelium-intact and endothelium-denuded arteries precontracted by NE. Nomega-Nitro-L-arginine methyl ester (L-NAME, nitric oxide synthase inhabitor), indomethacin (cyclooxygenase inhibitor), propranolol (general beta adrenoceptor antagonist) and glibenclamide (ATP sensitive potassium channel inhibitor) showed no effect on vasodilation of atropine. Atropine did not affect the concentration-contraction curve of K+. However, atropine suppressed the contraction induced by NE and CaCl2, but not that by caffeine in the Ca+ -free Krebs solution. CONCLUSION: Atropine showed significant vasodilation effect which may derive, in part, from endothelium. Besides, atropine could inhibit the receptor-mediated Ca2+ -influx and Ca2+ -release, which was inferred to the mechanism of atropine on vasodilation.
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