| 1. |
- Yang, Heyi, et al.
(författare)
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Composition-Conditioning Agent for Doped Spiro-OMeTAD to Realize Highly Efficient and Stable Perovskite Solar Cells
- 2022
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Ingår i: Advanced Energy Materials. - : WILEY-V C H VERLAG GMBH. - 1614-6832 .- 1614-6840. ; 12:44
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Tidskriftsartikel (refereegranskat)abstract
- The doped Spiro-OMeTAD hole transport layer (HTL) formed using the lithium bis(trifluoromethane) sulfonimide salt and 4-tert-butylpyridine with phenethylammonium iodide surface treatment on a perovskite film has continuously dominated the record power conversion efficiencies (PCEs) of perovskite solar cells (pero-SCs). However, unstable HTL compositions and iodide salts can cause severe device degradation. In this study, an HTL composition-conditioning agent (CCA), Spiro-BD-2OEG, is designed, which contains a Spiro-OMeTAD-like backbone, functional pyridine units, and oligo (ethylene glycol) chains. This finely designed CCA presents good miscibility with Spiro-OMeTAD and its dopants and acts as a conditioning agent through weak bond interactions. As a result, the CCA-regulated HTL shows a pinhole-free and smooth morphology with enhanced Spiro-OMeTAD ordering and improves dopant stability. In addition, the gradient-distributed CCA in the HTL can narrow the energy level offset with the valence band of the perovskite. The resultant pero-SCs exhibit an excellent PCE of 24.19% without any interface treatment and weak size dependence. A remarkable PCE of 22.63% is obtained even for a 1.004-cm(2) device. Importantly, the strategy shows good universality and significantly promotes the long-term stability of the pero-SCs based on the classical doped Spiro-OMeTAD.
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| 2. |
- Lv, Wanzhi, et al.
(författare)
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Lipoxin A4 attenuation of endothelial inflammation response mimicking pancreatitis-induced lung injury
- 2013
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Ingår i: Experimental Biology and Medicine. - : SAGE Publications. - 1535-3702 .- 1535-3699. ; 238:12, s. 1388-1395
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Tidskriftsartikel (refereegranskat)abstract
- Lipoxins (LXs) and their analogues are known to display potent anti-inflammatory actions. Previously, we reported that lipoxin A4 (LXA4) possessed powerful anti-inflammatory properties in acute pancreatitis in rats and that it may ameliorate the concomitant acute lung injury by reducing cytokine generation and inhibiting neutrophil activation. Considering that the vascular endothelium plays an important role during adherence, migration and activation of leukocytes, the present study was designed to investigate the effects of LXA4 on the inflammatory response induced by tumor necrosis factor a (TNF-alpha) in human pulmonary microvascular endothelial cells (HPMECs) and explore the potential mechanisms involved in these processes. We found that LXA4 markedly down-regulated the expression of monocyte chemotactic protein-1 (MCP-1), E-selectin, and interleukin-6 (IL-6) mRNA, as well as intercellular adhesion molecule-1 (ICAM-1) in TNF-alpha-exposed HPMECs. Moreover, LXA4 inhibited the phosphorylation and nuclear translocation of nuclear factor-kappa B/p65 (NF-kappa B/p65) and phosphorylation of p38 mitogen-activated protein kinase (p38 MAPK) in HPMECs following TNF-alpha stimulation. Heme oxygenase-1 (HO-1), a cytoprotective enzyme, was up-regulated by LXA4 in both non- and TNF-alpha-stimulated HPMECs. In conclusion, the protective effects of LXA4 to ALI may be executed through inhibition inflammation pathways of NF-kappa B and p38 MAPK and up-regulation of cytoprotective HO-1.
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