| 1. |
- Zhang, Bin, et al.
(author)
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Perylene Diimide-Based Low-Cost and Thickness-Tolerant Electron Transport Layer Enables Polymer Solar Cells Approaching 19% Efficiency
- 2024
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In: Advanced Functional Materials. - 1616-3028 .- 1616-301X. ; In Press
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Journal article (peer-reviewed)abstract
- The materials for electron transport layers (ETLs) play a significant role in the performance of polymer solar cells (PSCs) but face challenges, such as low electron transport mobility and conductivity, low solution processibility, and extreme thickness sensitivity, which will undermine the photovoltaic performance and hinder compatibility of large-scale fabrication technique. To address these challenges, a new n-type perylene diimide-based molecule (PDINB) with two special amine-anchored long-side chains is designed and synthesized feasibly. PDINB shows very high solubility in common organic solvents, such as dichloromethane (>75 mg ml−1) and methanol with acetic acid as an additive (>37 mg ml−1), which leads to excellent film formability when deposited on active layers. With PDINB as ETLs, the photovoltaic performance of the PSCs is boosted comprehensively, leading to power conversion efficiency (PCE) up to 18.81%. Thanks to the strong self-doping effect and high conductivity of PDINB, it displays an appreciable thickness-tolerant property as ETLs, where the devices remain consistently high PCE values with the thickness varying from 5 to 30 nm. Interestingly, PDINB can be used as a generic ETL in different types of PSCs including non-fullerene PSCs and all-polymer PSCs. Therefore, PDINB can be a potentially competitive candidate as an efficient ETL for PSCs.
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| 2. |
- Fu, Jinrong, et al.
(author)
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Anti-ischemia/reperfusion of C1 inhibitor in myocardial cell injury via regulation of local myocardial C3 activity.
- 2006
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In: Biochemical and Biophysical Research Communications - BBRC. - : Elsevier BV. - 0006-291X .- 1090-2104. ; 350:1, s. 162-8
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Journal article (peer-reviewed)abstract
- C3 is common to all pathways of complement activation augmenting ischemia/reperfusion (I/R)-induced myocardial injury and cardiac dysfunction. Complement inhibition with the complement regulatory protein, C1 inhibitor (C1INH), obviously exerts cardioprotective effects. Here, we examine whether C1INH regulates C3 activity in the ischemic myocardial tissue. C1INH markedly suppressed C3 mRNA expression and protein synthesis in both a model of I/R-induced rat acute myocardial infarction (AMI) and the cultured rat H9c2 heart myocytes. At least, this regulation was at the transcriptional level in response to oxygen tension. In vitro, C3 deposition on, and binding to, the surface of rat myocardial cells were significantly blocked by C1INH treatment. C1INH could inhibit classical complement-mediated cell lysis via suppressing the biological activity of C3. Therefore, C1INH, in addition to inhibition of the systemic complement activation, prevents myocardial cell injury via a direct inhibitory role in the local myocardial C3 activity.
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