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1.
ACS Appl Mater Interfaces ; 15(40): 46925-46932, 2023 Oct 11.
Artigo em Inglês | MEDLINE | ID: mdl-37769342

RESUMO

Titania nanospheres have been utilized as building blocks of electron transporting layers (ETLs) for mesoscopic perovskite solar cells (PSCs). Nevertheless, the power conversion efficiencies (PCEs) reported so far for the mesoscopic PSCs containing titania nanospheres are generally lower than those of the state-of-the-art planar PSCs. Here, we have prepared Li-doped hollow titania nanospheres (Li-HTS) through a "cation-exchange" approach and used them for the first time to modify the SnO2 ETL/perovskite interfaces of planar PSCs. The Li-HTS-modified PSC delivered a PCE of 23.28% with a fill factor (FF) of over 80%, which is significantly higher than the PCE of the control device (20.51%). This is the best PCE achieved for PSCs containing titania nanospheres. Moreover, interfacial modification using Li-HTS greatly improves the stability of the PSCs. This work demonstrates the potential of interface modification using inorganic nanostructures for enhancing the efficiency and stability of planar PSCs.

2.
ACS Appl Mater Interfaces ; 14(11): 13352-13360, 2022 Mar 23.
Artigo em Inglês | MEDLINE | ID: mdl-35289163

RESUMO

The interfaces between the absorber and charge transport layers are shown to be critical for the performance of perovskite solar cells (PSCs). PSCs based on the Spiro-OMeTAD hole transport layers generally suffer from the problems of stability and reproducibility. Inorganic hole transport materials CuCrO2 have good chemical stability and high hole mobility. Herein, we reported the preparation of the delafossite-type CuCrO2 nanocrystals with a template-etching-calcination method and the incorporation of the as-obtained CuCrO2 nanocrystals at the perovskite/Spiro-OMeTAD interfaces of planar PSCs to improve the device efficiency and stability. Compared with the traditional hydrothermal method, the template-etching-calcination method used less calcination time to prepare CuCrO2 nanocrystals. After the CuCrO2 interface modification, the efficiency of PSCs improved from 18.08% to 20.66%. Additionally, the CuCrO2-modified PSCs showed good stability by retaining nearly 90% of the initial PCE after being stored in a drybox for 30 days. The template-etching-calcination strategy will pave a new approach for the synthesis of high-performance inorganic hole-transporting materials.

3.
J Cardiovasc Med (Hagerstown) ; 15(7): 565-71, 2014 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-23751595

RESUMO

AIMS: Heat shock protein 70 (HSP70) protects against cardiac diseases such as ischemia/reperfusion injury and myocardial infarction. However, the underlying mechanisms have not yet been fully characterized. METHODS: In this study, we investigated the effects of reactive oxygen species (ROS) and transforming growth factor-ß-activated kinase 1 (TAK1) on HSP70-regulated cardiomyocyte protection. Cultured cardiomyocytes of neonatal rats were transfected with HSP70, TAK1 or both of them before exposure to H2O2, and the ROS generation, p38 mitogen-activated protein kinase (p38) activity and apoptosis were examined. RESULTS: H2O2 significantly enhanced intracellular ROS generation and apoptosis as expected, and all these cellular events were greatly abolished by overexpression of HSP70. However, H2O2-induced increments in p38 phosphorylation and cardiac cell apoptosis were largely enhanced by TAK1 overexpression, whereas the similar transfection did not affect the ROS generation in the cardiomyocytes. Moreover, inhibition of H2O2-increased ROS generation, p38 phosphorylation, and cardiomyocytes apoptosis by overexpression of HSP70 tended to disappear when the cells were cotransfected with TAK1. CONCLUSION: Our data suggest that HSP70 protects cardiomyocytes from apoptosis under oxidative stress through downregulation of intracellular ROS generation and inhibition of p38 phosphorylation. Although TAK1 itself has no effect on intracellular ROS accumulation, it may affect the inhibitory effects of HSP70 on ROS generation, p38 activity and cardiomyocyte injury.


Assuntos
Apoptose , Regulação da Expressão Gênica no Desenvolvimento , Peróxido de Hidrogênio/farmacologia , MAP Quinase Quinase Quinases/genética , Miócitos Cardíacos/metabolismo , RNA/genética , Espécies Reativas de Oxigênio/metabolismo , Animais , Animais Recém-Nascidos , Western Blotting , Células Cultivadas , Modelos Animais de Doenças , Regulação para Baixo , Ensaio de Imunoadsorção Enzimática , MAP Quinase Quinase Quinases/biossíntese , Miócitos Cardíacos/patologia , Estresse Oxidativo , Fosforilação , Ratos , Ratos Sprague-Dawley , Reação em Cadeia da Polimerase em Tempo Real , Transdução de Sinais
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