Tin selenide (Sn1−xSe) polycrystalline thin films were prepared by thermal co-evaporation, and the thermoelectric properties of the Sn1−xSe thin films were investigated.
Sb2Se3 possesses a quasi‐1D (Q1D) structure, which creates an anisotropic charge transporting behavior in which the carrier transport is very efficient along the Q1D direction, which is beneficial for solar cells as long as the absorber is properly aligned along the preferred orientation. However, Sb2Se3 is prone to form donor‐like defects, such as VSe, that are detrimental to the performance. Therefore, both growth of Sb2Se3 along the preferred orientations and the suppression of the formation of VSe are crucial in achieving Sb2Se3 solar cells with a high efficiency. Herein, the importance of fine control of the extra supply of Se during the deposition of Sb2Se3 in controlling crystallographic orientations and the population of VSe in the Sb2Se3 films is described. This control determines the performance of the resulting solar cells in a superstrate configuration with a CdS buffer. Incorporation of Se during the growth resulted in a larger open‐circuit voltage due to the passivation of VSe. However, an excess supply of Se disrupts the favorable orientation by selenizing the top region of the CdS, and therefore degraded the short‐circuit current. Through the optimization of the extra supply of Se vapor, the power conversion efficiency is improved from 3.7% to 5.2%.
Sb2Se3, a quasi-1D structured binary chalcogenide, has great potential as a solar cell light absorber owing to its anisotropic carrier transport and benign grain boundaries when the absorber layer is...
Carnosol, a naturally occurring bioactive phenolic diterpene originating from rosemary and sage, has been shown to exert antioxidant and anti-inflammatory effects. This study examined possible protective effects of carnosol on sodium nitroprusside (SNP)-induced cytotoxicity in C6 glial cells. Carnosol (1-10 microM) dose-dependently attenuated SNP (100 microM)-induced cell death and NO production. SNP-induced apoptotic characteristics, including DNA fragmentation, caspase-3 activation, and c-jun N-terminal protein kinase (JNK) phosphorylation, were significantly suppressed by carnosol (10 microM). In addition, carnosol pretreatment restored the level of reduced glutathione (GSH), which was diminished by SNP treatment. Although both SNP (100 microM) and carnosol (10 microM) stimulated the HO-1 expression time-dependently, SNP caused a temporal increase in HO-1 in early time periods (3-6 h) before cell death occurred. In contrast, carnosol induced the sustained expression of HO-1 until a late time point (24 h). The addition of 1 microM zinc protoporphyrin IX (ZnPP), a specific HO inhibitor, with SNP or carnosol further reduced cell viability. Also, the addition of ZnPP inhibited the protective effect of carnosol against SNP-induced cytotoxicity in C6 cells. These results suggest that carnosol possesses abilities to inhibit SNP-mediated glial cell death through modulation of apoptotic events and induction of HO-1 expression.
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