In this study, facile synthesis, characterization, and stability tests of highly luminescent Zn-doped CsPbBr3 perovskite nanocrystals (NCs) were demonstrated. The doping procedure was performed via partial replacement of PbBr2 with ZnBr2 in the precursor solution. Via Zn-doping, the photoluminescence quantum yield (PLQY) of the NCs was increased from 41.3% to 82.9%, with a blue-shifted peak at 503.7 nm and narrower spectral width of 18.7 nm which was consistent with the highly uniform size distribution of NCs observed from the TEM image. In the water-resistance stability test, the doped NCs exhibited an extended period-over four days until complete decomposition, under the harsh circumstances of hexane-ethanol-water mixing solution. The Zn-doped NC film maintained its 94% photoluminescence (PL) intensity after undergoing a heating/cooling cycle, surpassing the un-doped NC film with only 67% PL remaining. Based on our demonstrations, the in-situ Zn-doping procedure for the synthesis of CsPbBr3 NCs could be a promising strategy toward robust and PL-efficient nanomaterial to pave the way for realizing practical optoelectronic devices.

An ad hoc review committee appointed by ASPET's Board of Publications Trustees has reviewed the articles concerned. Generally, but not exclusively, the plagiarized text and appropriation of ideas occur in the Introduction and Discussion sections of the article. There is no allegation that the data reported in the article is unsound, and the main subject of the article is different from the topics of the articles by Blanchard et al. (2002) and Burhans et al. (2002). Nevertheless, the ASPET committee concurs with the Roswell Park internal inquiry committee in its decision that this extent of unattributed textual copying amounts to plagiarism as defined by the U. Department of Pharmacology and Therapeutics, Grace Cancer Drug Center, Roswell Park Cancer Institute, Buffalo, New York Received November 19, 2003; accepted April 12, 2004 This article is available online at http://molpharm.aspetjournals.org ABSTRACT Methylselenocysteine (MSC) is an organic selenium compound in preventative clinical trials involving prostate, lung, and colon carcinoma. We found that methioninase-activated MSC potentiates 7-ethyl-10-hydroxycamptothecin (SN-38)-induced cell lethality in vitro in the p53-defective human head and neck carcinoma A253 cells. Activated MSC increases chk2 phosphorylation at threonine-68 induced by SN-38, with no significant effect on chk1 phosphorylation. Cell cycle arrest induced by SN-38, however, was not abrogated or potentiated by MSC. These results suggest that the enhanced cellular lethality of SN-38 by MSC was not associated with cell cycle regulation pathways. Because chk2, in addition to its role in cell cycle arrest, can induce apoptosis by phosphorylation/activation, we examined whether increased chk2 phosphorylation could induce preapoptotic DNA fragmentation. DNA damage analysis showed that megabase DNA fragmentation is decreased, accompanied by the increased 30 to 300 kilobase pairs of DNA fragmentation after exposure to SN-38 with MSC,