ABSTRACT
It is unclear at the molecular level why HY (HY = RSH, or ROH, or RNH2) with HPPh2 additives kinetically affects the reaction pathway to the formation of different monomers (Ph2P-SeCd-Y or Ph2P-SeCdSe-Y) in the systhesis of semiconductor nanocrystals. In the present work, it was found that in a [Cd(OA)2 + Se[double bond, length as m-dash]P(C8H17)3 + HPPh2 + HY] mixture, HY behaves as a mediator for the formation of the initial kind of monomer, besides as a hydrogen/proton donor in the release of oleic acid and as an accelerant in the Se-P bond cleavage, which follows the mechanism of hydrogen-shift/nucleophilic-attack. The capability of the HY additive to provide a H-source decreases in the order SePPh2H > RSH > HPPh2 > ROH > RNH2, while the performance of HY to accelerate Se-P bond cleavage decreases in the order HPPh2 > RSH > RNH2 > ROH. The capacity of HY to promote the formation of the Ph2P-SeCd-Y monomer decreases in the order RSH > HPPh2 > ROH > RNH2, while the effect of HY to drive the formation of the Ph2P-SeCdSe-Y monomer decreases in the order HPPh2 > RSH > RNH2 > ROH. The activation strain energy plays a key role in both the Se-P and H-Y bond cleavage, which correlates negatively to the size of the coordinated atom radius. When only HPPh2 is present without other HY species (HY = RNH2, or RSH, or ROH), Ph2P-SeCdSe-PPh2 is preferentially formed. Alternatively, when both HY (HY = RNH2, or RSH, or ROH) and HPPh2 are present, Ph2P-SeCd-Y is favorably formed. For the formation of Ph2P-SeCd-Y (Y = -PPh2, -SR, -OR, and -NHR), SePPh2H embodies the catalytic performance, while HPPh2 serves as the catalyst for the formation of Ph2P-SeCdSe-Y (Y = -NHR or -OR). Our study brings a molecular-level insight into the relationship between the CdSe monomer and the phosphorous-containing side-product, which may advance the rational design and synthesis of quantum dots.
ABSTRACT
BACKGROUND: Lung cancer is the leading cause of cancer deaths in most countries. In patients with metastases, such as the brain, the 1-year survival is 10% and most of these patients die in 1-3 months. Data from large phase II trials of non-small cell lung cancer (NSCLC) suggested that the histologic subtype of adenocarcinoma may be a prognostic factor for patients treated with gefitinib. To evaluate the efficacy of gefitinib in palliative therapy for advanced patients with adenocarcinoma and brain metastases, we conducted a phase II study. PATIENTS AND METHODS: Eligible patients had histologically confirmed adenocarcinoma and brain metastases confirmed with radiological studies. All eligible patients had undergone chemotherapy previously. From December 2003 to December 2004, 40 patients received 250mg doses of gefitinib daily. The symptomatic response, survival, and toxicity were recorded. RESULTS: The overall objective response rate was 32% with a disease control rate of 77%. Altogether, 45% of the patients experienced symptom improvement. The median progression-free survival and overall survival were 9.0 months and 15.0 months, respectively. Gefitinib was well-tolerated, with cutaneous reactions as the most frequent toxicity. CONCLUSIONS: Our data suggest that gefitinib has promising activity in palliative therapy for patients with advanced lung adenocarcinoma and brain metastasis.