Surface Treatment on Nickel Oxide to Enhance the Efficiency of Inverted Perovskite Solar Cells

The organic-inorganic hybrid perovskites such as CH3NH3PbI3 have been considered as one of the most promising candidates for the next-generation photovoltaic materials due to its high absorption coefficient, low exciton binding energy, and long diffusion length. Herein, we have chosen NiOx as the hole transport material because metal oxides exhibit robust properties in air. We synthesized the NiOx film by a common sol-gel method. It is found that high-temperature annealing (500 degrees C) is required to ensure the perovskite solar cell (PSC) with an efficiency over 15%. Low-temperature annealing (100 degrees C) cannot convert the precursor materials to fully covered NiOx film, while the PSC based on mediate-temperature annealing (300 degrees C) NiOx has larger resistance and thus lower efficiency. Fortunately, we have found that UV-ozone treatment on the NiOx film can reduce the resistance of the device based on 300 degrees C annealed NiOx. The champion device can reach 16% efficiency with UV-ozone-treated 300 degrees C annealed NiOx. This work has made it possible to reduce the annealing temperature of the sol-gel NiOx for high-efficiency PSCs, and it is believed that this simple surface treatment can be further employed in other metal oxide-based optoelectronic devices

Prediction of prognosis and immunotherapy response in lung adenocarcinoma based on CD79A, DKK1 and VEGFC

Background: Tumor immune microenvironment (TIME) is crucial for tumor initiation, progression, and metastasis; however, its relationship with lung adenocarcinoma (LUAD) is unknown. Traditional predictive models screen for biomarkers that are too general and infrequently associated with immune genes. Methods: RNA sequencing data of LUAD patients and immune-related gene sets were retrieved from public databases. Using the common genes shared by The Cancer Genome Atlas (TCGA) and Immunology Database and Analysis Portal (ImmPort), differential gene expression analysis, survival analysis, Lasso regression analysis, and univariate and multivariate Cox regression analyses were performed to generate a novel risk score model. LUAD cohort in International Cancer Genome Consortium (ICGC), GSE68465 cohort in Gene Expression Omnibus (GEO) and an immunohistochemical assay were used to validate the key genes constructed risk score. The LUAD-related prognosis, clinical indicators, immune infiltrate characteristics, response to immunotherapy, and response to chemotherapeutic agents in different risk groups were evaluated by CIBERSORT, ImmuCellAI, pRRophetic and other tools. Results: The risk score model was constructed using CD79a molecule (CD79A), Dickkopf WNT signaling pathway inhibitor 1 (DKK1), and vascular endothelial growth factor C (VEGFC). High risk score was identified as a negative predictor for overall survival (OS) in subgroup analyses with tumor stage, TNM classification, therapy outcome, and ESTIMATE scores (P < 0.05). Low risk score was positively associated with plasma cells, memory B cells, CD8 T cells, regulatory T cells and γδT cells (P < 0.05). In low-risk group, programmed cell death 1 receptor (PD1), cytotoxic T-lymphocyte associated protein 4 (CTLA4), and lymphocyte activating 3 (LAG3) and indoleamine 2,3-dioxygenase (IDO) were more robustly expressed (P < 0.05). The treatment responses of immune checkpoint blockade (ICB) therapy and chemotherapy were likewise superior in low-risk group (P < 0.05). In immunohistochemical analysis, the tumor group had significantly higher levels of CD79A, DKK1, and VEGFC than the adjacent normal group (P < 0.01). Conclusions: CD79A, DKK1 and VEGFC are important differential genes related to LUAD, risk score could reliably predict prognosis, composition of TIME and immunotherapy responses in LUAD patients. The excellent performance of the risk model shows its strong and broad application potential

Mechanistic Insight into the Nickel-Catalyzed Cross-Coupling of Aryl Phosphates with Arylboronic Acids: Potassium Phosphate is Not a Spectator Base but is Involved in the Transmetalation Step in the Suzuki-Miyaura Reaction

National Basic Research Program of China [2013CB910700, 2012CB821600, 2011CB808504]; National Natural Science Foundation of China [21232005, 21103142, 21172184, 21133007]; Program for Changjiang Scholars and Innovative Research Team in University; Fundamental Research Funds for the Central Universities [2012121021

A novel salt-induced gene from sheepgrass, LcSAIN2, enhances salt tolerance in transgenic Arabidopsis

Salt stress affects plant growth and development, and limits the productivity of crops. Sheepgrass can grow well under various environmental and soil conditions and is a good wild resource in Triticeae. Using 454 high throughout sequencing technique, a large number of salt stress responsive genes have been picked out from sheepgrass. In this study, a novel salt-induced gene and its promoter were cloned and the gene was designated as LcSAIN2 (Leymus chinensis salt-induced 2). Bioinformatics analysis predicted that LcSAIN2 has one transmembrane helix and is localized in nucleus. Experiments of subcellular localization in tobacco leaf cells also indicated that it was mainly localized in nucleus. Several stress responsive elements were found in the promoter region of the LcSAIN2 gene. The expression analysis confirmed that LcSAIN2 was induced by salinity, PEG, ABA, and cold stresses, especially by high salinity. Overexpression of LcSAIN2 in Arabidopsis enhanced salt tolerance of transgenic plants by accumulating osmolytes, such as soluble sugars and free proline, and improving the expression levels of some stress-responsive transcription factors and key genes. Our results suggest that LcSAIN2 might play an important positive modulation role in salt stress tolerance and be a candidate gene utilized for enhancing stress tolerance in wheat and other crops. (C) 2013 Elsevier Masson SAS. All rights reserved

Base-to-Base Organocatalytic Approach for One-Pot Construction of Poly(ethylene oxide)-Based Macromolecular Structures

A base-to-base organocatalytic approach has been developed for one-pot synthesis of poly­(ethylene oxide)-<i>block</i>-polyesters and poly­(ethylene oxide)-based polyurethanes. Ethylene oxide is first polymerized from a diol in the presence of a phosphazene superbase; then a thiourea is added to be deprotonated by the strongly basic alkoxide, which attenuates the basicity of the catalytic system and thus allows for controlled polymerization of the subsequently added cyclic ester from the polyether chain end or for step-growth polymerization of an added diisocyanate with the macrodiol which is free from anionic homopolymerization of the diisocyanate. The approach shows several advantages in addition to the one-pot facile character, e.g., a wide applicability toward different “second monmers” including (but not limited to) ε-caprolactone, l-lactide, and diisocyanate, and a low amount of “second catalyst” required as the deprotonated thiourea itself serves as the mildly or weakly basic organocatalyst. Impact of the N-substituent, i.e., p<i>K</i>_a of the thiourea, on the catalytic efficacy of the deprotonated thiourea has also been preliminarily revealed

[Effect of the chemoprotectant tempol on anti-tumor activity of cisplatin].

ObjectiveTo investigate the effect of the chemoprotectant tempol on the anti-tumor activity of cisplatin (DDP).MethodsThe cellular toxicity of tempol in human colon cancer SW480 cells and mouse colon cancer CT26 cells were evaluated using MTT and cell counting kit-8 assays. CalcuSyn software analysis was used to determine the interaction between tempol and DDP in inhibition of the cell viability. A subcutaneous homograft mouse model of colon cancer was established. The mice were randomly divided into control group, tempol group, cisplatin group and tempol + DDP treatment group with intraperitoneal injections of the indicated agents. The tumor size, body weight and lifespan of the mice were measured, and HE staining was used to analyze the cytotoxic effect of the agents on the kidney and liver. Immunohistochemistry and Western blotting were performed to detect the expression of Bax and Bcl2 in the tumor tissue, and TUNEL staining was used to analyze the tumor cell apoptosis. The level of reactive oxygen species (ROS) in the tumor tissue was determined using flow cytometry.ResultsTempol showed inhibitory effects on the viability of SW480 and CT26 cells. CalcuSyn software analysis showed that tempol had a synergistic anti-tumor effect with DDP (CI &lt; 1). In the homograft mouse model, tempol treatment alone did not produce obvious anti-tumor effect. HE staining showed that the combined use of tempol and DDP alleviated DDP-induced fibrogenesis in the kidneys, but tempol also reduced the anti-tumor activity of DDP. Compared with the mice treated with DDP alone, the mice treated with both tempol and DDP had a significantly larger tumor size (P &lt; 0.01) and a shorter lifespan (P &lt; 0.05). Tempol significantly reversed DDP-induced expression of Bax and Bcl2 in the tumor tissue and tumor cell apoptosis (P &lt; 0.001), and obviously reduced the elevation of ROS level in the tumor tissue induced by DDP treatment (P &lt; 0.05).ConclusionsTempol can attenuate the anti-tumor effect of DDP while reducing the side effects of DDP. Caution must be taken and the risks and benefits should be carefully weighed when considering the use of tempol as an anti-oxidant to reduce the toxicities of DDP