Low-Temperature Discrimination of Defect States by Exciton Dynamics in Thin-Film MAPbBr₃ Perovskite

Exciton dynamics significantly influences the performance of the optoelectronic devices, which is intensively studied in the light-emitting perovskite of CH3NH3PbBr3 (MAPbBr3). However, most of the existing investigations have focused on the free excitons. In this study, we investigate the emissive recombination from defect states in MAPbBr3 using temperature- and excitation-dependent photoluminescence measurements. It is revealed that two emission peaks centered at about 550 and 590 nm are presented at temperatures as low as 10 K, instead of one peak at 535 nm for the observation at room temperature. These two peaks are attributed to the emission of bound excitons after self-absorption and bulk defects, respectively. It is found that the distribution of the bound and trapped excitons is strongly influenced by the morphology of the MAPbBr3 films. These results provide deep insights into the exciton dynamics in MAPbBr3, facilitating new physics for the design of related optoelectronic materials and devices

Efficient and Practical Synthesis of Saflufenacil

Efficient and Practical Synthesis of Saflufenaci

Table_3_Integrating Genome-Wide Association Studies With Pathway Analysis and Gene Expression Analysis Highlights Novel Osteoarthritis Risk Pathways and Genes.xls

Osteoarthritis (OA) is the most common degenerative joint disorder worldwide. To identify more genetic signals, genome-wide association study (GWAS) has been widely used and elucidated some OA susceptibility genes. However, these susceptibility genes could only explain only a small part of heritability of OA. It is suggested that the identification of disease-related pathways may contribute to understand the genomic etiology of OA. Here, we integrated the GWAS into pathway analysis to identify novel OA risk pathways. In this study, we first selected 187 independent genetic variants identified by GWAS (P < 1.00E−05) and found that most of these genetic variants are noncoding mutations. We then conducted an expression quantitative trait loci analysis and found that 165 of these 187 genetic variants could significantly regulate the expression of nearby genes. Third, we identified OA susceptibility genes corresponding to these genetic variants, conducted a pathway analysis, and identified novel OA-related KEGG pathways, GO biological processes, GO molecular functions, and GO cellular components. In KEGG database, transforming growth factor β signaling pathway is the most significant signal (P = 5.98E−05) and is the only pathway after the BH multiple-test adjustment with false discovery rate (FDR) = 0.02. In GO database, we identified 24 statistically significant GO biological processes, one statistically significant GO molecular function, and five statistically significant GO cellular components (FDR < 0.05). These signals are related with chondrocyte differentiation and development, which are all known biological pathways associated with OA. Finally, we conducted an OA case–control gene expression analysis to evaluate the differential expression of these OA risk genes. Using an OA case–control gene expression analysis, we showed that 44 risk genes were suggestively differentially expressed in OA cases compared with controls (P < 0.05). Three genes, WWP2, COG5, and MAPT, were statistically differentially expressed in OA cases compared with controls (P < 0.05/122 = 4.10E−04). Hence, our findings may contribute to understanding the genomic etiology of OA.</p

Table_2_Integrating Genome-Wide Association Studies With Pathway Analysis and Gene Expression Analysis Highlights Novel Osteoarthritis Risk Pathways and Genes.xls

Osteoarthritis (OA) is the most common degenerative joint disorder worldwide. To identify more genetic signals, genome-wide association study (GWAS) has been widely used and elucidated some OA susceptibility genes. However, these susceptibility genes could only explain only a small part of heritability of OA. It is suggested that the identification of disease-related pathways may contribute to understand the genomic etiology of OA. Here, we integrated the GWAS into pathway analysis to identify novel OA risk pathways. In this study, we first selected 187 independent genetic variants identified by GWAS (P < 1.00E−05) and found that most of these genetic variants are noncoding mutations. We then conducted an expression quantitative trait loci analysis and found that 165 of these 187 genetic variants could significantly regulate the expression of nearby genes. Third, we identified OA susceptibility genes corresponding to these genetic variants, conducted a pathway analysis, and identified novel OA-related KEGG pathways, GO biological processes, GO molecular functions, and GO cellular components. In KEGG database, transforming growth factor β signaling pathway is the most significant signal (P = 5.98E−05) and is the only pathway after the BH multiple-test adjustment with false discovery rate (FDR) = 0.02. In GO database, we identified 24 statistically significant GO biological processes, one statistically significant GO molecular function, and five statistically significant GO cellular components (FDR < 0.05). These signals are related with chondrocyte differentiation and development, which are all known biological pathways associated with OA. Finally, we conducted an OA case–control gene expression analysis to evaluate the differential expression of these OA risk genes. Using an OA case–control gene expression analysis, we showed that 44 risk genes were suggestively differentially expressed in OA cases compared with controls (P < 0.05). Three genes, WWP2, COG5, and MAPT, were statistically differentially expressed in OA cases compared with controls (P < 0.05/122 = 4.10E−04). Hence, our findings may contribute to understanding the genomic etiology of OA.</p

Table_1_Integrating Genome-Wide Association Studies With Pathway Analysis and Gene Expression Analysis Highlights Novel Osteoarthritis Risk Pathways and Genes.xls

Osteoarthritis (OA) is the most common degenerative joint disorder worldwide. To identify more genetic signals, genome-wide association study (GWAS) has been widely used and elucidated some OA susceptibility genes. However, these susceptibility genes could only explain only a small part of heritability of OA. It is suggested that the identification of disease-related pathways may contribute to understand the genomic etiology of OA. Here, we integrated the GWAS into pathway analysis to identify novel OA risk pathways. In this study, we first selected 187 independent genetic variants identified by GWAS (P < 1.00E−05) and found that most of these genetic variants are noncoding mutations. We then conducted an expression quantitative trait loci analysis and found that 165 of these 187 genetic variants could significantly regulate the expression of nearby genes. Third, we identified OA susceptibility genes corresponding to these genetic variants, conducted a pathway analysis, and identified novel OA-related KEGG pathways, GO biological processes, GO molecular functions, and GO cellular components. In KEGG database, transforming growth factor β signaling pathway is the most significant signal (P = 5.98E−05) and is the only pathway after the BH multiple-test adjustment with false discovery rate (FDR) = 0.02. In GO database, we identified 24 statistically significant GO biological processes, one statistically significant GO molecular function, and five statistically significant GO cellular components (FDR < 0.05). These signals are related with chondrocyte differentiation and development, which are all known biological pathways associated with OA. Finally, we conducted an OA case–control gene expression analysis to evaluate the differential expression of these OA risk genes. Using an OA case–control gene expression analysis, we showed that 44 risk genes were suggestively differentially expressed in OA cases compared with controls (P < 0.05). Three genes, WWP2, COG5, and MAPT, were statistically differentially expressed in OA cases compared with controls (P < 0.05/122 = 4.10E−04). Hence, our findings may contribute to understanding the genomic etiology of OA.</p

DataSheet_1_Analyzing Genome-Wide Association Study Dataset Highlights Immune Pathways in Lip Bone Mineral Density.xls

Osteoporosis is a common complex human disease. Until now, large-scale genome-wide association studies (GWAS) using single genetic variant have reported some novel osteoporosis susceptibility variants. However, these risk variants only explain a small proportion of osteoporosis genetic risk, and most genetic risk is largely unknown. Interestingly, the pathway analysis method has been used in investigation of osteoporosis mechanisms and reported some novel pathways. Until now, it remains unclear whether there are other risk pathways involved in BMD. Here, we selected a lip BMD GWAS with 301,019 SNPs in 5,858 Europeans, and conducted a gene-based analysis (SET SCREEN TEST) and a pathway-based analysis (WebGestalt). On the gene level, BMD susceptibility genes reported by previous GWAS were identified to be the top 10 significant signals. On the pathway level, we identified 27 significant KEGG pathways. Three immune pathways including T cell receptor signaling pathway (hsa04660), complement and coagulation cascades (hsa04610), and intestinal immune network for IgA production (hsa04672) are ranked the top three significant signals. Evidence from the PubMed and Google Scholar databases further supports our findings. In summary, our findings provide complementary information to these nine risk pathways.</p

Table_4_Integrating Genome-Wide Association Studies With Pathway Analysis and Gene Expression Analysis Highlights Novel Osteoarthritis Risk Pathways and Genes.xls

Osteoarthritis (OA) is the most common degenerative joint disorder worldwide. To identify more genetic signals, genome-wide association study (GWAS) has been widely used and elucidated some OA susceptibility genes. However, these susceptibility genes could only explain only a small part of heritability of OA. It is suggested that the identification of disease-related pathways may contribute to understand the genomic etiology of OA. Here, we integrated the GWAS into pathway analysis to identify novel OA risk pathways. In this study, we first selected 187 independent genetic variants identified by GWAS (P < 1.00E−05) and found that most of these genetic variants are noncoding mutations. We then conducted an expression quantitative trait loci analysis and found that 165 of these 187 genetic variants could significantly regulate the expression of nearby genes. Third, we identified OA susceptibility genes corresponding to these genetic variants, conducted a pathway analysis, and identified novel OA-related KEGG pathways, GO biological processes, GO molecular functions, and GO cellular components. In KEGG database, transforming growth factor β signaling pathway is the most significant signal (P = 5.98E−05) and is the only pathway after the BH multiple-test adjustment with false discovery rate (FDR) = 0.02. In GO database, we identified 24 statistically significant GO biological processes, one statistically significant GO molecular function, and five statistically significant GO cellular components (FDR < 0.05). These signals are related with chondrocyte differentiation and development, which are all known biological pathways associated with OA. Finally, we conducted an OA case–control gene expression analysis to evaluate the differential expression of these OA risk genes. Using an OA case–control gene expression analysis, we showed that 44 risk genes were suggestively differentially expressed in OA cases compared with controls (P < 0.05). Three genes, WWP2, COG5, and MAPT, were statistically differentially expressed in OA cases compared with controls (P < 0.05/122 = 4.10E−04). Hence, our findings may contribute to understanding the genomic etiology of OA.</p

Table_1_Analyzing Genome-Wide Association Study Dataset Highlights Immune Pathways in Lip Bone Mineral Density.doc

Osteoporosis is a common complex human disease. Until now, large-scale genome-wide association studies (GWAS) using single genetic variant have reported some novel osteoporosis susceptibility variants. However, these risk variants only explain a small proportion of osteoporosis genetic risk, and most genetic risk is largely unknown. Interestingly, the pathway analysis method has been used in investigation of osteoporosis mechanisms and reported some novel pathways. Until now, it remains unclear whether there are other risk pathways involved in BMD. Here, we selected a lip BMD GWAS with 301,019 SNPs in 5,858 Europeans, and conducted a gene-based analysis (SET SCREEN TEST) and a pathway-based analysis (WebGestalt). On the gene level, BMD susceptibility genes reported by previous GWAS were identified to be the top 10 significant signals. On the pathway level, we identified 27 significant KEGG pathways. Three immune pathways including T cell receptor signaling pathway (hsa04660), complement and coagulation cascades (hsa04610), and intestinal immune network for IgA production (hsa04672) are ranked the top three significant signals. Evidence from the PubMed and Google Scholar databases further supports our findings. In summary, our findings provide complementary information to these nine risk pathways.</p

Supplemental Material - Beauty May Not Be Effective: The Effects of Imaginative Display on Green Product Evaluation

Supplemental Material for Beauty May Not Be Effective: The Effects of Imaginative Display on Green Product Evaluation by Shichang Liang, Jingyi Li, Tingting Zhang, Yiwei Zhang, and Pin Xie in The Journal of Environment & Development.</p

Sn-Modified ZSM-5 As Support for Platinum Catalyst in Propane Dehydrogenation

Sn modified ZSM-5 was hydrothermally synthesized and this kind of zeolite was used as the support for platinum catalyst in propane dehydrogenation. In this tin-doped material, XRD results established the presence of highly crystalline and the analysis of SEM showed the deterioration in crystal quality. The incorporation of Sn into the framework of ZSM-5 zeolite introduced the strong interactions between Sn species and the support, thus more amounts of tin could exist in oxidized form. Moreover, on the Sn-containing PtNa/Sn-ZSM-5 catalyst, the substitution of Sn changed the interfacial character between Pt and the support, which in consequence promoted the occurrence of spillover hydrogen and facilitated the reduction of Pt species. Compared with the conventional impregnated PtNa/HZSM-5 and PtSnNa/HZSM-5 catalysts, the Sn-modified ZSM-5-based Pt catalyst exhibited higher reaction activity and stability. It showed the lowest deactivation parameter (6.2%) and exhibited a selectivity to propene higher than 98% with the corresponding propane conversion of about 39.0% after the reaction for 9 h