Reinforcing 2D Single-Crystal Bi2O2CO3 with Additional Interlayer Carbonates by CO2-Assisted Solid-to-Solid Phase Transition.

A facile gaseous CO2 mediated solid-to-solid transformation principle is adopted to insert additional CO3 2- anions into the thin single-crystal nanosheets of Bi2O2CO3, which is built of periodic arrays of intrinsic CO3 2- anions and (Bi2O2)2+ layers. The additional CO3 2- anions create abundant defects. The Bi2O2CO3 nanosheets with rich interlayer CO3 2- exhibit superior electronic properties and charge transfer kinetics than the pristine single-crystal 2D Bi2O2CO3 and display enhanced catalytic activity in photocatalytic CO2 reduction reaction and the photocatalytic oxidative degradation of organic pollutants. This work thus illustrates interlayer engineering as a flexible means to build layered 2D materials with excellent properties.

Toxic footprint and materials profile of electronic components in printed circuit boards.

Waste printed circuit boards (WPCBs) contain valuable material resources and hazardous substances, thereby posing a challenge for sustainable resource recovery and environmental protection initiatives. Overcoming this challenge will require mapping the toxic footprint of WPCBs to specific materials and substances used in manufacturing electronic components (ECs). Therefore, this work collected 50 EC specimens from WPCBs in five ubiquitous consumer products, such as television, refrigerator, air conditioner, washing machine and computer. The work extracted and analyzed metal contents and used leachability assessments based on tests adopted by the regulatory policies from China and the United States. The work found that copper and iron are the most abundant constituents in ECs, with concentrations ranging 5.90-796.62 g/kg and 0-831.53 g/kg, respectively; whereas abundance of precious metal content is in the order of silver > gold > palladium > platinum, with silver concentration ranging 15-5290 mg/kg. The content of marginally-regulated toxic substance arsenic ranged 0-9700 mg/kg; whereas fully regulated toxic metals such as chromium, lead and mercury did not exceed the thresholds set by China and US standards. The work found new toxic threats from arsenic and selenium leached from 20 of 50 ECs exceeding regulatory standards. These results will aid manufacturers and recyclers in protecting workers' health and environmental quality from arsenic and selenium pollution, and should initiate discussion about regulating these toxic components as part of a comprehensive program to reduce the toxic footprint of electronic products.

A rapid method and mechanism to identify the active compounds in Malus micromalus Makino fruit with spectrum-effect relationship, components knock-out and molecular docking technology.

Fingerprints of 20 batches of Malus micromalus Makino fruit were established by HPLC coupled with hierarchical cluster analysis (HCA) and principal component analysis (PCA) to estimate the common peaks on the basis of traditional similarity evaluation methods. Chromatographic peaks were identified as p-coumaric acid (P2), ferulic acid glycoside (P6), 4-O-ß-Glucopyranosyl-cis-coumaric acid (P8), phloretin-2'-xyloglucoside (P10), phloridzin (P11) and quercetin-3-O-α-rhamnoside (P12) by UPLC-MS/MS method. The results of tyrosinase kinetics experiments showed that: P2 and the concentration of P11 was greater than 0.50 mmol/L mainly had a competitive inhibitory effect on tyrosinase, and the concentration of phlorizin was less than at 0.25 mmol/L, it has a mixed inhibitory effect. P8 was mainly a non-competitive activation type in the concentration range, while P12 was a mixed activation type. The results of tyrosinase molecular docking showed that: P2, P8, P11, P12 was located in the active center of the hydrophobic pocket of the enzyme. They bound to tyrosinase residues by hydrogen bonds and interacted with many hydrophobic residues around them to maintain the structure of the complex. This research provides a rapid method to determine the active compounds in edible plants with the technology of spectrum-effect relationship, component knock-out and molecular docking.

Downregulations of miR-449a and miR-145-5p Act as Prognostic Biomarkers for Endometrial Cancer.

This investigation aimed to explore the underlying prognosis-associated microRNA (miRNA) biomarkers in endometrial cancer. Homo sapiens miRNA data set GSE35794 and miRNA data in TGGA database were downloaded and applied to screen the differentially expressed miRNAs (DE-miRNAs) using unpaired t-test in limma package in R. Basing on Venn analysis, the overlapped DE-miRNAs were screened and their potential targets were predicted according to miRWalk followed by target functional enrichment analyses and protein-protein interaction network visualized using Cytoscape. Finally, according to the information provided by the The Cancer Genome Atlas (TCGA) database, correlations between miRNAs or targets and patient prognosis were analyzed by survival package in R. A total of 24 overlapped DE-miRNAs were identified between endometrioid endometrial cancer samples and normal samples. Then, the miRNA-target regulatory network was constructed, including 11 upregulated miRNAs (e.g., miR-200a, miR-200b, and miR-200c) and five downregulated miRNAs (e.g., miR-449a, miR-145-5p, and miR-145-3p). Lymphocyte enhancer factor-1 (LEF1) was predicted to be a target of miR-449a and SOX11 was a target of miR-145-5p. Functional enrichment analyses of these targets were significantly related to the biological process of "negative regulation of transcription from RNA polymerase II promoter" and "positive regulation of transcription from RNA polymerase II promoter" (e.g., NOTCH1, LEF1, and SOX11). In addition, survival analysis showed that miR-449a, miR-145-5p, and LEF1 were approximately correlated with the overall survival prognosis of endometrial cancer patients. Downregulations of miR-449a and miR-145-5p might be involved in the pathogenesis of endometrial cancer and could act as prognostic biomarkers for endometrial cancer patients.

Genes and transcription factors related to the adverse effects of maternal type I diabetes mellitus on fetal development.

PURPOSE: Maternal type I diabetes mellitus (T1DM) increases the risk of adverse pregnancy outcomes, but the corresponding mechanism is unclear. This study aims to investigate the mechanism underlying the adverse pregnancy outcomes of maternal T1DM. METHODS: Gene expression microarray (GSE51546) was down-loaded from the Gene Expression Omnibus. This dataset included 12 umbilical cord samples from the newborns of T1DM mothers (T1DM group, N = six) and non-diabetic mothers (control group, N = six). RESULTS: Consequently, 1051 differentially expressed genes (DEGs) were found between the two groups. The up-regulated DEGs enriched in 30 KEGG pathways. HLA-DPA1, HLA-DMA, HLA-DMB, HLA-DQA1, HLA-DQA2 and HLA-DRA enriched in "Type I diabetes mellitus". This pathway was strongly related to 14 pathways, most of which were associated with diseases. Then, a protein-protein interaction network was constructed, and 45 potential key DEGs were identified. The 45 DEGs enriched in pathways such as "Rheumatoid arthritis", "Chemokine signaling pathway" and "Cytokine-cytokine receptor interaction" (e.g. CXCL12 and CCL5). Transcription factors (TFs) of key DEGs were predicted, and a TF-DEG regulatory network was constructed. CONCLUSIONS: Some genes (e.g. CXCL12 and CCL5) and their TFs were significantly and abnormally regulated in the umbilical cord tissue from the pregnancies of T1DM mothers compared to that from non-T1DM mothers.