Improved Birefringence Activated by Tetrahedra Decorated with a Single Linear Unit.

Performance enhancement induced by structural modification has long been the target in materials science fields. Direct evidence to witness the effectivity of one strategy is challenging and necessary. In this work, a tetrahedra-decoration strategy was proposed to improve the birefringent performance sharply, namely decorating the tetrahedra with a single linear [S2 ] unit. The strategy was verified by comprehensive characterization of two thiogermanates K2 BaGeS4 and K2 BaGeS5 , which crystallize in the same space group, have similar unit cells and the same units arrangements. Theoretical characterization verified that the [GeS5 ] group has much larger polarization anisotropy than [GeS4 ], further demonstrated that the linear [S2 ] led to the sharp birefringence enlargement of K2 BaGeS5 (0.19 vs 0.03 of K2 BaGeS4 ). This work provides a new guiding thought to improve the birefringence performance.

Small area mean estimation after effect clustering.

Providing reliable estimates of subpopulation/area parameters has attracted increased attention due to their importance in applications such as policymaking. Due to low or even no samples from some areas, we must adopt indirect model approaches. Existing indirect small area estimation methods often assume that a single nested error regression model is suitable for all the small areas. In particular, the effects of the auxiliary variables are either fixed or have a single attraction center. In some applications, it can be more appropriate to cluster the small areas so that the effects of the auxiliary variables are fixed but have multiple centers in the nested error regression model. In this paper, we examine an extended nested error regression model in which the auxiliary variables have mixed effects with multiple centers. We use a penalty approach to identify these centers and estimate the model parameters simultaneously. We then propose two new small area mean estimators and construct estimators of their mean square errors. Simulations based on artificial and realistic finite populations show that the new estimators can be efficient. Furthermore, the confidence intervals based on the new methods have accurate coverage probabilities. We illustrate the proposed methods with the Survey of Labour and Income Dynamics conducted in Canada.

Integrated analysis and knockdown of RAB23 indicate the role of RAB23 in gastric adenocarcinoma.

BACKGROUND: The present study aimed to identify key differentially expressed genes (DEGs) and miRNAs (DEmiRNAs) in gastric adenocarcinoma. METHODS: We performed integrated analysis to determine DEGs and DEmiRNAs of gastric adenocarcinoma based on the GEO database. A DEmiRNA-target interaction network was established. GO and KEGG pathway enrichment analyses were utilized. Then, MKN45 cells were transfected with shRNA-RAB23 to knock down the expression of RAB23. CCK-8, transwell and flow cytometry assays were utilized to measure the capacities for cell proliferation, migration and apoptosis, and the apoptosis-related gene and protein levels were measured by using polymerase chain reaction (PCR) and Western blot, respectively. Colocalization analysis of Snc1 with the vesicular protein VAMP3 and the endoplasmic reticulum protein Calnexin was performed to assess the influence of RAB23 on vesicle transport. Finally, we performed metabolomic analysis by using gas chromatography mass spectrometry (GC-MS). RESULTS: We performed MMIA of gastric adenocarcinoma based on two miRNA datasets and two mRNA datasets. A total of 4,586 DEmRNAs and 30 DEmiRNAs were obtained. The DEmRNAs of gastric adenocarcinoma were significantly enriched in PI3K/Akt signaling. We identified three interactions, hsa-miR-23a-3p-PTPN4, hsa-miR-20b-5p (hsa-miR-130a-3p)-TNFRSF10B, and hsa-miR-130a-3p (hsa-miR-363-3p)-RAB23, that may be related to the pathogenesis of gastric adenocarcinoma. The growth of MKN45 cells was inhibited by RAB23 knockdown via shRNA-RAB23 transfection. Metabolic analysis of three groups revealed a number of significantly altered metabolites, including glycerol, niacinamide, and nonadecanoic acid methylester. CONCLUSIONS: RAB23 might be a target gene of hsa-miR-130a-3p and hsa-miR-363-3p. In gastric adenocarcinoma cells, knockdown of RAB23 inhibited cell proliferation, migration, and invasion and increased apoptosis by downregulating the PI3K/Akt pathway.