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Given the increased frequency and destructive nature of seismic events, the exigencies for enhanced management protocols for urban edifices in the milieu of seismic disaster scenarios have intensified. The role of Building Information Modeling (BIM) and Geographic Information Systems (GIS) in the governance of seismic-induced disasters is integral and merits recognition. The synergistic application of BIM and GIS technologies empowers the strategic articulation of measures that substantially abate the potential hazards associated with seismic events. The present manuscript conducts a comprehensive review of the applications of BIM-GIS synergy in the domains of seismic disaster prevention, emergency response, and in the evaluative and recovery phases following such calamities. It also examines the associated data paradigms and advancements in data interoperability techniques while addressing the prevailing limitations within the scope of contemporary research. This study endeavors to enhance the acumen of urban disaster management operatives in discerning and capitalizing on the collective strengths of BIM and GIS, with the aim of optimizing urban strategies for managing seismic disasters and diminishing the resultant losses sustained by the populace.

Given the increased frequency and destructive nature of seismic events, the exigencies for enhanced management protocols for urban edifices in the milieu of seismic disaster scenarios have intensified. The role of Building Information Modeling (BIM) and Geographic Information Systems (GIS) in the governance of seismic-induced disasters is integral and merits recognition. The synergistic application of BIM and GIS technologies empowers the strategic articulation of measures that substantially abate the potential hazards associated with seismic events. The present manuscript conducts a comprehensive review of the applications of BIM-GIS synergy in the domains of seismic disaster prevention, emergency response, and in the evaluative and recovery phases following such calamities. It also examines the associated data paradigms and advancements in data interoperability techniques while addressing the prevailing limitations within the scope of contemporary research. This study endeavors to enhance the acumen of urban disaster management operatives in discerning and capitalizing on the collective strengths of BIM and GIS, with the aim of optimizing urban strategies for managing seismic disasters and diminishing the resultant losses sustained by the populace.

Pancreatic cancer (PCa) is one of the most fatal human malignancies. The enhanced infiltration of stromal tissue into the PCa tumor microenvironment limits the identification of key tumor‐specific transcription factors and epigenomic abnormalities in malignant epithelial cells. Integrated transcriptome and epigenetic multiomics analyses of the paired PCa organoids indicate that the basic helix‐loop‐helix transcription factor 40 (BHLHE40) is significantly upregulated in tumor samples. Increased chromatin accessibility at the promoter region and enhanced mTOR pathway activity contribute to the elevated expression of BHLHE40. Integrated analysis of chromatin immunoprecipitation‐seq, RNA‐seq, and high‐throughput chromosome conformation capture data, together with chromosome conformation capture assays, indicate that BHLHE40 not only regulates sterol regulatory element‐binding factor 1 (SREBF1) transcription as a classic transcription factor but also links the enhancer and promoter regions of SREBF1. It is found that the BHLHE40‐SREBF1‐stearoyl‐CoA desaturase axis protects PCa cells from ferroptosis, resulting in the reduced accumulation of lipid peroxidation. Moreover, fatostatin, an SREBF1 inhibitor, significantly suppresses the growth of PCa tumors with high expressions of BHLHE40. This study highlights the important roles of BHLHE40‐mediated lipid peroxidation in inducing ferroptosis in PCa cells and provides a novel mechanism underlying SREBF1 overexpression in PCa. [ABSTRACT FROM AUTHOR]

This study aimed to explore novel long non-coding RNAs (lncRNAs) and the underlying mechanisms involved in childhood acute lymphoblastic leukemia (cALL). The GSE67684 dataset was downloaded from the Gene Expression Omnibus. Differentially expressed genes (DEGs) and lncRNAs (DELs) between Days 0, 8, 15 and 33 were isolated using random variance model corrective analysis of variance. Overlapping DEGs and DELs were clustered using Cluster 3.0. Bio-functional enrichment analysis was performed using Gene Ontology (GO) and the Kyoto Encyclopedia of Genes and Genomes (KEGG). Interactions between lncRNAs and mRNAs were calculated using dynamic simulations, and interactions among mRNAs were predicted using the STRING database. lncRNA-mRNA and protein-protein interaction (PPI) networks were visualized using Cytoscape. Subsequently, the expression levels of lncRNAs in biological samples from children with or without cALL were validated using reverse transcription-quantitative polymerase chain reaction (RT-qPCR). A total of 593 overlapping DEGs and 21 DELs were identified. After clustering, Profile 26 exhibited a continuously increasing temporal trend, whereas Profile 1 exhibited a continuous decreasing trend. Upregulated DEGs were significantly enriched in 1,825 GO terms and 166 KEGG pathways, whereas downregulated DEGs were significantly enriched in 196 GO terms and 90 KEGG pathways. The lncRNAs NONHSAT027612.2 and NONHSAT134556.2 were the top two regulators in the lncRNA-mRNA network. Toll-like receptor 4, cathepsin G, nucleotide-binding oligomerization domain containing 2 and cathepsin S may be considered the hub genes of the PPI network. RT-qPCR results indicated that the expression levels of the lncRNAs NONHSAT027612.2 and NONHSAT134556.2 were significantly elevated in the blood and bone marrow of patients with cALL compared with the controls. In conclusion, the lncRNAs NONHSAT027612.2 and NONHSAT134556.2 may serve important roles in the pathogenesis of cALL via regulating immune response-associated pathways. [ABSTRACT FROM AUTHOR]

Ubiquitylation of the epithelial Na + channel (ENaC) plays a critical role in cellular functions, including transmembrane transport of Na + , Na + and water balance, and blood pressure stabilization. Published studies have suggested that ENaC subunits are targets of ER-related degradation (ERAD) in yeast systems. However, the molecular mechanism underlying proteasome-mediated degradation of ENaC subunits remains to be established. Derlin-1, an E3 ligase mediator, links recognized target proteins to ubiquitin-mediated proteasomal degradation in the cytosol. In the present study, we found that derlin-1 suppressed the expression of ENaC at the protein level and that the subunit α-ENaC (also known as SCNN1A) physically interacted with derlin-1 at the membrane-anchored domains or the loop regions, and that derlin-1 initiated α-ENaC retrotranslocation. In addition, HUWE1, an endoplasmic reticulum (ER)-resident E3 ubiquitin ligase, was recruited and promoted K11-linked polyubiquitylation of α-ENaC and, hence, formation of an α-ENaC ubiquitin-mediated degradation complex. These findings suggest that derlin-1 promotes ENaC ubiquitylation and enhances ENaC ubiquitin- mediated proteasome degradation. The derlin-1 pathway therefore may represent a significant early checkpoint in the recognition and degradation of ENaC in mammalian cells., (© 2017. Published by The Company of Biologists Ltd.)