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Background: Circular RNAs (circRNAs) have been shown to mediate tumor‐associated macrophages (TAMs) to regulate the development of many cancers, including lung adenocarcinoma (LUAD). However, whether circ_0001715 regulates LUAD progression by mediating TAMs polarization remains uncertain. Methods: Monocytes (THP‐1) were treated with PMA to induce M0 macrophages. M0 macrophages were incubated with LUAD cells‐derived exosomes and then cocultured with LUAD cells. The levels of circ_0001715, M2 macrophage markers, microRNA (miR)‐205‐5p, and triggering receptor expressed on myeloid cells‐2 (TREM2) were examined using quantitative real‐time PCR. Flow cytometry was performed to assess M2 macrophage surface marker CD206. Cell proliferation, migration and invasion were determined using cell counting kit 8, EdU, colony formation and transwell assays. Dual‐luciferase reporter assay was used to investigate the interactions between miR‐205‐5p and circ_0001715 or TREM2. Results: Circ_0001715 knockdown inhibited M2 macrophage polarization and its overexpression had an opposite effect. After M0 macrophages transfected with si‐circ_0001715 were cocultured with LUAD cells, the proliferation and metastasis of LUAD cells were markedly reduced. Exosomes transferred circ_0001715 between M0 macrophages and LUAD cells. Exosomal circ_0001715 promoted M2 macrophage polarization to increase LUAD cell proliferation and metastasis. In terms of mechanism, circ_0001715 sponged miR‐205‐5p to positively regulate TREM2. TREM2 upregulation also could promote LUAD cell proliferation and metastasis via increasing M2 macrophage polarization. In addition, TREM2 knockdown reversed the effect of exosomal circ_0001715 on M2 macrophage polarization and LUAD cell progression. Conclusion: Exosomal circ_0001715 led to LUAD cell proliferation and metastasis by promoting M2 macrophage polarization via the miR‐205‐5p/TREM2 axis. [ABSTRACT FROM AUTHOR]

Compared with cement stone, epoxy resin has a higher compressive strength, lower elastic modulus, and better seepage capacity in repairing cement sheath or cementing in special formations. The viscosity of epoxy resin is significantly affected by temperature, which causes a serious decrease in the settlement stability. In this study, the effects of the diluent, solid epoxy resin and rheological agents on the slurry viscosity, and settlement stability were evaluated. The results indicate that fumed silica and organic bentonite have a good effect on improving the settlement stability, but have negative effects on pumpability. Therefore, a method to improve the settlement stability of epoxy resin-based cementing slurry was developed. Fumed silica and organic bentonite were compounded to increase the settlement stability and lower dosage (fumed silica less than 3 wt.%) can avoid too much negative effect on pumpability. Viscosity tests showed that diluent work more effectively at low temperatures while solid ER and Xanthan gum are more effective at high temperatures. When they use together, the viscosity at 90 °C is increased by 33% while decrease by 86% at 25 °C. When the temperature increases downhole, the viscosity of diluent is closed to ER, and tackifying materials dominate, increasing the viscosity at high temperatures. Based on the method proposed in this paper, the epoxy resin-based cementing slurry can increase the settlement stability to less than 0.01 g/cm3 when the slurry density is less than 1.3 g/cm3 and a settlement stability of less than g/cm3 when slurry density is less than 1.59 g/cm3. [ABSTRACT FROM AUTHOR]

According to the World Health Organization, Mycobacterium tuberculosis infections affect approximately 25% of the world's population. There is mounting evidence linking autophagy and immunological dysregulation to tuberculosis (TB). As a result, this research set out to discover TB-related autophagy-related biomarkers and prospective treatment targets. We used five autophagy databases to get genes linked to autophagy and Gene Expression Omnibus databases to get genes connected to TB. Then, functional modules associated with autophagy were obtained by analyzing them using weighted gene co-expression network analysis. Both Gene Ontology and Kyoto Encyclopedia of Genes and Genomes were used to examine the autophagy-related genes (ATGs) of important modules. Limma was used to identify differentially expressed ATGs (DE-ATGs), and the external datasets were used to further confirm their identification. We used DE-ATGs and a protein-protein interaction network to search the hub genes. CIBERSORT was used to estimate the kinds and amounts of immune cells. After that, we built a drug-gene interaction network and a network that included messenger RNA, small RNA, and DNA. At last, the differential expression of hub ATGs was confirmed by RT-qPCR, immunohistochemistry, and western blotting. The diagnostic usefulness of hub ATGs was evaluated using receiver operating characteristic curve analysis. Including 508 ATGs, four of the nine modules strongly linked with TB were deemed essential. Interleukin 1B ( IL1B ), CAPS1 , and signal transducer and activator of transcription 1 ( STAT1 ) were identified by intersection out of 22 DE-ATGs discovered by differential expression analysis. Research into immune cell infiltration found that patients with TB had an increased proportion of plasma cells, CD8 T cells, and M0 macrophages. A competitive endogenous RNA network utilized 10 long non-coding RNAs and 2 miRNAs. Then, the IL1B -targeted drug Cankinumad was assessed using this network. During bioinformatics analysis, three hub genes were validated in mouse and macrophage infection models. We found that IL1B , CASP1 , and STAT1 are important biomarkers for TB. As a result, these crucial hub genes may hold promise as TB treatment targets.