RESUMEN
The calcium looping technology employing CaO-based sorbents is pivotal for capturing CO2 from flue gas. However, the intrinsic low thermodynamic stability of CaO-based sorbents and the requisite molding step induce severe sintering issues, diminishing their cyclic stability. Herein, a high-entropy fluorite oxide (HEFO) inert stabilizer premised on entropy stabilization and synergistic effect strategies is introduced. HEFO-modified, CaO-based sorbent pellets are synthesized via a rapid cigarette butt-assisted combustion process (15 min) combined with the graphite molding method. Post-multiple cycles, their CO2 capture capacity reaches 0.373 g g-1, which is 2.6-fold superior to that of pure CaO, demonstrating markedly enhanced anti-sintering properties. First, the subtle morphological and crystallographic modifications suggest that the inherent entropy stability of HEFO imparts robust thermal resistance. Concurrently, the disordered structure of single-phase HEFO exhibits a high affinity for CaO, resulting in an interface binding energy of -1.83 eV, in sharp contrast to the -0.112 eV of pure CaO, thereby restricting CaO migration. Additionally, the multi-element synergistic effect of HEFO reduces the energy barrier by 0.15 eV, leading to a 40% and 140% increase in carbonation and calcination rates, respectively. This work presents highly efficient and rapidly synthesized CaO-based sorbent pellets, showcasing promising potential for industrial application.
RESUMEN
Colon adenocarcinoma (COAD) is one of the most common cancers, and its carcinogenesis and progression is influenced by multiple long non-coding RNAs (lncRNA), especially through the miRNA sponge effect. In this study, more than 4000 lncRNAs were re-annotated from the microarray datasets through probe sequence mapping to obtain reliable lncRNA expression profiles. As a systems biology method for describing the correlation patterns among genes across microarray samples, weighted gene co-expression network analysis was conducted to identify lncRNA modules associated with the five stepwise stages from normal colonic samples to COAD (n = 94). In the most relevant module (R2 = -0.78, P = 4E-20), four hub lncRNAs were identified (CTD-2396E7.11, PCGF5, RP11-33O4.1, and RP11-164P12.5). Then, these four hub lncRNAs were validated using two other independent datasets including GSE20916 (n = 145) and GSE39582 (n = 552). The results indicated that all hub lncRNAs were significantly negatively correlated with the three-stage colonic carcinogenesis, as well as TNM stages in COAD (one-way analysis of variance P < 0.05). Kaplan-Meier survival curve showed that patients with higher expression of each hub lncRNA had a significantly higher overall survival rate and lower relapse risk (log-rank P < 0.05). In conclusion, through co-expression analysis, we identified and validated four key lncRNAs in association with the carcinogenesis and progression of COAD, and these lncRNAs might have important clinical implications for improving the risk stratification, therapeutic decision and prognosis prediction in COAD patients.
