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Amine-based CO2 capture technology suffers from great energy penalty drawbacks, hindering its industrial application. The large capture energy consumption primarily rests in the enthalpy irreversibility of the CO2 capture process where the reaction heat released in CO2-absorption is wasted but the same amount of CO2 reaction enthalpy is supplied to liberate CO2 in CO2-desorption. The present study proposes a new method of metal-ion-mediated amine regeneration (MMAR) that employs the metal–amine complexes as an internal energy buffer to tune the CO2 reaction enthalpy. Using Ni(II) metal ions, we performed experimental calorimetric measurements to provide direct evidence that Ni(II)-ion additives reduce the CO2 reaction enthalpy over the cyclic CO2 loading, i.e., from 89.1 kJ per mol CO2 to 78.5 kJ per mol CO2 in the benchmark MEA solvent (11.9% reduction), and further to 62.9 kJ per mol CO2 in the blended MEA/AMP solvent (29.4% reduction) at a Ni(II) concentration of 0.3 M. The decreased reaction heat is primarily attributed to the change in the reaction pathway from carbamate to bicarbonate formation, as well as the chemical heat buffer of the Ni(II)-MEA complex for enthalpy recovery and its in situ utilization. The reduced CO2 reaction heat contributed to a decreased regeneration energy from 128.3 kJ per mol to 101.5 kJ per mol CO2 in the blended MEA/AMP system, a 20.9% energy reduction as compared to the reference MEA. A comprehensive experimental investigation also revealed that the Ni(II)-ion additive has a negligible effect on cyclic CO2 capacity, absorption kinetics, and solvent viscosity, and more importantly, it has a marginal influence on solvent degradation. The new chemistry of the MMAR system is anticipated to provide the amine solvent system with tunable reaction enthalpy, enabling a better energy performance in amine-based CO2 capture. [ABSTRACT FROM AUTHOR]

Background: The main obstacle encountered in microarray technology is how to mine the valuable information under the profiles and study the genes function.Objective: Maximal information coefficient (MIC) is a novel, non-parametric statistic that has been successfully applied to genome-wide association studies and differentially gene and miRNA expression analysis. However, the data used in these applications are not gold standard but real data.Methods: Therefore, this study attempts to test the feasibility of MIC for differentially expressed gene identification with simulation data.Results: Our experiments indicate that, MIC perfermance is better than Limma always, which is almost the same level of SAM, ROTS or DESeq2. However, the count of AUC < 0.5 of MIC is significantly smaller than the three methods, and MIC does not exhibit an abnormal phenomenon in which the AUC increases as the noise increases.Conclusions: Compared to the existing methods, our experiments show that MIC is not only in the first tier in identifying differentially expressed genes and noise immunity, but also shows better robustness and stronger data/environment adaptability. [ABSTRACT FROM AUTHOR]

Objective: Long non‐coding RNA (lncRNA) has become an important regulator of many human malignancies. However, the biological role and clinical significance of most lncRNA in gastric cancer (GC) remain unclear. Methods: We investigate the biological function, mechanism of action and clinical expression of lncRNA MYOSLID in GC. First, we analysed the differential expression of lncRNA MYOSLID in GC tissues and non‐cancerous tissues by analysing the sequencing data obtained from The Cancer Genome Atlas. Subsequently, we verified that lncRNA MYOSLID regulates the proliferation and apoptosis of GC cells by acting as a ceRNA against miR‐29c‐3p. The nude mouse xenograft was used to further confirm the functional significance of lncRNA MYOSLID in vivo. Results: We found for the first time that the expression of lncRNA MYOSLID was significantly up‐regulated in GC tissues, and the up‐regulation of lncRNA MYOSLID in GC was correlated with tumour size, AJCC stage, depth of invasion and survival time. In addition, apoptosis and growth arrest can be induced in vitro after knockdown of lncRNA MYOSLID, which inhibits tumorigenesis in mouse xenografts in vivo. Further in‐depth studies revealed that lncRNA MYOSLID acts as a ceRNA of miR‐29c‐3p, resulting in de‐repression of its downstream target gene MCL‐1. Conclusion: The lncRNA MYOSLID‐miR‐29c‐3p‐MCL‐1 axis plays a key role in the development of GC. Our findings may provide potential new targets for the diagnosis and treatment of human GC. [ABSTRACT FROM AUTHOR]