RESUMEN
We show here that attaching -NH2, -NHCH3, or -N(CH3)2 to ethylene oxide can dramatically reduce the CO2 cycloaddition barrier, from 69.5 kcal/mol (R = -H) down to 22.1 kcal/mol [R = -N(CH3)2], which may enable CO2 fixation under milder conditions without the help of catalysts. A joint analysis of local charges, frontier orbital energies, molecular electronegativity, and partial electron transfer explains how these substituents facilitate CO2 cycloaddition to ethylene oxide. The distortion/interaction-activation strain model (D/I-ASM) simulation reveals that the computed low reaction barrier results from the decreased activation strain energy and increased intermolecular interaction energy in the transition state. Density functional theory calculations show that -N(CH3)2-monosubstituted ethylene oxide (NEO) can greatly lower the energy threshold for CO2 sequestration. NEO can also work with the common organic catalyst 1,5,7-triazabicyclo[4.4.0]dec-5-ene (TBD) that assists CO2 for further conversion into dimethyl carbonate (via alcoholysis) and N,N'-dimethylurea (via ammonolysis) with maximal barrier heights as low as 24.2 and 21.9 kcal/mol, respectively. The facile coupling of NEO with CO2 and the undemanding alcoholysis/ammonolysis of NCC with TBD would promise the inclusion of amino functionalities to small-molecule-based epoxides, or polymeric epoxy resins, in the fixation and further economic conversions of CO2.
RESUMEN
The abuse of adamantanamine (ADA) and its derivatives as veterinary drugs in the poultry industry could cause severe health problems for humans. It is of great need to develop a rapid, cheap and ultrasensitive method for ADA detection. In this study, a sensitive conical nanochannel sensor was established for the rapid quantitative detection of ADA with the distinctive design of the host-guest competition. The sensor was constructed by functionalizing the nanochannel surface with p-toluidine and was then assembled with Cucurbit [7]uril (CB [7]). When ADA is added, it could occupy the cavity of CB [7] due to the host-guest competition and makes CB [7] to release from the CB [7]-p-toluidine complex, resulting in a distinct change of hydrophobicity of the nanochannel, which could be determined by the ionic current. Under the optimal conditions, the strategy permitted sensitive detection of ADA in a linear range of 10-1000 nM. The nanochannel based ADA sensing platform showed both high sensitivity and excellent reproducibility and the limit of detection was 4.54 nM. For the first time, the rapid and sensitive recognition of an illegal medicine was realized based on the host-guest competition method with the nanochannel system and the principle and feasibility of this method were described at length. This strategy provides a simple, reliable, and effective way to apply host-guest system in the development of nanochannel sensor for small-molecule drug detection.
RESUMEN
Interleukin 6 (IL-6) was abundant in the tumor microenvironment and played potential roles in tumor progression. In our study, the expression of IL-6 in tumor tissues from 36 gastric cancer (GC) patients was significantly higher than in non-tumor tissues. Moreover, the number of CD163+CD206+ M2 macrophages that infiltrated in tumor tissues was significantly greater than those infiltrated in non-tumor tissues. The frequencies of M2 macrophages were positively correlated with the IL-6 expression in GC tumors. We also found that IL-6 could induce normal macrophages to differentiate into M2 macrophages with higher IL-10 and TGF-ß expression, and lower IL-12 expression, via activating STAT3 phosphorylation. Accordingly, knocking down STAT3 using small interfering RNA decreased the expression of M2 macrophages-related cytokines (IL-10 and TGF-ß). Furthermore, supernatants from IL-6-induced M2 macrophages promote GC cell proliferation and migration. Moreover, IL-6 production and CD163+CD206+ M2 macrophage infiltration in tumors were associated with disease progression and reduced GC patient survival. In conclusion, our data indicate that IL-6 induces M2 macrophage differentiation (IL-10highTGF-ßhighIL-12 p35low ) by activating STAT3 phosphorylation, and the IL-6-induced M2 macrophages exert a pro-tumor function by promoting GC cell proliferation and migration.
