Effect of Alkyl Chain Length on the Corrosion Inhibition Performance of Imidazolium-Based Ionic Liquids for Carbon Steel in 1 M HCl Solution: Experimental Evaluation and Theoretical Analysis.

In this study, five kinds of 1-alkyl-3-methylimidazolium bromide ([CXami]Br) ionic liquids with different alkyl chain lengths (8, 10, 12, 14, and 16) were selected as inhibitors. Then, their corrosion inhibition performances for Q235 steel in 1.0 mol L-1 HCl solution were investigated via a weight loss test, polarization curve method, and surface analysis techniques. The results show that these five imidazolium-based ionic liquids are all mixed-type inhibitors, and they can be spontaneously adsorbed onto the Q235 steel surface. The adsorption process follows the Langmuir model and involves mixed physical-chemical adsorption. Theoretical calculations confirm that the increase in alkyl chain length is conducive to the imidazolium-based ionic liquids exhibiting stronger chemical bonding abilities and forming denser adsorption films. The inhibition efficiency significantly increases below the critical micelle concentration (CMC) with an increase in alkyl chain length, and the highest inhibition efficiency is 95.17% for the [C16ami]Br inhibitor at the concentration of 0.005 mM. However, above the CMC, the inhibition efficiency is minimally affected by the alkyl chain length since all ionic liquid inhibitors have reached adsorption saturation on the steel surface.

Enhanced electromagnetic wave absorption properties of SiCN(Ni)/BN ceramics by in situ generated Ni and Ni3Si.

In this paper, the SiCN(Ni)/BN ceramic with excellent electromagnetic wave (EMW) absorption performance was successfully prepared. The Ni and Ni3Si were in situ formed by the introduction of nickel acetylacetonate (NA), which effectively improved the impedance matching performance of SiCN(Ni)/BN ceramics. The EMW absorption properties of the SiCN(Ni)/BN ceramics showed a trend of first increasing and then decreasing with the increase in content of NA. When the NA content reached 7 wt%, the impedance matching range of SiCN-7 was optimal. The minimum reflection loss (RLmin) of SiCN-7 reached -53.47 dB at 4.2 mm and the effective absorption bandwidth (EAB) was 2.32 GHz at 3.48 mm. Through the analysis of electrical conductivity, it was found that the proportion of polarization loss in dielectric loss was more than 99%. It is worth noting that the radar cross section (RCS) value of SiCN-7 absorber was lower than that of the perfect electrical conductor (PEC) plate in the range of -90-90°, and showed a larger coverage angle, indicating that it possessed a good practical application prospect in the field of electromagnetic wave absorption.

Metformin alleviates bevacizumab-induced vascular endothelial injury in mice through growth differentiation factor 15 upregulation.

Objectives: Bevacizumab is a commonly used anticancer drug in clinical practice, but it often leads to adverse reactions such as vascular endothelial damage, hypertension, arterial and venous thrombosis, and bleeding. This study investigated the protective effects of metformin against bevacizumab-induced vascular injury in a mouse model and examined the possible involvement of GDF15/PI3K/AKT/FOXO/PPARγ signaling in the effects. Materials and Methods: C57 male mice were purchased. To investigate metformin, the mice were assigned to the saline, bevacizumab (15 mg every 3 days), metformin (1200 mg/day), and bevacizumab+metformin groups. To investigate GDF15, the mice were assigned to the siNC+bevacizumab, siNC+bevacizumab+metformin, siGDF15+bevacizumab, and siGDF15+bevacizumab+metformin groups. Histological staining was used to evaluate vascular injury. Flow cytometry was used to evaluate apoptosis. ELISA was used to measure plasma endothelial injury markers and proinflammatory cytokines. qRT-PCR and western blot were used to determine the expression of GDF15 and PI3K/AKT/FOXO/PPARγ in aortic tissues. Results: Metformin alleviated bevacizumab-induced abdominal aortic injury, endothelial cell apoptosis, and systemic inflammation in mice (all P<0.05). Metformin up-regulated GDF15 expression and PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05). siGDF15 abolished the vascular protective and anti-inflammatory effects of metformin (all P<0.05). siGDF15 suppressed PI3K/AKT/FOXO/PPARγ signaling in the abdominal aorta of mice treated with bevacizumab (all P<0.05). Conclusion: Metformin attenuates bevacizumab-induced vascular endothelial injury, apoptosis, and systemic inflammation by activating GDF15/PI3K/AKT/FOXO/PPARγ signaling.