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Aluminum nanoparticles (nAl) have received sustained interest due to their higher reactivity than micron aluminum particles (mAl). However, in practice, the densities of explosive formulations with nAl are far smaller than those with mAl, which greatly undercuts the energy release performance. To take advantages of both kinds of Al particles, in situ integration of mAl@nAl composites was proposed and evaluated. The mAl@nAl composites were prepared by in situ electrical explosion of Al wire. Their morphology, density, and specific surface area (SSA) were characterized by scanning electron microscope (SEM), densimetry, and Brunauer–Emmett–Teller (BET), respectively. SEM showed that nAl uniformly adhered to the surface of mAl. With the increase in voltage, the average diameter and density of the composites decreased, but the SSA of the composites increased. And the largest density of the composites was 1.13 g/cm3, comparable to that of the commercial graded Al product (1.25 g/cm3). Meanwhile, the highest SSA of the composites was 12.1192 m2/g. In addition, the combustion efficiency of mAl@nAl composites at 20 kV was 8.26% higher than that of physically graded counterparts. The constant-volume combustion test under zero oxygen balance revealed that the pressurization rate and peak pressure of mAl@nAl composites prepared at 20 kV were the highest of all. Furthermore, constant-volume combustion under constant heat showed that the combustion temperatures of mAl@nAl composites were 1.15–1.45 times higher than those of physically graded counterparts. Finally, the ignition delay of mAl@nAl composites was reduced with the increase in explosion voltage. [ABSTRACT FROM AUTHOR]

Objective: CD147 is an important glycoprotein that participates in the progression of diverse cancers. This study aims to explore the specific function of CD147 in lung adenocarcinoma (LUAD) and to reveal related downstream molecular mechanisms. Methods: Followed by silencing of CD147, the viability, migration, invasion, and apoptosis of LUAD cells were measured by CCK8, wound healing, transwell assay, and flow cytometer, respectively. The expression of CD147 and two markers of lipid metabolism (FASN and ACOX1) were detected by qRT-PCR. A xenograft tumor model was constructed to investigate the function of CD147 in vivo. Then transcriptome sequencing was performed to explore the potential mechanisms. After measuring the expression of Rap1 and p-p38 MAPK/p38 MAPK by western blot, the changes of CD147 and lipid metabolism markers (FASN, ACOX1) was detected by Immunohistochemistry. Moreover, a Rap1 activator and a Rap1 inhibitor were applied for feedback functional experiments. Results: CD147 was up-regulated in LUAD cells, and its silencing inhibited cell proliferation, migration, invasion, lipid metabolism dysregulation and promoted apoptosis, while overexpression of CD147 showed the opposite results. Silencing of CD147 also inhibited the growth of tumor xenografts in mice. Transcriptome sequencing revealed 834 up-regulated differentially expressed genes (DEGs) and 602 down-regulated DEGs. After functional enrichment, the Rap1 signaling pathway was selected as a potential target, which was then verified to be blocked by CD147 silencing. In addition, the treatment of Rap1 activator weakened the inhibiting effects of si-CD147 on the proliferation, migration, invasion, and lipid metabolism in LUAD cells, while the intervention of RAP1 inhibitor showed the opposite results. Conclusions: Silencing of CD147 inhibited the proliferation, migration, invasion, lipid metabolism dysregulation and promoted apoptosis of LUAD cells through blocking the Rap1 signaling pathway. [ABSTRACT FROM AUTHOR]

This correction notice addresses an error in the original article titled "Silencing of CD147 inhibits cell proliferation, migration, invasion, lipid metabolism dysregulation and promotes apoptosis in lung adenocarcinoma via blocking the Rap1 signaling pathway." The authors identified that Figures 1 and 2 were inadvertently swapped. The correction provides the correct figures and captions, and assures readers that the corrections do not alter the interpretations or validity of the research. The error does not significantly impact the overall findings and conclusions of the paper. [Extracted from the article]