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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]

Incorporating consumer choice behavior into a product line design optimization model enhances the understanding of consumer choices and improves the opportunities to increase profit. Most product line optimization problems assume that parameters are precisely known in consumer choice model. However, the decision maker does not precisely know the model parameters because of insufficient sample data, measurement problems, and other factors. We investigate the problem of establishing robust product line pricing under a multinomial logit model to account for the uncertainty of the valuation parameter. First, we present a nominal product line model to maximize profit. We then establish a robust product line model to maximize the worst-case expected profit, where the valuation parameter lies in an uncertainty set. We consider both single and multiple products development and derive the optimal prices' closed-form expressions. Through numerical experiments, we illustrate the benefit of robust product line pricing to address parameter uncertainty. We demonstrate that the difference between the expected nominal profit and the worst-case profit increases with the increase of the interval of the uncertainty set, and the robust profit relative to the worst-case nominal profit improves. The robust product line design can ensure steadier, even higher profit. [ABSTRACT FROM AUTHOR]

The complex network effect of the product exhibits has a significant impact on the product line optimization design. The multinomial logit (MNL) model which is used to simulate consumer choice behavior is applied in most of product line optimization problems. However, its assumptions, independence of irrelevant alternatives (IIA) and the same Gumbel distribution of random error terms, are usually difficult to be met in practice. The marginal moment model (MMM) can be used when the mean and variance of consumer's utility error are known. The MMM not only has weak assumption conditions but also overcomes the IIA problem of MNL model. In this paper, we study the product pricing problem based on MMM with endogenous negative network effect. Firstly, we construct a variant of MMM considering network effect in product line optimization design. Secondly, we prove that the revenue function is concave in market share. We propose the solving methods of the model to obtain the optimal price, the corresponding market share, and the revenue under three different scenarios, i.e., developing single product, homogeneous products, and heterogeneous products. Finally, numerical experiments show that the proposed model can better simulate consumer choice behavior and potentially increase revenue. [ABSTRACT FROM AUTHOR]

Understanding biodiversity changes, along with its driving factors and mechanisms, is crucial in biogeography and community ecology. Beta diversity is an indicator for discerning the compositional variations among communities and is essential role in fostering a comprehensive understanding of the ecological processes shaping biodiversity distribution patterns. This study quantitatively evaluated the beta diversity of macroinvertebrates in the Wei River Basin, focusing on: (i) contributions of turnover and nestedness to taxonomic, functional, and phylogenetic total beta diversity, (ii) correlations between these beta diversity dimensions, and (iii) the influences of local, climatic, and spatial factors on beta diversity. We analyzed macroinvertebrate data from 51 sampling locations in the Wei River Basin and explored the relationships between different beta diversity dimensions using the Mantel test. Additionally, we assessed the relative influence of local, climatic, and spatial factors on beta diversity through distance-based redundancy analysis and variance partitioning methods. The results indicated that turnover predominantly affects taxonomic and phylogenetic beta diversity, while nestedness mainly drives functional beta diversity. Functional beta diversity was more weakly associated with the other dimensions. Local environmental factors significantly influenced taxonomic and phylogenetic beta diversity, whereas spatial factors had a stronger influence on functional beta diversity. Our findings highlight the need for conservation strategies to integrate taxonomic, functional, and phylogenetic dimensions, transcending traditional species-level approaches. [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]

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]