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This paper conducts an analysis of the site selection methods for power grid material distribution centers. It proposes the fundamental principles for site selection and organizes and compares representative models and commonly used methods in site selection issues. Taking the establishment and solving process of the site selection model for power grid material distribution centers as an example, the specific methods and procedures of Sparrow Search Algorithm applied to site selection problems are explained, and analyzes the shortcomings of this method. Finally, building upon the comparison and summary of simulated annealing algorithm and Sparrow Search Algorithm in the preceding sections, this paper combines their strengths to propose an approach for optimizing the solution method that is, using the former to update the iterative optimal solution of the latter, in order to reduce the risk of falling into local optimization, enhance the accuracy of problem-solving, and improve distribution efficiency. This contributes as a reference for similar site planning and decision-making processes.

Longitudinal optical field modulation is of critical importance in a wide range of applications, including optical imaging, spectroscopy, and optical manipulation. However, it remains a considerable challenge to realize a uniformly distributed light field with extended depth-of-focus. Here, a high-efficiency extended depth-of-focus metalens is proposed by adjoint-based topology-shape optimization approach, wherein the theoretical electric field intensity corresponding to a variable focal-length phase is utilized as the figure of merit. Using a dozen of metalens with random structure parameters as initial structures, the average focal depth of topology-shape optimized metalens is greatly improved up to 18.80 μm (about 29.7λ), which is 1.54 times higher than the diffraction-limited focal depth. Moreover, all the topology-shape optimized metalens exhibit high diffraction efficiency exceeding 0.7 over the whole focal depth range, which is approximately three times greater than that of the forward design. Our results offer a new insight into the design of extended depth-of-focus metalens and may find potential applications in imaging, holography, and optical fabrication.

Summary: Plant leaf senescence, caused by multiple internal and environmental factors, has an important impact on agricultural production. The lectin receptor‐like kinase (LecRLK) family members participate in plant development and responses to biotic and abiotic stresses, but their roles in regulating leaf senescence remain elusive. Here, we identify and characterize a rice premature withered leaf 1 (pwl1) mutant, which exhibits premature leaf senescence throughout the plant life cycle. The pwl1 mutant displayed withered and whitish leaf tips, decreased chlorophyll content, and accelerated chloroplast degradation. Map‐based cloning revealed an amino acid substitution (Gly412Arg) in LOC_Os03g62180 (PWL1) was responsible for the phenotypes of pwl1. The expression of PWL1 was detected in all tissues, but predominantly in tillering and mature leaves. PWL1 encodes a G‐type LecRLK with active kinase and autophosphorylation activities. PWL1 is localized to the plasma membrane and can self‐associate, mainly mediated by the plasminogen‐apple‐nematode (PAN) domain. Substitution of the PAN domain significantly diminished the self‐interaction of PWL1. Moreover, the pwl1 mutant showed enhanced reactive oxygen species (ROS) accumulation, cell death, and severe DNA fragmentation. RNA sequencing analysis revealed that PWL1 was involved in the regulation of multiple biological processes, like carbon metabolism, ribosome, and peroxisome pathways. Meanwhile, interfering of biological processes induced by the PWL1 mutation also enhanced heat sensitivity and resistance to bacterial blight and bacterial leaf streak with excessive accumulation of ROS and impaired chloroplast development in rice. Natural variation analysis indicated more variations in indica varieties, and the vast majority of japonica varieties harbour the PWL1Hap1 allele. Together, our results suggest that PWL1, a member of LecRLKs, exerts multiple roles in regulating plant growth and development, heat‐tolerance, and resistance to bacterial pathogens. [ABSTRACT FROM AUTHOR]

N6‐methyladenosine (m6A) modification has been implicated in the progression of obesity and metabolic diseases. However, its impact on beige fat biology is not well understood. Here, via m6A‐sequencing and RNA‐sequencing, this work reports that upon beige adipocytes activation, glycolytic genes undergo major events of m6A modification and transcriptional activation. Genetic ablation of m6A writer Mettl3 in fat tissues reveals that Mettl3 deficiency in mature beige adipocytes leads to suppressed glycolytic capability and thermogenesis, as well as reduced preadipocytes proliferation via glycolytic product lactate. In addition, specific modulation of Mettl3 in beige fat via AAV delivery demonstrates consistently Mettl3's role in glucose metabolism, thermogenesis, and beige fat hyperplasia. Mechanistically, Mettl3 and m6A reader Igf2bp2 control mRNA stability of key glycolytic genes in beige adipocytes. Overall, these findings highlight the significance of m6A on fat biology and systemic energy homeostasis. [ABSTRACT FROM AUTHOR]

N6-methyladenosine (m 6 A) modification has been implicated in the progression of obesity and metabolic diseases. However, its impact on beige fat biology is not well understood. Here, via m 6 A-sequencing and RNA-sequencing, this work reports that upon beige adipocytes activation, glycolytic genes undergo major events of m 6 A modification and transcriptional activation. Genetic ablation of m 6 A writer Mettl3 in fat tissues reveals that Mettl3 deficiency in mature beige adipocytes leads to suppressed glycolytic capability and thermogenesis, as well as reduced preadipocytes proliferation via glycolytic product lactate. In addition, specific modulation of Mettl3 in beige fat via AAV delivery demonstrates consistently Mettl3's role in glucose metabolism, thermogenesis, and beige fat hyperplasia. Mechanistically, Mettl3 and m 6 A reader Igf2bp2 control mRNA stability of key glycolytic genes in beige adipocytes. Overall, these findings highlight the significance of m 6 A on fat biology and systemic energy homeostasis., (© 2023 The Authors. Advanced Science published by Wiley-VCH GmbH.)

Objective: To investigate the effect of Golgi phosphoprotein 3 (Golph3) on paclitaxel- induced apoptosis and autophagy in HeLa cells., Methods: HeLa cells were transfected with a lentiviral vector expressing Golph3 or a small interfering RNA (siRNA) targeting Golph3 for up-regulation or down-regulation of Golph3 which was verified by Western blotting. The autophagic bodies in the cells were observed using transmission electron microscopy. The expression of autophagy markers p62 and LC3 were detected using Western blotting, and the cell apoptosis was examined by PI/Anexin V-FITC double staining and flow cytometry. The effects of blocking autophagy was evaluated by treatment of the cells with the autophagy inhibitor 3-MA., Results: Transmission electron microscopy showed that the lentivirus-mediated overexpression of Golph3 significantly increased the number of autophagic bodies and interference of Golph3 expression significantly decreased autophagic bodies in HeLa cells. Western blotting showed that Golph3 overexpression caused an increased expression of LC3 and decreased the accumulation of p62 in the cells, and interference of Golph3 resulted in the reverse changes. The cell apoptosis induced by paclitaxel was significantly decreased in Golph3-overexpressing HeLa cells and increased in the cells with Golph3 knockdown ( P >0.01). Treatment with 3-MA alone did not obviously affect HeLa cell apoptosis, but in cells with Golph3 knockdown, 3-MA significantly enhanced paclitaxel-induced apoptosis ( P >0.01)., Conclusions: Up-regulation of Golph3 promotes autophagy and inhibits paclitaxel-induced apoptosis, whereas suppression of Golph3 inhibits autophagy and enhances paclitaxel- induced apoptosis in HeLa cells.