Search

In this study, calibrated hot box and finite element simulation methods were used to study the influence of a slotted web on the thermal performance of a lightweight steel stud composite wall. By comparing the results from the simulations and experiments, the accuracy of the finite element method was verified; this method was then used for parameter analyses. The results showed that the wall's thermal transfer coefficient is inversely proportional to increases in the length of the slot and height of the stud web, leading to improvements in the thermal insulation effect; vice versa, the wall thermal transfer coefficient increases when the slot transverse spacing and stud thickness increase, and the insulation effect correspondingly worsens. The stud spacing influences the insulation performance of the wall by changing the proportion of studs within a certain wall. The greater the proportion of studs, the greater the stud thermal bridging, the faster the thermal loss, and the worse the insulation effect of the wall. In practice, the height of the stud web can be set as required. Preferably, for practical applications, the number of rows of slots is 5–7, the length of the slots is 70–80 mm, the transverse distance of the slots is 6–8 mm, the thickness of each stud is 1 or 1.2 mm, and the distance of each stud is 600 mm. [ABSTRACT FROM AUTHOR]

We will introduce four new geometric constants closely related to the James constant J (X) , which have symmetric structure, along with a discussion on the relationships among them and some other well-known geometric constants via several inequalities, together with the calculation of several values on some specific spaces. In addition, we will characterize geometric properties of J 1 (X) , such as uniform non-squareness and uniformly normal structure. [ABSTRACT FROM AUTHOR]

We will introduce some new geometric constants based on the constant H (X) proposed by Gao and the constant A 2 (X) proposed by M. Baronti et al. We first provide a study of a new constant M 1 (X) closely related to the midlines of equilateral triangles, including a discussion of some of its properties and the connections with other parameters of the sphere. Next, we focus on a new constant M 2 (X) and its generalized form M 2 (X , p , q) , along with some of their basic properties. Finally, we concentrate on a new constant M 3 (X) and discuss some of its properties. [ABSTRACT FROM AUTHOR]

Osteoarthritis (OA) is a type of arthritis that causes joint pain and limited mobility. In recent years, some studies have shown that the pathological process of OA chondrocytes is related to ferroptosis. Our study aims to identify and validate differentially expressed ferroptosis-related genes (DEFRGs) in OA chondrocytes and to investigate the potential molecular mechanisms. RNA-sequencing and microarray datasets were downloaded from Gene Expression Omnibus (GEO) data repository. Differentially expressed genes (DEGs) were screened by four methods: limma-voom, edgeR, DESeq2, and Wilcoxon rank-sum test. Weighted correlation network analysis (WGCNA), protein-protein interactions (PPI), and cytoHubba of Cytoscape were applied to identify hub genes. Clinical OA cartilage specimens were collected for quantitative reverse transcription-polymerase chain reaction (qRT-PCR) analysis, western blotting (WB), histological staining, transmission electron microscopy (TEM), and transfection. Sankey diagram was used to visualize the relationships between the expression level of SLC3A2 in the damaged area and clinical factors. Based on bioinformatics analysis, clinical factors, and experiment validation, SLC3A2 was identified as a hub gene. It was down-regulated in OA cartilage compared to normal cartilage (p < 0.05). Functional enrichment analysis revealed that SLC3A2 was associated with ferroptosis-related functions. Spearman correlation analysis showed that the expression level of SLC3A2 in the OA cartilage-damaged area was closely related to BMI, obesity grade, and Kellgren-Lawrence grade. Furthermore, in vitro experiments validated that SLC3A2 inhibited ferroptosis and suppressed cartilage degeneration in OA. In summary, we demonstrated that SLC3A2 inhibited ferroptosis and suppressed cartilage degeneration in OA. These findings provide a new idea for the study of the pathogenesis of OA, thus providing new means for the clinical diagnosis and targeted therapy of OA. [ABSTRACT FROM AUTHOR]