Haoyu Tian

Longitudinal T-shaped finned tubes are important heat-transfer components in spacecraft thermal control systems, and their forming accuracy and quality during bending have a significant influence on heat-transfer efficiency. Therefore, the analysis and control of nonuniform sectional deformation and nonlinear springback are essential for precision forming. In this study, a semi-analytical springback correction model coupling neutral-axis shift and equivalent unloading modulus degradation was proposed based on axial force equilibrium and sectional stress integration. Based on numerical simulations and experiments, the relationship between free-bending die eccentricity and formed curvature was established, and the effects of forming radius and bending angle on springback were analyzed. The results show that the formed curvature increases approximately linearly with die eccentricity, the radius springback increases with forming radius, and the springback angle first increases and then decreases with increasing bending angle. The constant-modulus model systematically underestimated springback, whereas the equivalent unloading modulus correction improved agreement with experimental measurements. Furthermore, a coupled angle-curvature inverse compensation method was proposed to determine the pre-compensated forming radius, free-bending die eccentricity, and over-bending angle from the target geometry. After compensation, the forming accuracy reached ±0.28° for bending angle and ±0.33 mm for bending radius, compared with ±3.16° and ±2.51 mm before compensation, respectively. The proposed coupled prediction-compensation framework provides an effective approach for precision free bending of longitudinal T-shaped finned tubes.

A publicly accessible online database was utilized in this study to investigate COMP, which is aberrantly expressed in a range of malignancies. It was discovered that colorectal cancer had significant levels of COMP expression. This finding was corroborated by Western Blot and RT-qPCR analysis tests on colorectal cancer cell lines. In order to study the effect of COMP on colorectal cancer migration, we investigated the expression of mRNA and protein levels in colorectal cancer cell lines knocked down by COMP, and the effect of COMP on the migration of SW480 cell line was studied using Transwell, wound healing assay. The findings demonstrated that the migration of colorectal cancer cell lines was suppressed by COMP expression knockdown. These findings offer a theoretical foundation for the use of COMP as a novel clinical treatment target and possible marker for the identification of colorectal cancer metastases.

Cervical cancer is a disease that develops from an abnormal proliferation of cervical tissue to a malignant tumor. The primary etiological factor in the development of cervical cancer is the infection with high-risk human papillomavirus (HPV), particularly the HPV types 16 and 18. Cholesterol is an essential component of cell membranes and an important substance for cell signaling. DHCR24, also known as 24-dehydrocholesterol reductase, is a gene that encodes a flavin adenine dinucleotide (FAD)-dependent oxidoreductase. DHCR24 is involved in cholesterol synthesis through the enzymes it encodes, which in turn affects lipid metabolism and various pathophysiological processes. Studies have demonstrated that variants in the DHCR24 gene can result in the rare syndrome of multiple tissue congenital anomalies. In this study, we employed informatics analysis to investigate the role of DHCR24 in the development and prognosis of cervical cancer. The transcriptional profiles of DHCR24 were evaluated in pan-cancer and cervical cancer, respectively, using the online website TIMER. We evaluated the overexpression of DHCR24 mRNA in cervical cancer and 18 other cancers. Gene set enrichment analysis (GSEA) demonstrated that DHCR24 is associated with cell cycle and tumor cell adhesion molecules. Furthermore, the expression of DHCR24 may be related to the proliferation and migration of cervical cancer cells, as well as the stem cell capacity of the tumor cells. To verify these findings, we constructed normal cervical cancer cells and DHCR24 knockdown cells and performed scratch and cell cloning experiments. Subsequently, the relationship between DHCR24 expression level and immune cell infiltration was analyzed using XIANTAO and TIMER tools. The findings indicated that the upregulation of DHCR24 was negatively correlated with the majority of immune infiltrating cells. The findings of this study indicate that DHCR24 may be associated with the progression of cervical cancer and may serve as a potential marker for the diagnosis of cervical cancer.

Increasing evidence suggests that RHBDD2 is involved in the development and progression of a variety of tumors, but its role in colorectal adenocarcinoma (COAD) remains unclear. Therefore, the aim of our study was to investigate the exact role of RHBDD2 in COAD. The expression levels of RHBDD2 in COAD were analyzed based on The Cancer Genome Atlas (TCGA) database. Survival analysis of RHBDD2 in COAD was analyzed using the TCGA dataset. In addition, the functional role of RHBDD2 was detected by GO, KEGG, and immune infiltration analysis. The results showed that RHBDD2 was significantly upregulated in COAD samples. High RHBDD2 expression in COAD was significantly correlated with T, N, and M stages and pathological stage. Elevated RHBDD2 expression was unfavorable for overall survival (OS), progression-free interval (PFI), and disease-specific survival (DSS). Receiver operating characteristic (ROC) analysis showed that RHBDD2 may serve as a potential diagnostic biomarker for COAD patients. In addition, RHBDD2 was significantly correlated with the level of immune cell infiltration. The current study suggests that elevated RHBDD2 expression is closely associated with poor prognosis and immune cell infiltration in COAD, and may serve as a promising independent prognostic biomarker and potential therapeutic target.