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This study proposes a single-axis registration system based on monocular vision and CAD modelling without employing three-dimensional scanning or reconstruction techniques. The developed system uses dynamic modelling and image projection methods to estimate the single-axis rotation angle of an inspected workpiece. The estimated rotation angle of the inspected workpiece is achieved using the pose of the virtual model. Dynamic modelling significantly reduces both the data storage and computing time required to match the virtual model. Through experiments, we found that the average root-mean-square (RMS) error between the true centre location of special features within the inspected workpiece and those constructed within the virtual model was 2.19 pixels, and the RMS overlap rate was 96.44%. Thus, a monocular vision three-dimensional workpiece registration system with a dynamic model is effectively realised. [ABSTRACT FROM AUTHOR]

Despite its high prevalence, effective treatment for degenerative mitral regurgitation (MR) remains elusive. Although the mineralocorticoid-receptor antagonist spironolactone, in conjunction with renin-angiotensin system (RAS) inhibitors, has been shown to reduce mortality in patients with heart failure with reduced ejection fraction (HFrEF), its efficacy in managing degenerative MR is uncertain. In this study, we aimed to compare the effectiveness of valsartan (a renin-angiotensin system inhibitor), spironolactone, and combination therapy in mitigating MR-induced myocardial dysfunction. Using a mini-invasive model of degenerative MR, we administered valsartan (31 mg/kg/day), spironolactone (80 mg/kg/day), or a combination of both to rats over a 4-week period. Serial echocardiography and pressure-volume loops were utilized to assess cardiac function and hemodynamics. Rats with degenerative MR treated with valsartan or spironolactone alone did not show significant improvement in myocardial dysfunction. In contrast, combination therapy resulted in significant improvement. Similarly, the pressure-volume relationship was significantly improved in rats treated with the combination therapy compared to that in rats treated with a single therapy. Mechanistically, combination therapy effectively suppressed circulating and cardiac expression of aldosterone- and apoptosis-associated proteins. Overall, combination treatment with valsartan and spironolactone significantly attenuated the degenerative MR-induced myocardial stress and dysfunction, suggesting a potential therapeutic avenue for managing degenerative MR-induced HF., (Copyright © 2024 Wolters Kluwer Health, Inc. All rights reserved.)

Aberrant chondroitin sulfate (CS) accumulation in glioblastoma (GBM) tissue has been documented, but the role of excessive CS in GBM progression and whether it can be a druggable target are largely unknown. The aim of this study is to clarify the biological functions of CHST11 in GBM cells, and evaluate therapeutic effects of blocking CHST11-derived chondroitin 4-sulfate (C4S). We investigated the expression of CHST11 in glioma tissue by immunohistochemistry, and analyzed CHST11 associated genes using public RNA sequencing datasets. The effects of CHST11 on aggressive cell behaviors have been studied in vitro and in vivo . We demonstrated that CHST11 is frequently overexpressed in GBM tissue, promoting GBM cell mobility and modulating C4S on GBM cells. We further discovered that CSPG4 is positively correlated with CHST11, and CSPG4 involved in CHST11-mediated cell invasiveness. In addition, GBM patients with high expression of CHST11 and CSPG4 have a significantly shorter survival time. We examined the effects of treating C4S-specific binding peptide (C4Sp) as a therapeutic agent in vitro and in vivo . C4Sp treatment attenuated GBM cell invasiveness and, notably, improved survival rate of orthotopic glioma cell transplant mice. Our results propose a possible mechanism of CHST11 in regulating GBM malignancy and highlight a novel strategy for targeting aberrant chondroitin sulfate in GBM cells., Competing Interests: None., (AJCR Copyright © 2023.)

Liver cancers, such as hepatocellular carcinoma (HCC), are a highly prevalent cause of cancer-related deaths. Current treatments to combat liver cancer are limited. (-)-Agelasidine A, a compound isolated from the methanol extract of Agelas nakamurai , a sesquiterpene guanidine derived from sea sponge, has antibacterial activity. We demonstrated its anticancer capabilities by researching the associated mechanism of (-)-agelasidine A in human liver cancer cells. We found that (-)-agelasidine A significantly reduced viability in Hep3B and HepG2 cells, and we determined that apoptosis was involved in the (-)-agelasidine A-induced Hep3B cell deaths. (-)-Agelasidine A activated caspases 9, 8, and 3, as well as PARP. This effect was reversed by caspase inhibitors, suggesting caspase-mediated apoptosis in the (-)-agelasidine A-treated Hep3B cells. Moreover, the reduced mitochondrial membrane potential (MMP) and the release of cytochrome c indicated that the (-)-agelasidine A-mediated mitochondrial apoptosis was mechanistic. (-)-Agelasidine A also increased apoptosis-associated proteins (DR4, DR5, FAS), which are related to extrinsic pathways. These events were accompanied by an increase in Bim and Bax, proteins that promote apoptosis, and a decrease in the antiapoptotic protein, Bcl-2. Furthermore, our results presented that (-)-agelasidine A treatment bridged the intrinsic and extrinsic apoptotic pathways. Western blot analysis of Hep3B cells treated with (-)-agelasidine A showed that endoplasmic reticulum (ER) stress-related proteins (GRP78, phosphorylated PERK, phosphorylated eIF2α, ATF4, truncated ATF6, and CHOP) were upregulated. Moreover, 4-PBA, an ER stress inhibitor, could also abrogate (-)-agelasidine A-induced cell viability reduction, annexin V+ apoptosis, death receptor (DR4, DR5, FAS) expression, mitochondrial dysfunction, and cytochrome c release. In conclusion, by activating ER stress, (-)-agelasidine A induced the extrinsic and intrinsic apoptotic pathways of human HCC.

Alteration of extracellular glycosylation is a hallmark of malignant characteristics. In this study, we revealed that fucosyltransferase 8 (FUT8), an enzyme that mediates the core fucosylation of N-linked glycosylation, is an important regulator of malignant characteristics in human glioma that acts by modifying the activities of both the HGF receptor (MET) and epidermal growth factor receptor (EGFR). mRNA and protein expression levels of FUT8 were frequently upregulated in gliomas, and these events were showed positive correlations with advanced tumor grade, recurrence, and decreased overall survival. Silencing FUT8 expression in glioma cells suppressed cell growth, migration, and invasion, whereas overexpression of FUT8 was sufficient to enhance these phenotypes. Mechanistic investigations revealed that FUT8 was involved in the alteration of fucosylation status that was attached to MET and EGFR, changing MET responses after HGF stimulation, as well as in the transactivation of EGFR. Importantly, altering FUT8 expression or using the fucosylation inhibitor 2F-peracetyl-fucose sensitized the efficacy of of temozolomide (TMZ) therapy. Collectively, these results suggested that FUT8 dysregulation contributed to the malignant behaviors of glioma cells and provide novel insights into the significance of fucosylation in receptor tyrosine kinase activity and TMZ resistance., Competing Interests: None., (AJCR Copyright © 2021.)

Cytochrome P450 2E1 (CYP2E1) is involved in the metabolic activation of various carcinogens. CYP2E1 RsaI/PstI polymorphism has been identified in urologic cancer patients, while studies of the polymorphism have shown inconclusive trends in the risk of urologic cancers. Therefore, we performed this systematic review to provide a complete picture and conducted a meta-analysis to derive a precise estimation. We searched PubMed, Embase and Web of Science to identify eligible studies up to December 15, 2014. 12 studies with 2712 cases and 2977 controls were included in the meta-analysis.The odds ratio with a 95% confidence interval was used to assess the strength of associations. We observed that the c2 allele of CYP2E1 RsaI/PstI polymorphism was associated with a decreased risk of urologic cancer under all genetic models (c2 vs. c1: OR = 0.742, 95% CI = 0.659-0.835); c2c2 vs. c1c1: OR = 0.516, 95% CI = 0.357-0.745; c1c2 vs. c1c1: OR = 0.748, 95% CI = 0.748 (0.648-0.863; c2c2 + c1c2 vs. c1c1: OR = 0.722, 95% CI = 0.629-0.829; c2c2 vs. c1c1 + c1c2: OR = 0.578, 95% CI = 0.401-0.832). In the subgroup analysis by cancer type, statistically significant associations were found in urothelial cancer in all genetic models. When stratified by ethnicity, a same trend was also indicated in Asians in all genetic models.To conclude, our results support the conclusion that the CYP2E1 RsaI/PstI polymorphism may be associated with urologic cancer susceptibility. The c2 allele is a low-penetrance risk factor for urologic cancer development.