Objective: This study aims to evaluate the difference of palatal morphology between subjects with skeletal Class III and skeletal Class I in different vertical patterns using digital technology. Materials and Methods: In this study, 89 subjects with skeletal Class III (49 females, 40 males; 25.45±3.81 years) and 85 subjects with skeletal Class I (45 females, 40 males; 23.95±4.45 years) were collected retrospectively and divided into hyperdivergent, normodivergent and hypodivergent groups. Dolphin software was used to reorient the CBCT images of these subjects. After using ProPlan software to segment three-dimensional (3D) object of maxilla from the 3D skull, Geomagic Studio software was used to reconstruct 3D palatal morphology. The differences of 3D palatal morphology between different groups were compare by deviation patterns on 3D colored map analysis. Results: 3D colored map analysis showed the posterior part of male’s palate was higher and wider than that of female in skeletal Class III subjects. In skeletal Class III subjects, males with hyperdivergent had a higher and narrower palate compared with hypodivergent subjects, while females with hyperdivergent had a higher but no obvious narrower palate compared with hypodivergent subjects. In the similar vertical patterns, skeletal Class III subjects had a flatter but not narrower palate compared with skeletal Class I, along with a smaller palate volume. Conclusions: In skeletal Class III subjects, as the vertical dimension increased, the palate tended to be higher and narrower. Clinical Relevance: The influence of vertical patterns on the palatal morphology should be fully considered in the orthodontic and orthognathic treatment of skeletal Class III subjects.

Background Long interspersed nuclear element-1 (LINE-1 or L1) comprises 17% of the human genome. As the only autonomous and active retrotransposon, L1 plays an essential role in cancer initiation and progression. The studies of L1 in cancer mainly focus on the impact of L1 insertion into the new genome locus. The L1 5´ untranslated region (UTR) also contains antisense promoter (ASP) activity, generating L1-gene chimeric transcripts to a neighbor exon. Some of these ASP-driven genes have been reported to be overexpressed in cancer and promote cancer cell growth. However, little is known about overall expression patterns and the roles of L1 ASP-driven genes in human cancers.Results L1 ASP-driven genes were frequently dysregulated in cancer and associated with the cell cycle, the P13K/AKT pathway, and the GTPase signaling pathway. The expression of L1 ASP-driven genes was correlated with tumor patient prognosis. Hub L1 ASP-driven genes CENPU and MCM2 showed a correlation with immune infiltration, clinical T stage, and cancer stemness in pan-cancer. Knockdown of L1 ASP-driven gene LINC00491 resulted in a significant decrease in the ability of tumor growth and migration.Conclusions The expression of L1 ASP-driven genes is significantly dysregulated at the pan-cancer level, which is closely related to the tumor microenvironment and progression, as well as patient prognosis. Hub genes CENPU and MCM2 are expected to be new tumor diagnostic markers and therapeutic targets.

Atherosclerosis is the most common disease of the vascular system and the metabolic disorder is one of its important molecular mechanisms. SAP protein is found to be highly expressed in atherosclerotic blood vessels. Our previous study found that SAP deficiency can significantly inhibit the development of atherosclerosis. However, the regulatory effect of SAP deficiency on AS metabolism is unknown. Based on 1H-NMR metabonomics, this study investigated the serum metabolic changes in ApoE−/−;SAP−/− mice compared with ApoE−/− mice during the whole progression of atherosclerosis. The results showed that acetate, pyruvate, choline and VLDL + LDL were statistically regulated to the normal levels as in C57 mice by SAP deficiency in ApoE−/−;SAP−/− mice at 8 w (without obvious plaques). With the appearance and aggravation of atherosclerotic plaques (8 + 4 w and 8 + 8 w), the four metabolites of acetate, pyruvate, choline and VLDL + LDL were continuously regulated, which were denoted as the metabolic regulatory markers of SAP deficiency. We also found that the changes in these four metabolites had nothing to do with high-fat diet. Therefore, it was revealed that SAP deficiency regulated the metabolic disorders in ApoE−/− prior to the appearance of obvious atherosclerotic plaques, which is one of the important mechanisms leading to the inhibition of atherosclerosis, providing a new basis for the application of SAP in atherosclerosis.

Purpose: Disulfidptosis, a novel form of cell death triggered by disulfide stress, could have significant implications in breast cancer (BC) pathogenesis. Despite this, the identification of disulfidptosis-related lncRNAs in BC remains has not been reported. Therefore, this study aimed to examine the prognostic potential of disulfidptosis-associated lncRNAs in BC. Methods: RNA-seq data and clinical information of BC patients were obtained from the TCGA database. Co-expression analysis was performed to identify disulfidptosis-associated lncRNAs. Subsequently, a risk signature was developed through univariate Cox and LASSO analyses, and its predictive ability was validated. Additionally, the association between the risk signature and immune cell infiltration, immune function, tumor mutational burden (TMB）, and immune checkpoints was investigated. Finally, potential anticancer drugs associated with the risk signatures were predicted. Results: A 10-lncRNA signature was established to stratify BC patients into high-risk and low-risk groups, where the high-risk group showed an unfavorable prognosis. This signature served as an independent prognostic factor in BC patients. Notably, the two subgroups displayed distinct mutation gene profiles, and the risk score exhibited a significant correlation with TMB. Furthermore, ssGSEA and immune checkpoint analysis revealed a significant association between the predictive signature and the immune status of BC patients. Finally, 55 potential anticancer drugs associated with the signature were identified. CONCLUSIONS: We successfully established an independent prognostic signature of disulfidptosis-related lncRNAs in BC patients. This signature provides a solid basis for future investigations into the functional significance of disulfidptosis-associated lncRNAs in breast cancer.