[Baicalin induces ferroptosis in HepG2 cells by inhibiting ROS-mediated PI3K/Akt/FoxO3a signaling pathway].

This study aims to investigate whether baicalin induces ferroptosis in HepG2 cells and decipher the underlying mechanisms based on network pharmacology and cell experiments. HepG2 cells were cultured in vitro and the cell viability was detected by the cell counting kit-8(CCK-8). The transcriptome data of hepatocellular carcinoma were obtained from the Cancer Genome Atlas(TCGA), and the ferroptosis gene data from FerrDb V2. The DEG2 package was used to screen the differentially expressed genes(DEGs), and the common genes between DEGs and ferroptosis genes were selected as the target genes that mediate ferroptosis to regulate hepatocellular carcinoma progression. The functions and structures of the target genes were analyzed by Gene Ontology(GO) functional annotation and Kyoto Encyclopedia of Genes and Genomes(KEGG) pathway enrichment with the thresholds of P<0.05 and |log_2(fold change)|>0.5. DCFH-DA probe was used to detect the changes in the levels of cellular reactive oxygen species(ROS) in each group. The reduced glutathione(GSH) assay kit was used to measure the cellular GSH level, and Fe~(2+) assay kit to determine the Fe~(2+) level. Real-time quantitative PCR(RT-PCR) was employed to measure the mRNA levels of glutathione peroxidase 4(GPX4) and solute carrier family 7 member 11(SLC7A11) in each group. Western blot was employed to determine the protein levels of GPX4, SLC7A11, phosphatidylinositol 3-kinase(PI3K), p-PI3K, protein kinase B(Akt), p-Akt, forkhead box protein O3a(FoxO3a), and p-FoxO3a in each group. The results showed that treatment with 200 µmol·L~(-1) baicalin for 48 h significantly inhibited the viability of HepG2 cells. Ferroptosis in hepatocellular carcinoma could be regulated via the PI3K/Akt signaling pathway. The cell experiments showed that baicalin down-regulated the expression of SLC7A11 and GPX4, lowered the GSH level, and increased ROS accumulation and Fe~(2+) production in HepG2 cells. However, ferrostatin-1, an ferroptosis inhibitor, reduced baicalin-induced ROS accumulation, up-regulated the expression of SLC7A11 and GPX4, elevated the GSH level, and decreased PI3K, Akt, and FoxO3a phosphorylation. In summary, baicalin can induce ferroptosis in HepG2 cells by inhibiting the ROS-mediated PI3K/Akt/FoxO3a pathway.

Longitudinal trajectories of disability among Chinese adults: the role of cardiometabolic multimorbidity.

BACKGROUND: Cardiometabolic multimorbidity (CM) has been found to be associated with higher mortality and functional limitations. However, few studies have investigated the longitudinal association between CM and disability in the Chinese population and whether these associations vary by smoking status. METHODS: The study included 16,754 participants from four waves (2011, 2013, 2015, and 2018) of China Health and Retirement Longitudinal Study (CHARLS) (mean age: 59, female: 51%). CM was assesed at baseline and defined as having two or more of diabetes, stroke, or heart disease. Disability was repeatedly measured by summing the number of impaired activities of daily living (ADL) and instrumental activities of daily living (IADL) during the 7-year follow-up. Linear mixed-effects model was used to determine the association of CM and trajectories of disability and to assess the modification effect of smoking status in these associations. RESULTS: Participants with CM at baseline had a faster progression of disability compared to those without CM (CM: ß = 0.13, 95% CI: 0.05 to 0.21). Current smokers with CM developed disability faster than their counterparts (Pinteraction for smoking=0.011). In addition, there was a significant association between CM and the annual change of disability in current smokers (ß = 0.34, 95% CI: 0.17 to 0.50) while no such association was observed in current non-smokers (ß = 0.08, 95% CI: -0.02 to 0.17). CONCLUSION: CM was associated with more a rapid disability progression. Notably, being current smokers may amplify the adverse effects of CM on disability progression.

Mosquito swarm counting via attention-based multi-scale convolutional neural network.

Monitoring mosquito density to predict the risk of transmission of the virus and develop a response in advance is an important part of prevention efforts. This paper aims to estimate accurately the mosquito swarm count from a given image. To this end, we proposed an attention-based multi-scale mosquito swarm counting model that consists of the feature extraction network (FEN) and attention based multi-scale regression network (AMRN). The FEN uses VGG-16 network to extract low-level features of mosquitoes. The AMRN adopts a multi-scale convolutional neural network, and with a squeeze and excitation channel attention module in the branch with a 7 × 7 convolution kernel to extract high-level features, map the feature map to the mosquito swarm density map and estimate mosquitoes count. We collected and labelled a data set that includes 391 mosquito swarm images with 15,466 mosquitoes. Experiments show that our method performs well on the data set and achieves mean absolute error (MAE) of 1.810 and root mean square error (RMSE) of 3.467.

CircLATS2 Regulates miR-520a-3p/E2F7/p-VEGFR2 Signaling Pathway to Promote Hepatocellular Carcinoma Progression and Angiogenesis.

Objective: To investigate the effect of circLATS2 on the progression and angiogenesis of hepatocellular carcinoma and its molecular mechanism. Methods: The expression of circLATS2 in hepatocellular carcinoma was detected by qRT-PCR. The StarBase database was used to predict the potential miRNA, and the combination of the above was cytological verified by luciferase reporter gene assay and RNA pull down. The potential target genes of miRNA were predicted by TargetScan, verified by the above experiments, and the influence of circLATS2 on its expression was determined. The biological function of circLATS2 was investigated by in vitro and in vivo experiments. The effects of miRNA and target genes on the malignant behavior of HCC cells were determined by the reverse experiment. Results: circLATS2 was highly expressed in HCC and was positively correlated with tumor size and tumor stage. miR-520a-3p was sponged by circLATS2 and was low expressed in HCC tissues. As the target gene of miR-520a-3p, the expression level of E2F7 is affected by circLATS2. In vitro experiments showed that circLATS2 knockdown inhibited the proliferation, clone formation, migration, and invasion ability of hepatocellular carcinoma cells. In vivo knockdown of circLATS2 inhibits the proliferation of HCC cells, while overexpression of circLATS2 promotes the proliferation of HCC cells. Overexpression of miR-520a-3p and E2F7 knockdown reversed the role of circLATS2 in promoting malignant behavior of HCC cells and affected phosphorylation of VEGFR2. Conclusion: CircLATS2 promotes the progression of HCC by regulating miR-520a-3p/E2F7/P-VEGFR2 signaling pathway.

Core point pixel-level localization by fingerprint features in spatial domain.

Singular point detection is a primary step in fingerprint recognition, especially for fingerprint alignment and classification. But in present there are still some problems and challenges such as more false-positive singular points or inaccurate reference point localization. This paper proposes an accurate core point localization method based on spatial domain features of fingerprint images from a completely different viewpoint to improve the fingerprint core point displacement problem of singular point detection. The method first defines new fingerprint features, called furcation and confluence, to represent specific ridge/valley distribution in a core point area, and uses them to extract the innermost Curve of ridges. The summit of this Curve is regarded as the localization result. Furthermore, an approach for removing false Furcation and Confluence based on their correlations is developed to enhance the method robustness. Experimental results show that the proposed method achieves satisfactory core localization accuracy in a large number of samples.