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Background: Anemia significantly contributes to the global disease burden, with its incidence potentially influenced by the trace metal content within the body. Objective: This study aims to examine the associations between trace metals and anemia risk, with a particular focus on investigating the potential mediating roles of iron status and inflammation in these associations. Methods: Five trace metals (Ni, Co, Mn, Se, and Mo) were examined in 1274 US adults, utilizing data from the National Health and Nutrition Examination Survey (NHANES) 2017–2020. The individual and combined effects of these metals on anemia were assessed using logistic regression, quantile g-computation (QGC), and Bayesian kernel machine regression (BKMR). A sex-stratified analysis was conducted to discern any gender-specific susceptibilities. Additionally, mediation analysis was employed to explore the potential mediating roles of iron status and inflammation in the associations between these metals and anemia. Results: Increased risks of anemia were positively associated with Co and Ni levels but negatively correlated with Se and Mn levels (all with p < 0.05). The trace metal mixture was negatively associated with anemia, with the highest weights of Co and Se in different directions in both the QGC and BKMR models. In the sex-specific analysis, we observed less pronounced protective effects from trace metals in females. Moreover, the mediating proportion of the iron status and inflammation in these relationships ranged from 10.29% to 58.18%. Conclusion: Our findings suggest that the trace element mixture was associated with decreased anemia risk, among which Se was a protective factor while Co was a risk factor, and females were more susceptible. The effects of these trace metals on anemia may be mediated by the iron status and inflammation. [ABSTRACT FROM AUTHOR]

This study sought to understand the effects of vitronectin (VTN) on the growth of SMMC-7721 hepatoma cells. In addition, this study examined how VTN inhibits the induction of apoptosis in SMMC-7721 cells by 3,3'-diindolylmethane (DIM),a metabolite of natural phytochemicals, and preliminarily investigated the signaling molecules involved in this process. A cell proliferation reagent was used to observe the effects of VTN on cell proliferation rates. Laser scanning confocal microscopy was performed to observe the effects of VTN on the morphology of tubulin, a component of the cytoskeleton. Flow cytometry and Western blotting assays were used to observe the inhibitory effects of VTN on DIM-induced apoptosis in SMMC-7721 cells and changes in the expression levels of the signaling molecules involved in this process. VTN promoted tumor cell growth in a concentration-dependent manner and inhibited apoptosis caused by the effects of apoptosis-inducing agents. Under in vitro experimental conditions, VTN contributed to the growth of SMMC-7721 hepatoma cells and protected them from the effects of an apoptosis-inducing agent. These findings suggest that during hepatocellular carcinogenesis, VTN may promote tumor cell growth and inhibit chemically induced apoptosis. Key words: vitronectin, hepatocellular carcinoma, apoptosis, caspase. Cette etude visait a comprendre les effets de la vitronectine (VTN) sur la croissance des cellules d'hepatome SMMC-7721. De plus, cette etude a examine comment la VTN inhibait l'induction de l'apoptose chez les cellules SMMC-7721 par le 3,3=diindolylmethane (DIM), un metabolite de composes phytochimiques naturels, et examine de fa^on preliminaire les molecules de signalisation impliquees dans ce processus. Un reactif de mesure de la proliferation cellulaire a ete utilise pour observer les effets de la VTN sur les taux de proliferation. La microscopie confocale par balayage au laser a ete utilisee afin d'observer les effets de la VTN sur la morphologie de la tubuline, une composante du cytosquelette. La cytometrie en flux et le buvardage Western ont ete utilises pour observer les effets inhibiteurs de la VTN sur l'apoptose des SMMC-7721 induite par le DIM ainsi que les changements dans les niveaux d'expression des molecules de signalisation impliquees dans ce processus. La VTN favorisait la croissance tumorale en fonction de la concentration et inhibait l'apoptose resultant des effets des reactifs inducteurs d'apoptose. En conditions experimentales in vitro, le VTN contribuait a la croissance des cellules d'hepatome SMMC-7721 et les protegeait des effets d'un agent inducteur de l'apoptose. Ces donnees suggerent que lors de la carcinogenese hepatocellulaire, la VTN peut promouvoir la croissance cellulaire et inhiber l'apoptose induite chimiquement. [Traduit par la Redaction] Mots-cles: vitronectine, carcinome hepatocellulaire, apoptose, caspase., Introduction Hepatocellular carcinoma (HCC) is a very common cancer recently linked to obesity-related nonalcoholic fatty liver disease (NAFLD), metabolic syndrome, and type-2 diabetes mellitus, and to a lesser extent, to [...]

Soft magnetic composite (SMC) material is formed by surface-insulated iron powder particles, generating unique properties like magnetic and thermal isotropy, and very low eddy currents. This paper presents the design and analysis of a high-speed claw pole motor with an SMC stator core for reducing core losses and cost. The analyses of magnetic and thermal fields are conducted based on a comprehensive understanding of the property of SMC materials. The 3-D finite-element analysis (FEA) is performed for accurate parameter calculation, design optimization, and thermal calculation. Because of the importance of core loss in high-speed motors, rotational core loss model is employed, and the core losses are coupled directly into thermal calculation by keeping the same hexahedral mesh structure between magnetic field analysis and thermal analysis. Since the rotor modal analysis is very important to high-speed motors, the natural frequencies and mode of the rotor are studied. Index Terms--Core losses, finite-element field analysis, high-speed motors, modal analysis, soft magnetic composite (SMC) materials, thermal analysis.

Excessive exposure to N,N‐dimethylformamide (DMF) can lead to occupational liver poisoning in workers; however, the underlying mechanism is not fully clarified. The importance of microRNAs (miRNAs) in chemical‐induced hepatotoxicity has been demonstrated. To determine whether miRNAs are also involved in DMF‐induced hepatotoxicity, we systematically analyzed the miRNA expression profiles in DMF‐treated (75 and 150 mm) HL‐7702 liver cells and controls by high‐throughput sequencing. Among the altered miRNAs, miR‐192‐5p was the most significantly upregulated in HL‐7702 cells after DMF exposure and was involved in DMF‐mediated cell apoptosis. By contrast, suppression of miR‐192‐5p in HL‐7702 cells attenuated the apoptosis induced by DMF. Furthermore, the anti‐apoptotic gene (NIN1/RPN12 binding protein 1 homolog [NOB1]) was predicted to be a potential miR‐192‐5p target according to bioinformatics analysis. The direct interaction between miR‐192‐5p and NOB1 was confirmed by the dual‐luciferase activity assay in HEK293FT cells. Overexpression of miR‐192‐5p efficiently reduced NOB1 mRNA and protein expression in HL‐7702 cells. Alteration in NOB1 expression influenced DMF‐induced hepatotoxicity by affecting hepatic apoptosis. In addition, the inverse correlation between miR‐192‐5p expression levels and NOB1 expression was further confirmed in DMF‐exposed mouse liver tissue samples. These observations demonstrated that promotion of apoptosis from the suppression of NOB1 by miR‐192‐5p overexpression was responsible for the DMF‐induced hepatotoxicity. This work provides the molecular mechanism at the miRNA level for hepatic apoptosis induced by DMF. DMF can lead to occupational liver poisoning. DMF exposure can result in the upregulation of miR‐192‐5p expression in HL‐7702 cells and liver tissue of ICR mice. The anti‐apoptotic gene NOB1 is the direct target of miR‐192‐5p. Our observations demonstrated that miR‐192‐5p was involved in DMF‐induced hepatocyte apoptosis by inhibiting the expression of NOB1. This work provides the molecular mechanism at the miRNA level for hepatic apoptosis induced by DMF. [ABSTRACT FROM AUTHOR]

Gene knockdown and knockout using RNAi and CRISPR/Cas9 allow for efficient evaluation of gene function, but it is unclear how the choice of technology can influence the results. To compare the phenotypes obtained using siRNA and CRISPR/Cas9 technologies, aldehyde dehydrogenase 2 (ALDH2) was selected as an example. In this study, we constructed one HepG2 cell line with a homozygous mutation in the fifth exon of ALDH2 (ALDH2-KO1 cell) using the eukaryotic CRISPR/Cas9 expression system followed by the limited dilution method and one HepG2 cell line with different mutations in the ALDH2 gene (ALDH2-KO2 cell) using the lentivirus CRISPR/Cas9 system. Additionally, one ALDH2-knockdown (KD) HepG2 cell line was created using siRNA. The reproducibility of these methods was further verified in the HEK293FT cell line. We found that the mRNA expression level of ALDH2 was significantly decreased and the protein expression level of ALDH2 was completely abolished in the ALDH2-KO cell lines, but not in ALDH2-KD cells. Furthermore, the functional activity of ALDH2 was also markedly disrupted in the two ALDH2-KO cell lines compared with ALDH2-KD and wild-type cells. The lack of ALDH2 expression mediated by CRIPSR/Cas9 resulted in a more dramatic increase in the cellular susceptibility to chemical-induced reactive oxygen species generation, cytotoxicity, apoptosis, and inflammation, especially at low concentrations compared with ALDH2-KD and WT cells. Therefore, we consider the gene knockout cell line created by CRISPR/Cas9 to be a more useful tool for identifying the function of a gene. [ABSTRACT FROM AUTHOR]

The identification of aberrant microRNA (miRNA) expression during chemical-induced hepatic dysfunction will lead to a better understanding of the substantial role of miRNAs in liver diseases. 1,2-Dichloroethane (1,2-DCE), a chlorinated organic toxicant, can lead to hepatic abnormalities in occupationally exposed populations. To explore whether aberrant miRNA expression is involved in liver abnormalities mediated by 1,2-DCE exposure, we examined alterations in miRNA expression patterns in the livers of NIH Swiss mice after dynamic inhalation exposure to 350 or 700 mg m-3 1,2-DCE for 28 days. Using a microarray chip, we discovered that only mmumiR-451a was significantly upregulated in the liver tissue of mice exposed to 700 mg m-3 1,2-DCE; this finding was validated by quantitative real-time polymerase chain reaction. In vitro study revealed that it was metabolite 2-chloroacetic acid, not 1,2-DCE that resulted in the upregulation of mmu-miR-451a in the mouse AML12 cell line. Furthermore, our data showed that the upregulation of mmu-miR-451a induced by 2-chloroacetic acid could suppress the expression of glycerol kinase and lead to the inhibition of glycerol gluconeogenesis in mouse liver tissue and AML12 cells. These observations provide evidence that hepatic mmu-miR-451a responds to 1,2-DCE exposure and might induce glucose metabolism disorders by suppressing the glycerol gluconeogenesis process. [ABSTRACT FROM AUTHOR]