Higher serum ascorbic acid levels are associated with lower depression prevalence in US adults: a case-control study.

Background: Recent studies have shown that a higher intake of ascorbic acid was associated with a lower prevalence of depression. Nevertheless, the recall bias was common in dietary surveys in these studies, and it was ignored that there were differences in the absorption and utilization of ascorbic acid in the body. Hence, we aim to investigate the association between serum ascorbic acid levels and the prevalence of depression in US adults. Methods: A total of 3,404 participants from the 2017-2018 National Health and Nutrition Examination Survey (NHANES) that underwent measurement of the Patient Health Questionnaire-9 (PHQ-9) scores and serum levels of ascorbic acid. Propensity Score Matching (PSM) successfully established a case-control study, comprising 299 participants diagnosed with depression and 1,107 as controls. We used binary logistic regression to estimate odds ratios (ORs) and 95% confidence intervals (CIs) to explore associated risk factors for depression. Restricted cubic splines (RCS) were used to show the nonlinear relationship between serum ascorbic acid levels and the prevalence of depression. Results: The prevalence of depression was approximately 8.8%, with a median serum ascorbic acid level of 49.9 (36.0, 67.0) µmol/L. Results revealed that the serum ascorbic acid levels of depressed patients were significantly lower than those of non-depressed individuals (42.97 VS 52.97 µmol/L). The baseline data indicated that as serum ascorbic acid levels increased from Quartile 1 (Q1) to Quartile 4 (Q4), the depression prevalence decreased from 12.0 to 5.4% (p < 0.05). The results of the chi-square test after PSM showed that serum ascorbic acid was still statistically significant (p < 0.001) with the prevalence of depression. Forest plot showed that compared with the Q1 of serum ascorbic acid level, the OR and 95%CI of depression prevalence in Q4 was 0.42 (0.30 ~ 0.61), and the adjusted OR and 95%CI of depressive prevalence was 0.49 (0.33 ~ 0.73). RCS models showed an L-shaped nonlinear relationship (P for nonlinearity <0.05) between serum ascorbic acid and depression. Conclusion: Our results suggested that higher serum ascorbic acid levels are associated with a reduced prevalence of depression.

[Analysis the mechanism of cadmium-induced cytotoxicity in mouse testicular mesenchymal cells with miRNA transcriptomic].

OBJECTIVE: To analyze the mechanism of cadmium-induced cytotoxicity in mouse testicular mesenchymal cells(TM3) with transcriptome sequencing and bioinformatics techniques. METHODS: TM3 cells were selected as the cell model and divided into control group(no cadmium treatment) and cadmium-treated group(20 µmol/L CdCl_2). After 24 hours of administration, cells were harvested to extract total RNA, and then miRNA expression profiles were obtained by sequencing program after RNA quality detection. The fold change(FC) >2, P<0.05 was used as the standard to screen for differentially expressed miRNAs. The quantitative real-time polymerase chain reaction(qRT-PCR) was used to verify the differentially expressed miRNAs. Then, their target genes were predicted by miRanda software to construct miRNA-target gene interaction network, and their target genes were enriched by gene ontology(GO) and Kyoto encyclopedia of genes and genomes(KEGG) pathway function. RESULTS: A total of 26 differentially expressed miRNAs were identified which may be related to cadmium-induced TM3 cytotoxicity, including 19 up-regulated and 7 down-regulated miRNAs. The result of qRT-PCR were consistent with the miRNA sequencing result. Meanwhile, bioinformatics analysis result showed that the 26 differentially expressed miRNAs predicted 657 target genes. GO enrichment was mainly classified into biological regulation, metabolic process, protein binding and catalytic activity. KEGG pathway analysis showed that target genes were significantly involved in mitogen-activated protein kinase(MAPK) and tumor necrosis factor(TNF) signal pathways closely related to inflammatory response and apoptosis. CONCLUSION: Cadmium can lead to the differential expression of miRNAs in TM3 cells, and its target genes may be involved in Cd-induced TM3 cytotoxicity through signaling pathways such as MAPK and TNF.

Nano-selenium Alleviates Cadmium-Induced Mouse Leydig Cell Injury, via the Inhibition of Reactive Oxygen Species and the Restoration of Autophagic Flux.

Cadmium (Cd) is a well-known environmental pollutant that can contribute to male reproductive toxicity through oxidative stress. Nano-selenium (Nano-se) is an active single body of selenium with strong antioxidant properties and low toxicity. Some studies have addressed the potential ameliorative effect of Nano-se against Cd-induced testicular toxicity; however, the underlying mechanisms remain to be investigated. This study aimed to explore the protective effect of Nano-se on Cd-induced mouse testicular TM3 cell toxicity by regulating autophagy process. We showed that cadmium exposure to TM3 cells inhibited cell viability and elevated the level of reactive oxygen species (ROS) generation. Morphology observation by transmission electron microscope and the presence of mRFP-GFP-LC3 fluorescence puncta demonstrated that cadmium increased autophagosome formation and accumulation in TM3 cells, resulting in blocking the autophagic flux of TM3 cells. Meanwhile, cadmium remarkably increased the ratio of LC3-II to LC3-I protein expression (2.07 ± 0.31) and the Beclin-1 protein expression (1.97 ± 0.40) in TM3 cells (P < 0.01). Pretreatment with Nano-se significantly reduced Cd-induced TM3 cell toxicity (P < 0.01). Furthermore, Nano-se treatment reversed Cd-induced ROS production and autophagosome accumulation, and autophagy as evidenced by the ratio of LC3-II to LC3-I and Beclin-1 expression. In addition, ROS scavenger, N-acetyl-L-cysteine (NAC) or autophagy inhibitor, 3-methyladenine (3-MA) reversed cadmium-induced ROS generation, autophagosome accumulation, and autophagy-related protein expression levels, which confirmed that cadmium induced TM3 cell injury via ROS signal pathway and blockage of autophagic flux. Collectively, our results reveal that Nano-se attenuates Cd-induced TM3 cell toxicity through the inhibition of ROS production and the amelioration of autophagy disruption.

A Resilient Method for Visual-Inertial Fusion Based on Covariance Tuning.

To improve localization and pose precision of visual-inertial simultaneous localization and mapping (viSLAM) in complex scenarios, it is necessary to tune the weights of the visual and inertial inputs during sensor fusion. To this end, we propose a resilient viSLAM algorithm based on covariance tuning. During back-end optimization of the viSLAM process, the unit-weight root-mean-square error (RMSE) of the visual reprojection and IMU preintegration in each optimization is computed to construct a covariance tuning function, producing a new covariance matrix. This is used to perform another round of nonlinear optimization, effectively improving pose and localization precision without closed-loop detection. In the validation experiment, our algorithm outperformed the OKVIS, R-VIO, and VINS-Mono open-source viSLAM frameworks in pose and localization precision on the EuRoc dataset, at all difficulty levels.