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Because of the limitations of current PCB detection methods, such as low detection accuracy and high rate of false and missed detection, a PCB defect detection algorithm based on improved RetinaNet is proposed, that is, RetinaNet-line. Firstly, the algorithm uses PVT v2B2-Hi as the backbone network of the whole model, which can not only solve the deep feature redundancy caused by the residual network in RetinaNet but also improve the feature extraction ability of the network. Then, the CARAFE up-sampling module is used to enrich the semantic features of defective targets and promote the discrimination ability of the algorithm to defective targets. Finally, HSV color space is used to process the input feature image, and the color distribution is expanded by random perturbation in H, S, and V channels, with the data enhancement completed. In this paper, experiments are conducted on the publicly shared PCB defect detection dataset from the Intelligent Open Laboratory of Peking University, and the results show that the improved algorithm achieves 94.2% in the mAP index, which is better than other networks. [ABSTRACT FROM AUTHOR]

The causality between the urinary sodium–potassium ratio and upper urinary calculi has not been clarified and easily affected by confounders. We performed two-sample and multivariable Mendelian randomization (MR) analysis to evaluate the potential causal role of the urinary sodium–potassium ratio in upper urinary calculi. Data of the urinary sodium–potassium ratio (N = 326,938), upper urinary calculi (N = 337,199), and confounding factors including BMI (N = 336,107), ever-smoke (N = 461,066), hypertension (N = 218,754), diabetes (N = 218,792), and alcohol intake frequency (N = 462,346) were obtained from the IEU OpenGWAS Project database. The inverse-variance weighted (IVW), weighted median, and MR-Egger methods were used to estimate MR effects. The MR-Egger intercept test, Cochran's Q test, MR-PRESSO, leave-one-out method, and funnel plot were used for sensitivity analysis. A causal relationship was found between the urinary sodium–potassium ratio and upper urinary calculi (OR = 1.008, 95% CI = 1.002–1.013, P = 0.011). FinnGen data supported this conclusion (OR = 2.864, 95% CI = 1.235–6.641, P = 0.014). The multivariable Mendelian randomization analysis result showed that after adjusting for the effects of five confounders, the urinary sodium–potassium ratio was still positively correlated with upper urinary calculi (OR = 1.005, 95% CI = 1.001–1.009, P = 0.012). This study demonstrated a positive causal association between the urinary sodium–potassium ratio and upper urinary calculi using MR analysis. Timely identification of changes in urine composition and dietary regulation of sodium and potassium intake could greatly reduce the incidence of future urinary calculi. [ABSTRACT FROM AUTHOR]

Glioblastoma multiforme (GBM) is a malignant brain tumor with a poor prognosis. Aerobic glycolysis and an immunosuppressive microenvironment are potentially correlated with progression of GBM. However, the prognostic value of glycolysis–immune-related genes has not been studied in GBM. Using GBM-related data downloaded from Chinese Glioma Genome Atlas database, the overlapped differentially expressed genes were identified between the GBM patients with a different glycolysis status and immune score, which had also undergone functional enrichment. Univariate Cox regression analysis and LASSO (least absolute shrinkage and selection operator) Cox regression analysis were used for risk score construction. Multivariate Cox regression analysis and survival analysis determined the independent prognostic factors. We found 277 overlapped differentially expressed genes between high glycolysis and low glycolysis, a high immune score and low immune score, and a combination of low glycolysis status and a low immune score and high glycolysis status and a high immune score. These were significantly enriched in 301 gene otology terms and 25 Kyoto Encyclopedia of Genes and Genomes pathways. Of these, 8 genes were found to be optimal for building a risk score. The risk score was an independent prognostic factor for GBM patients, and patients with a high score had a worse prognosis. Moreover, between the high- and low-risk GBM patients, 17 types of immune cells were differentially infiltrated, and 5 immune checkpoints were differentially expressed. The glycolysis–immune-related risk score using CACNG2, CSMD3, GABRA3, KCNIP2, KSR2, PTPRT, TNFRSF12A, and TNR was able to predict the prognosis of GBM patients relatively reliably. [ABSTRACT FROM AUTHOR]

Background: Osteoarthritis is a chronic degenerative joint disease, and increasing evidences suggest that the pathogenic mechanism involves immune system and inflammation. Aims: The aim of current study was to uncover hub genes linked to immune infiltration in osteoarthritis synovial tissue using comprehensive bioinformatics analysis and experimental confirmation. Methods: Multiple microarray datasets (GSE55457, GSE55235, GSE12021 and GSE1919) for osteoarthritis in Gene Expression Omnibus database were downloaded for analysis. Differentially expressed genes (DEGs) were identified using Limma package in R software, and immune infiltration was evaluated by CIBERSORT algorithm. Then weighted gene co-expression network analysis (WGCNA) was performed to uncover immune infiltration-associated gene modules. Protein–protein interaction (PPI) network was constructed to select the hub genes, and the tissue distribution of these genes was analyzed using BioGPS database. Finally, the expression pattern of these genes was confirmed by RT-qPCR using clinical samples. Results: Totally 181 DEGs between osteoarthritis and normal control were screened. Macrophages, mast cells, memory CD4 T cells and B cells accounted for the majority of immune cell composition in synovial tissue. Osteoarthritis synovial showed high abundance of infiltrating resting mast cells, B cells memory and plasma cells. WGCNA screened 93 DEGs related to osteoarthritis immune infiltration. These genes were involved in TNF signaling pathway, IL-17 signaling pathway, response to steroid hormone, glucocorticoid and corticosteroid. Ten hub genes including MYC, JUN, DUSP1, NFKBIA, VEGFA, ATF3, IL-6, PTGS2, IL1B and SOCS3 were selected by using PPI network. Among them, four genes (MYC, JUN, DUSP1 and NFKBIA) specifically expressed in immune system were identified and clinical samples revealed consistent change of these four genes in synovial tissue retrieved from patients with osteoarthritis. Conclusion: A 4-gene-based diagnostic model was developed, which had well predictive performance in osteoarthritis. MYC, JUN, DUSP1 and NFKBIA might be biomarkers and potential therapeutic targets in osteoarthritis. [ABSTRACT FROM AUTHOR]

A Mediterranean-style diet (MED) can promote people lengthen the span of life and avoid atherosclerotic cardiovascular disease (ASCVD) in primary prevention. Metabolic syndrome (MetS) can significantly reduce life expectancy and increase the risk of ASCVD. However, few studies have focused on the role of the Mediterranean diet in patients with MetS. Participants in the National Health and Nutrition Examination Survey (NHANES) with MetS (N = 8301) from 2007 to 2018 were examined. A 9-point evaluation scorewas used to measure the degree of adherence to the MED diet. In order to compare the various levels of adherence to the MED diet and the effects of the specific MED diet components on all-cause and cardiovascular mortality, Cox regression models were utilized. Among the 8301 participants with MetS, about 13.0% (1080 of 8301) died after a median follow-up of 6.3 years. In this study, participants with MetS with adherence to high-quality and moderate-quality Mediterranean diet were significantly associated with lower all-cause mortality as well as cardiovascular mortality during the follow-up period. Futhermore, in joint analysis of the Mediterranean diet and sedentary behavior or depression, we found that high-quality or moderate-quality Mediterranean diet could attenuate, even reverse the adverse effects of sedentary behavior and depression on all-cause and cardiovascular mortality in participants with MetS. Among the components of the MED diet, greater intakes of vegetables, legumes, nuts and high MUFA/SFA ratio were significantly associated with lower all-cause mortality and greater vegetables intake was significantly associated with lower cardiovascular mortality, while more red/processed meat intake was significantly associated with higher cardiovascular mortality in participants with MetS. [ABSTRACT FROM AUTHOR]

Background: There is a bidirectional effect between sleep disorders and Mediterranean diet (MED), but the joint effect of MED and sleep disorders on mortality is unclear. The aim of this study was to investigate whether there is a synergistic effect of adherence to MED and sleep disorders on all-cause and cause-specific mortality. Methods: The study included 23,212 individuals in the National Health and Nutrition Examination Survey (NHANES) from 2005 to 2014. A 9-point evaluation score, alternative Mediterranean diet (aMED) index was used to assess adherence to MED. Sleep disorder and hours of sleep were assessed by structured questionnaires. Cox regression models were used to assess the relationship between sleep disorders, aMED and all-cause mortality, cause-specific mortality (cardiovascular-related death, cancer-related death). The interaction effect of sleep disorders with aMED on mortality was further assessed. Results: Results showed that participants with lower aMED and presence of sleep disorders had significantly higher risk of all-cause mortality and cardiovascular-related mortality (HR, 2.16, 95% CI, 1.49–3.13, P < 0.0001; HR, 2.68, 95% CI, 1.58–4.54, P = 0.0003). A significant interaction effect was found between aMED and sleep disorders on cardiovascular mortality (p for interaction = 0.033). No significant interaction existed between aMED and sleep disorders on all-cause mortality (p for interaction = 0.184) and cancer-related mortality (p for interaction = 0.955). Conclusions: Poorer adherence to MED and sleep disorders synergistically increased long-term all-cause mortality and cardiovascular mortality in NHANES population. [ABSTRACT FROM AUTHOR]

Parkinson's disease (PD) is characterized by both motor and non-motor symptoms, including hypokinesia, postural instability, dopaminergic (DA) neurons loss, and α-synuclein (α-syn) accumulation. A growing number of patients show negative responses towards the current therapies. Thus, preventative or disease-modifying treatment agents are worth to further research. In recent years, compounds extracted from natural sources become promising candidates to treat PD. Chlorogenic acid (CGA) is a phenolic compound appearing in coffee, honeysuckle, and eucommia that showed their potential as antioxidants and neuroprotectors. In this study, we investigated the anti-PD activity of CGA by testing its effect on 1-methyl-4-phenyl-1-1,2,3,6-tetrahydropyridine (MPTP) zebrafish model of PD. It was shown that CGA relieved MPTP-induced PD-like symptoms including DA neurons and blood vessel loss, locomotion reduction, and apoptosis events in brain. Moreover, CGA modulated the expression of PD- and autophagy-related genes (α -syn , lc3b , p62 , atg5 , atg7 , and ulk1b), showing its ability to promote the autophagy which was interrupted in the PD pathology. The unblocked effect of CGA on autophagy was further verified in 6-hydroxydopamine (6-OHDA)-modeled SHSY5Y cells. Our findings indicated that CGA might relieve PD by boosting the autophagy in neuronal cells that makes CGA a potential candidate for anti-PD treatment. [Display omitted] • CGA relieves PD-like symptoms in zebrafish PD model. • CGA regulates autophagy by affecting the expression of related genes. • CGA decreases the accumulation of LC3B in cellular PD model. • CGA plays a neuroprotective role in PD through boosting the autophagy. [ABSTRACT FROM AUTHOR]