The aim of this study was to analyze the differences in gut microbiota between selenium deficiency and T-2 toxin intervention rats. Knee joint and fecal samples of rats were collected. The pathological characteristics of knee cartilage were observed by safranin O/fast green staining. DNA was extracted from fecal samples for PCR amplification, and 16S rDNA sequencing was performed to compare the gut microbiota of rats. At the phylum level, Firmicutes (81.39% vs. 77.06%) and Bacteroidetes (11.11% vs. 14.85%) were dominant in the Se-deficient (SD) group and T-2 exposure (T-2) groups. At the genus level, the relative abundance of Ruminococcus_1 (12.62%) and Ruminococcaceae_UCG-005 (10.31%) in the SD group were higher. In the T-2 group, the relative abundance of Lactobacillus (11.71%) and Ruminococcaceae_UCG-005 (9.26%) were higher. At the species level, the high-quality bacteria in the SD group was Ruminococcus_1_unclassified, and Ruminococcaceae_UCG-005_unclassified in the T-2 group. Lactobacillus_sp__L_YJ and Lactobacillus_crispatus were the most significant biomarkers in the T-2 group. This study analyzed the different compositions of gut microbiota in rats induced by selenium deficiency and T-2 toxin, and revealed the changes in gut microbiota, so as to provide a certain basis for promoting the study of the pathogenesis of Kashin–Beck disease (KBD).

Chondropathies are a group of cartilage diseases, which share some common pathogenetic features. The etiology of chondropathies is still largely obscure now. A transcriptome-wide association study (TWAS) was performed using the UK Biobank genome-wide association study (GWAS) data of chondropathies (including 1314 chondropathy patients and 450,950 controls) with gene expression references of muscle skeleton (MS) and peripheral blood (YBL). The candidate genes identified by TWAS were further compared with three gene expression profiles of osteoarthritis (OA), cartilage tumor (CT), and spinal disc herniation (SDH), to confirm the functional relevance between the chondropathies and the candidate genes identified by TWAS. Functional mapping and annotation (FUMA) was used for the gene ontology enrichment analyses. Immunohistochemistry (IHC) was conducted to validate the accuracy of integrative analysis results. Integrating TWAS and mRNA expression profiles detected 84 candidate genes for knee OA, such as DDX20 (PTWAS YBL = 1.79 × 10− 3, fold change (FC) = 2.69), 10 candidate genes for CT, such as SRGN (PTWAS YBL = 1.46 × 10− 3, FC = 3.36), and 4 candidate genes for SDH, such as SUPV3L1 (PTWAS YBL = 3.59 × 10− 3, FC = 3.22). Gene set enrichment analysis detected 73 GO terms for knee OA, 3 GO terms for CT, and 1 GO term for SDH, such as mitochondrial protein complex (P = 7.31 × 10− 5) for knee OA, cytokine for CT (P = 1.13 × 10− 4), and ion binding for SDH (P = 3.55 × 10− 4). IHC confirmed that the protein expression level of DDX20 was significantly different between knee OA cartilage and healthy control cartilage (P = 0.0358). Multiple candidate genes and GO terms were detected for chondropathies. Our findings may provide a novel insight in the molecular mechanisms of chondropathies.

Kashin-Beck disease (KBD) is a serious human endemic chronic osteochondral disease. However, quantitative syntheses of X-ray detective rate studies for KBD are rare. We performed an initial systematic review and meta-analysis to assess the X-ray detective rate of KBD in China. For this systematic review and meta-analysis, we searched five databases (PubMed, Web of Science, Chinese National Knowledge Infrastructure (CNKI), WanFang Data and the China Science and Technology Journal Database (VIP))using a comprehensive search strategy to identify studies of KBD X-ray detective rate in China that were published from database inception to January 13, 2018. The X-ray detective rate of KBD was determined via an analysis of published studies using a random effect meta-analysis with the proportions approach. Subgroup analysis and meta-regression were used to explore heterogeneity, and study quality was assessed using the risk of bias tool. A total of 53 studies involving 14,039 samples with X-ray detective rate in 163,340 observations in total were included in this meta-analysis. These studies were geographically diverse (3 endemic areas). The pooled overall X-ray detective rate for KBD was 11% (95%CI,8–15%;Z = 13.14; p < 0.001). The pooled X-ray detective rate estimates were 11% (95%CI, 6–17%; Z = 7.06; p < 0.001) for northeast endemic areas, 13% (95%CI, 7–20%; Z = 7.45; p < 0.001) for northwest endemic areas, and 8% (95%CI, 5–12%; Z = 7.90; p < 0.001) for southwest endemic areas. There was a significant relationship between the survey year and the X-ray detective rate of KBD. Our systematic review found that the summary estimate of the X-ray detective rate of KBD was 11% and, that KBD X-ray positive rate ranged from 8.00 to 15.00% depending on the study. Further research is required to identify effective strategies for preventing and treating KBD.

The purpose of this study was clarify the relationship between the differential expression of cyclins CCNB1 and CCNG1 and chondrocyte damage in Kashin-Beck disease. Systematic review and high-throughput sequencing of chondrocytes derived from Kashin-Beck disease patients were combined to identify the differentially expressed cyclins and cyclin-dependent kinase genes. In parallel, weaned SD rats were treated with low selenium for 4 weeks and then T-2 toxin for 4 weeks. Knee cartilage was collected to harvest chondrocytes for gene expression profiling. Finally, the protein expression levels of CCNB1 and CCNG1 were verified in knee cartilage tissue of Kashin-Beck disease patients and normal controls by immunohistochemical staining. The systematic review found 52 cartilage disease-related cyclins and cyclin-dependent kinase genes, 23 of which were coexpressed in Kashin-Beck disease, including 15 upregulated and 8 downregulated genes. Under the intervention of a low selenium diet and T-2 toxin exposure, CCNB1 (FC = 0.36) and CCNG1 (FC = 0.73) showed a downward expression trend in rat articular cartilage. Furthermore, compared to normal controls, CCNB1 protein in Kashin-Beck disease articular cartilage was 71.98% and 66.27% downregulated in the superficial and middle zones, respectively, and 12.06% upregulated in the deep zone. CCNG1 protein was 45.66% downregulated in the superficial zone and 12.19% and 9.13% upregulated in the middle and deep zones, respectively. The differential expression of cyclins CCNB1 and CCNG1 may be related to articular cartilage damage in Kashin-Beck disease.