BMP7 ameliorates intervertebral disc degeneration in type 1 diabetic rats by inhibiting pyroptosis of nucleus pulposus cells and NLRP3 inflammasome activity.

Background: Accumulating evidence indicates that intervertebral disc degeneration (IDD) is associated with diabetes mellitus (DM), while the underlying mechanisms still remain elusive. Herein, the current study sought to explore the potential molecular mechanism of IDD in diabetic rats based on transcriptome sequencing data.

Methods: Streptozotocin (STZ)-induced diabetes mellitus type 1 (T1DM) rats were used to obtain the nucleus pulposus tissues for transcriptome sequencing.

Ferrostatin-1 Inhibits Toll-Like Receptor 4/NF-κB Signaling to Alleviate Intervertebral Disc Degeneration in Rats.

Ferrostatin-1 (Fer-1), an inhibitor of ferroptosis, is implicated in intervertebral disc degeneration (IDD). The current study explored the role of Fer-1 in IDD via the toll-like receptor 4 (TLR4)/NF-κB signaling pathway. IDD-related gene expression microarray GSE124272 and high-throughput sequencing data set GSE175710 were obtained through the Gene Expression Omnibus database.

Long-term results of trans-scaphoid perilunate fracture dislocations treated by open reduction and internal fixation.

Purpose: The paper holds the research purpose of confirming the long-term results of trans-scaphoid perilunate fracture dislocations (TSPFD) under the treatment of open reduction and internal fixation.

Methods: Anteroposterial-lateral radiographs of the patient's wrist were taken before and after surgery. We use a dorsal approach for all cases.

Retraction Notice to: Knockdown of KCNQ1OT1 Suppresses Cell Invasion and Sensitizes Osteosarcoma Cells to CDDP by Upregulating DNMT1-Mediated Kcnq1 Expression.

[This retracts the article DOI: 10.1016/j.omtn.

Knockdown of KCNQ1OT1 Suppresses Cell Invasion and Sensitizes Osteosarcoma Cells to CDDP by Upregulating DNMT1-Mediated Kcnq1 Expression.

Osteosarcoma is a malignant bone tumor, with a high incidence worldwide. The involvement of long non-coding RNAs (lncRNAs) in cancers and their molecular association with the progression of osteosarcoma have been previously discussed. We conducted the present study to examine the effect of lncRNA KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) on osteosarcoma cell invasion and chemosensitivity to cisplatin (CDDP).

SIRT1-ZEB1-positive feedback promotes epithelial-mesenchymal transition process and metastasis of osteosarcoma.

Osteosarcoma is the most common malignant bone cancer that mainly affects children and young adults. Recently, the NAD -dependent deacetylase, sirtuin 1 (SIRT1), has been reported to play a key role in the development of malignant tumors. The study aimed to investigate the role of SIRT1 in osteosarcoma and explore its underlying oncogenic mechanisms.

Discontinuation of antiviral prophylaxis increased the risk of hepatitis B virus reactivation in glomerulonephritis patients under immunotherapy: a real-life observation.

Purpose: Antiviral prophylaxis is proved to be effective in reducing the risk of hepatitis B virus (HBV) reactivation in hepatitis B surface antigen (HBsAg)-positive patients under immunotherapy. But outcomes referring to discontinuation of antiviral prophylaxis in these patients are lacking.

Methods: We performed a retrospective study of 105 HBsAg-positive patients under immunotherapy for glomerulonephritis and evaluated the incidence and risk factors for HBV reactivation.

Osteoclast regulation of osteoblasts via RANK‑RANKL reverse signal transduction in vitro.

The treatment of osteoporosis typically inhibits the activity of osteoclasts, which subsequently results in the suppression of bone formation and maintenance, however the underlying mechanism remains to be elucidated. The receptor activator of nuclear factor κ‑B ligand (RANKL)‑receptor activator of nuclear factor κ‑B (RANK) signaling axis is important in the osteoblast regulation of osteoclasts. RANKL surface‑bound molecules expressed on T cells stimulate a reverse signaling transduction in order to regulate the T cells, therefore the present study hypothesized that RANKL expressed on osteoblasts may transfer reverse signals to regulate osteoblasts.

Burden of infections in China: a systematic review and meta-analysis.

Background: is a leading cause of bacterial meningitis and septicemia in children and young adults worldwide. The disease burden associated with infections has not been systematically assessed in China. Therefore, we undertook this study to determine the burden of meningococcal disease in China.

A single nucleotide polymorphism in the 3'-untranslated region of the KRAS gene disrupts the interaction with let-7a and enhances the metastatic potential of osteosarcoma cells.

The objective of the present study was to explore the molecular mechanism with which a single nucleotide polymorphism (rs61764370) interferes with the interaction between the 3'-untranslated region (3'-UTR) of Kirsten rat sarcoma viral oncogene homolog (KRAS) and let-7a, and its association with the metastasis of osteosarcoma (OS). In this study, we confirmed that KRAS is a target of let-7a in OS cells, and the introduction of rs61764370 minor allele into KRAS 3'-UTR significantly compromised the microRNA (miRNA)/mRNA interaction using a luciferase reporter system. Additionally, a total of 36 OS tissue samples of three different genotypes (TT,22; TG,10; GG,4) were obtained, and the expression of let-7a and KRAS was determined.

MicroRNA-503 represses epithelial-mesenchymal transition and inhibits metastasis of osteosarcoma by targeting c-myb.

Deregulated expression of miRNAs contributes to the development of osteosarcoma. Our previous study has showed that miR-503 was downregulated in osteosarcoma tissues. However, the mechanism of the miR-503 in osteosarcoma development still remains largely undefined.

MicroRNA-503 acts as a tumor suppressor in osteosarcoma by targeting L1CAM.

Deregulated microRNAs and their roles in tumorigenesis have attracted much attention in recent years. Although miR-503 was shown to be important in tumorigenesis, its role in osteosarcoma remains unknown. In this study, we focused on the expression and mechanisms of miR-503 in osteosarcoma development.