Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were involved in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. Based on different transfection, MEG3 cells were grouped into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics group. The RT-qPCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Moreover, western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis in cartilage cells. Finally, the histological analysis and immunostaining were performed on OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Finally, rat model analysis showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes.

This study aimed to explore the potential molecular pathways and targets of Alzheimer's disease leading to osteoporosis using bioinformatics tools. The Alzheimer's and osteoporosis microarray gene expression data were retrieved from the Gene Expression Omnibus, and differentially expressed genes in the blood microenvironment related to Alzheimer's disease and osteoporosis were identified. The intersection of the three datasets (GSE97760, GSE168813, and GSE62402) was used to obtain 21 co-expressed targets in the peripheral blood samples in patients with Alzheimer's disease and osteoporosis. Based on the degree algorithm, the top 10 potential core target genes related to these diseases were identified, which included CLEC4D, PROK2, SIGLEC7, PDGFB, PTCRA, ECH1, etc. Two differentially expressed mRNAs, Prokineticin 2 (PROK2) and three colony-stimulating factor 3 (CSF3), were screened in the GSE62402 dataset associated with osteoporosis. Protein–protein rigid docking with ZDOCK revealed that PROK2 and CSF3 could form a stable protein docking model. The interaction of PROK2 and CSF3, core genes related to osteoporosis inflammation, plays an important role in the mechanism of osteoporosis in patients with Alzheimer's. Therefore, abnormalities or alterations in the inflammatory pathways in the peripheral blood samples of Alzheimer's patients may affect the course of osteoporosis.

Objective. Hip fractures are quite common worldwide, especially among the elderly, and are associated with a high incidence of postoperative delirium, which worsens functional results and increases death. The causes of postoperative delirium in patients with hip fractures are unknown, and a separate pathobiology has been hypothesized. Substance P is a neuropeptide that has been linked to a number of immune-inflammatory and neurological conditions. The purpose of this study was to see if serum substance P levels could predict postoperative delirium in a group of hip fracture patients. Methods. A total of 148 hip fracture patients were enrolled in the study, all of whom had no substantial pre-existing medical or cognitive issues. Demographic and regular laboratory data were gathered as a starting point. ELISA was used to examine substance P levels before and after surgery (after 1 day). Patients were then divided into two groups: “postoperative delirium” and “no postoperative delirium.” Intergroup comparisons, study of delirium prevalence rates in postoperative serum substance P quartile categories, and binary logistic regression for postoperative delirium category as outcome were all done. Results. Except for serum low-density lipoprotein (LDL) levels, there were no statistically significant variations in preoperative substance P levels or other baseline characteristics between the two groups. The “postoperative delirium” group had significantly higher postoperative substance P levels than the “no postoperative delirium” group (46.36.1 versus 31.94.7 pg/ml). There was a significant difference in postoperative delirium rates between the quartile categories of postoperative substance P, with the fourth quartile having the highest rate. Regression analysis revealed that postoperative substance P levels were related with a significantly increased OR (1.265, CI: 1.172-1.283) of postoperative delirium. Conclusion. In the current sample of hip fracture patients, a higher postoperative serum substance P level was linked to a higher risk of postoperative delirium. Further research into the utility of early postoperative serum substance P as a delirium indicator in hip fracture patients is needed.

Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms in osteoarthritis (OA). Methods: Patients with OA and patients undergoing thigh amputation were enrolled in OA group and normal group, respectively. Cartilage tissues of all patients were isolated and cultured. After different transfections, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. The qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1. Western blot, luciferase reporter assay, RIP, CCK-8 and flow cytometry analysis were performed to reveal the morphology, proliferation and apoptosis of cartilage cells. Histological analysis and immunostaining were conducted in OA rat model. Results: The expression of MEG3 and FOXO1 in OA was significantly decreased while miR-361-5p was increased compared with the normal group. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, the western blot and CCK-8 assay showed that MEG3, targeted miR-361-5p/FOXO1, might elevate cell proliferation and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed the cartilage matrix degradation. Conclusion: Taken together, MEG3 can contribute to cell proliferation, inhibit cell apoptosis and extracellular matrix (ECM) degradation via miR-361-5p/FOXO1 axis in OA chondrocytes. BackgroundOsteoarthritis (OA) is a disease increasing with age and even induces serious pain and disability 1 , which characterized by various pathological changes, such as articular cartilage degradation, synovial inflammation and subchondral osteoblast activation 2 . Although various genetic, biological, and biomechanical components have been proved to be associated with OA 3 , the underlying molecular mechanisms of OA progression remains unclear and the efficacious cure is still not available.Accumulating reports have indicated that lncRNAs are implicated in the various cancerogenesisrelated signaling pathways 4-8 . Moreover, lncRNAs have also been reported to be associated with knee OA progression 9 . As a member of lncRNA, maternally expressed 3 (MEG3) has been regarded as an important factor in the development of tumors 10 . Increasing publications have found that MEG3 is

Background: This study aimed to investigate the role of long non-coding RNA (lncRNA) maternally expressed 3 (MEG3) and related molecular mechanisms, in osteoarthritis (OA). Methods: Cartilage tissues of OA patients and healthy volunteers were isolated and cultured. After transfection with the appropriate construct, chondrocytes were classified into Blank, pcDNA3.1-NC, pcDNA3.1-MEG3, si-NC, si-MEG3, pcDNA3.1-NC + mimics NC, pcDNA3.1-MEG3 + mimics NC, pcDNA3.1-NC + miR-361-5p mimics and pcDNA3.1-MEG3 + miR-361-5p mimics groups. qRT-PCR was used to detect the expression of MEG3, miR-361-5p and FOXO1 . Western blot, luciferase reporter assay, RIP, CCK-8, and flow cytometry analysis were performed to reveal the morphology, proliferation, and apoptotic status of cartilage cells. Histological analysis and immunostaining were conducted in the OA rat model. Results: Expression of MEG3 and FOXO1 was significantly decreased in OA compared with the normal group, while the expression of miR-361-5p was increased. MEG3 might serve as a ceRNA of miR-361-5p in OA chondrocytes. Moreover, using western blot analyses and the CCK-8 assay, MEG3 was shown to target miR-361-5p/FOXO1, elevate cell proliferation, and impair cell apoptosis. Functional analysis in vivo showed that MEG3 suppressed degradation of the cartilage matrix. Conclusion: MEG3 can contribute to cell proliferation and inhibit cell apoptosis and degradation of extracellular matrix (ECM) via the miR-361-5p/FOXO1 axis in OA chondrocytes.