The role of Bacillus acidophilus in osteoporosis and its roles in proliferation and differentiation.

BACKGROUND: Osteoporosis is one of the most closely related diseases associated with the elderly. In recent years, the studies found that gut microbiota can cause osteoporosis. We evaluated the role of Bacillus acidophilus in osteoporosis and its roles in proliferation and differentiation. METHODS: We selected 5 healthy people and 10 osteoporosis patients and analyzed their level of 25-hydroxyvitamin D and procollagen type I N-terminal peptide (PINP), the characteristic of gut microbiota. The effect of lactobacillus acidophilus and Lactobacillus rhamnosus supernatant and butanoic acids on proliferation, differentiation, and maturity of osteoblasts MC3T3-E1 and osteoclasts RAW 264.7 cells and the activity of alkaline phosphatase, concentration of osteocalcin, and the expression of RUNX2, RANK, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 were measured in the above cell lines. RESULTS: The diversity of gut microbiota in osteoporosis patients is decreased and imbalanced with lower abundance of lactobacillus and butyric acid bacteria; meanwhile, 25-hydroxyvitamin D and PINP of osteoporosis patient were significantly lower than the normal group. The proliferation, differentiation, and maturity of MC3T3-E1 cells were stimulated; the activity of alkaline phosphatase, concentration of osteocalcin, and the expression of RUNX2, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 were improved by supernatant of lactobacillus acidophilus, Lactobacillus rhamnosus and butanoic acids; however, the proliferation, differentiation, maturity, and the expression of RANK, NFATc1, cathepsin K, DC-STAMP, OSCAR, WNT2, and CTNNB1 in RAW 264.7 cells were suppressed. CONCLUSIONS: The lactobacillus acidophilus and Lactobacillus rhamnosus supernatant could stimulate the proliferation, differentiation, and maturation of osteoblasts; the production of butyric acid may be the potential mechanism.

Comprehensive analysis to identify PUS7 as a prognostic biomarker from pan-cancer analysis to osteosarcoma validation.

AIM: Pseudouridylation has demonstrated the potential to control the development of numerous malignancies. PUS7(Pseudouridine Synthase 7) is one of the pseudouridine synthases, but the literature on this enzyme is limited to several cancer types. Currently, no investigation has been performed on the systematic pan-cancer analysis concerning PUS7 role in cancer diagnosis and prognosis. METHODS: Employing public databases, including The Cancer Genome Atlas (TCGA), Genotype-Tissue Expression Project (GTEx), Human Protein Atlas (HPA), UALCAN and Tumor Immune Single-cell Hub (TISCH), this work investigated the PUS7 carcinogenesis in pan-cancer. Differential expression analysis, prognostic survival analysis and biological function were systematically performed. Furthermore, PUS7 potential as an osteosarcoma biomarker for diagnosis and prognosis was assessed in this study. RESULTS: The findings indicated that PUS7 was overexpressed in the majority of malignancies. High PUS7 expression contributed to the poor prognosis among 11 cancer types, including Adrenocortical Cancer (ACC), Bladder Cancer (BLCA), Liver Cancer (LIHC), Kidney Papillary Cell Carcinoma (KIRP), Mesothelioma (MESO), Lower Grade Glioma (LGG), Kidney Chromophobe (KICH), Sarcoma (SARC), osteosarcoma (OS), Pancreatic Cancer (PAAD), and Thyroid Cancer (THCA). In addition, elevated PUS7 expression was linked to advanced TNM across multiple malignancies, including ACC, BLCA, KIRP, LIHC and PAAD. The function enrichment analysis revealed that PUS7 participates in E2F targets, G2M checkpoint, ribosome biogenesis, and rRNA metabolic process. Moreover, PUS7 is also a reliable biomarker and a potential therapeutic target for osteosarcoma. CONCLUSIONS: In summary, PUS7 is a putative pan-cancer biomarker that reliably forecasts cancer patients' prognosis. In addition, this enzyme regulates the cell cycle, ribosome biogenesis, and rRNA metabolism. Most importantly, PUS7 possibly regulates osteosarcoma initiation and progression.

[A new method to reconstruct the spatial structure of human proximal femur and establishment of the finite element model].

In current study of femoral head necrosis and femoral neck fractures, more attentions has been paid to relationship between the femoral head trabecular bone within the spatial structure and its biomechanics. In this connection, PMMA (polymethyl methacrylate), special square iron, dental base acrylic resin liquid and powder were used to embed and fix human dry femur. Then, M618 Lie Axle Rectangle Desk Plane Grinding Machine was applied to grind the femur specimen, and then air blower clean, two-dimensional cross section image was obtained by using scanner. With Mimics software reconstruction, a three-dimensional model of spatial structure of trabecular bone was obtained, and the trabecular bone three-dimensional parameters were calculated. The authors obtained clear three-dimensional model of trabecular bone, reconstructed the real anatomic morphology of proximal femur. This is a good method to research into the interior structure of femur and to provide the foundation for the three-dimensional finite element analysis.

BTG2 inhibits the proliferation and metastasis of osteosarcoma cells by suppressing the PI3K/AKT pathway.

B cell translocation gene 2 (BTG2) has been reported to be a potential tumor suppressor in many types of tumors. However, the roles and molecular mechanisms of BTG2 in osteosarcoma progression are still unknown. In this study, we investigated the role of BTG2 in proliferation and metastasis of osteosarcoma and the underlying mechanism. BTG2 expression levels were measured in fresh osteosarcoma tissues and cell lines. The effects of BTG2 on cell proliferation, migration and invasion were explored by MTT, transwell assays, western blot, and in vivo tumorigenesis in nude mice. We found that BTG2 was down-regulated in human osteosarcoma tissues and cell lines. Overexpression of BTG2 inhibited the proliferation and migration/invasion of human osteosarcoma cells in vitro, it also markedly inhibited xenograft tumor growth in vivo. Furthermore, BTG2 significantly decreased the expression of phosphorylated PI3K and AKT in osteosarcoma cells. Taken together, our data indicate that BTG2 might suppress the tumor growth and metastasis via PI3K/AKT signaling pathway, implying that BTG2 may serve as a potential molecular target for the treatment of osteosarcoma.

Elevated serum chemerin levels are associated with the presence of coronary artery disease in patients with metabolic syndrome.

OBJECTIVE: Patients with metabolic syndrome (MetS) are at a high risk for developing atherosclerosis and cardiovascular disease. Serum levels of chemerin have been found elevated in subjects with MetS and are associated with several cardiovascular factors. This study was undertaken to determine whether serum chemerin levels are associated with coronary artery disease (CAD) in patients with MetS. METHODS: A total of 112 patients with MetS (66 patients with CAD and 46 without CAD) and 52 healthy subjects who underwent coronary angiography for the evaluation of CAD were enrolled in this study. Serum levels of chemerin were measured by enzyme-linked immunosorbent assay. RESULTS: Serum chemerin levels were significantly elevated in MetS patients with CAD compared to in those without CAD and healthy subjects. MetS patients without CAD also had higher serum chemerin levels compared with healthy subjects. Multivariate logistic regression analysis revealed that serum chemerin levels were significantly associated with the presence of CAD in patients with MetS. Simple linear regression analysis showed that the serum levels of chemerin were positively correlated with body mass index (BMI), systolic blood pressure (SBP), serum triglycerides and C-reactive protein (CRP) in patients with MetS. Only BMI and CRP remained significantly associated with serum chemerin after multiple stepwise regression analysis. CONCLUSION: Elevated serum chemerin levels could be considered as an independent predictive marker of the presence of CAD in patients with MetS.