BackgroundDairy product consumption may affect the risk of hip fracture, but previous studies have reported inconsistent findings. The primary aim of our meta-analysis was to examine and quantify the potential association of dairy product consumption with risk of hip fracture.MethodsWe searched the databases of PubMed and EMBASE for relevant articles from their inception through April 17, 2017. The final analysis included 10 cohort studies and 8 case-control studies. Random-effects models were used to estimate the pooled risk. Subgroup and dose-response analyses were conducted to explore the relationships between the consumption of milk and the risk of hip fracture.ResultsAfter pooling the data from the included studies, the summary relative risk (RR) for hip fracture for highest versus lowest consumption were 0.91 (95% CI: 0.74–1.12), 0.75 (95% CI: 0.66–0.86), 0.68 (95% CI: 0.61–0. 77), 1.02 (95% CI: 0.93–1.12) for milk, yogurt, cheese, and total dairy products in cohort studies, respectively. Higher milk consumption [Odds ratio (OR), 0.71, 95% CI: 0.55–0. 91] was associated with lower risk of hip fracture for highest versus lowest consumption in case-control studies. After quantifying the specific dose of milk, the summary RR/OR for an increased milk consumption of 200 g/day was 1.00 (95% CI: 0.94–1.07), and 0.89 (95%CI: 0.64–1.24) with significant heterogeneity for cohort and case-control studies, respectively; There was a nonlinear association between milk consumption and hip fracture risk in cohort, and case-control studies.ConclusionsOur findings indicate that consumption of yogurt and cheese was associated with lower risk of hip fracture in cohort studies. However, the consumption of total dairy products and cream was not significantly associated with the risk of hip fracture. There was insufficient evidence to deduce the association between milk consumption and risk of hip fracture. A lower threshold of 200 g/day milk intake may have beneficial effects, whereas the effects of a higher threshold of milk intake are unclear.Electronic supplementary materialThe online version of this article (10.1186/s12889-018-5041-5) contains supplementary material, which is available to authorized users.

The Chinese medicinal herb, Panax notoginseng, has long been used to treat bone fractures and Panax notoginseng saponins (PNS) could promote bone formation. Here, we investigated whether PNS could promote osteogenesis of bone marrow stromal cells (BMSCs) through modulating the MAPK signaling pathways, which are implicated in BMSC osteogenesis. We found that PNS markedly increased the mineralization of BMSCs by alizarin red S assays and stimulate alkaline phosphatase activity of these cells. Additionally, PNS significantly increased the mRNA levels of alkaline phosphatase, core-binding factor a1, and bone sialoprotein while decreasing PPAR 2 mRNA levels. Furthermore, inhibitors of ERK, PD98059, and p38, SB203580 inhibited the osteogenesis-potentiating effects by PNS. PNS stimulated the activation of ERK and p38 as evidenced by increased phosphorylation of these proteins, which was inhibited by PD98059 and SB203580. Our findings indicate that PNS could promote BMSC osteogenesis by activating the ERK and p38 signaling pathways.

Background Osteosarcoma is the most common bone tumor that occurs in children. Methods To identify co-expression modules and pathways correlated with osteosarcoma and its clinical characteristics, we performed weighted gene co-expression network analysis (WGCNA) on RNA-seq data of osteosarcoma with 52 samples. Then we performed pathway enrichment analysis on genes from significant modules. Results A total of 5471 genes were included in WGCNA, and 16 modules were identified. Module-trait analysis identified that a module involved in microtubule bundle formation, drug metabolism-cytochrome P450, and IL-17 signaling pathway was negatively correlated with osteosarcoma and positively correlated with metastasis; a module involved in DNA replication was positively correlated with osteosarcoma; a module involved in cell junction was positively correlated with metastasis; and a module involved in heparin binding negatively correlated with osteosarcoma. Moreover, expression levels in four of the top ten differentially expressed genes were validated in another independent dataset. Conclusions Our analysis might provide insight for molecular mechanisms of osteosarcoma. Electronic supplementary material The online version of this article (10.1186/s12957-019-1587-7) contains supplementary material, which is available to authorized users.

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Objective: To compare the preventive effects of teriparatide and alendronate on the progression of vertebral body collapse in postmenopausal single-level Kümmell's disease (KD). Methods: From March 2013 to December 2020, the medical records for 53 postmenopausal single-level KD patients who received conservative treatment with teriparatide (25 patients, teriparatide group) or alendronate (28 patients, alendronate group) were retrospectively reviewed. Midsagittal computed tomography (CT) images were analyzed by ImageJ to assess the intravertebral bone formation (mineralized bone) by calculating the ratio of area of intravertebral mineralized bone (AIMB) to the area of fractured vertebral body (AFVB). The changes in radiological parameters of the fractured vertebral body including kyphosis angle (KA), anterior and posterior border heights (ABH and PBH) and spinal canal diameter (SCD), bone turnover biomarkers (BTMs), and bone mineral density (BMD) were analyzed to evaluate the therapeutic effect. Results: At month 12, the ratio of AIMB to AFVB was significantly greater in teriparatide group (54.28% AE 15.30%) than in alendronate group (35.57% AE 17.61%) (P < 0.001). Sagittal CT substantiated the formation of bone bridge in 16 patients in teriparatide group. No bone bridge was detected in alendronate group. The KA was significantly smaller and the ABH, PBH, and SCD was greater in teriparatide group than in alendronate group (all P < 0.001). The KA increments were significantly smaller in teriparatide group (3.98 AE 1.30) than in alendronate group (11.43 AE 3.73) (P < 0.001). The ABH and PBH decrement were significantly lower in teriparatide group (11.96% AE 1.93% and 2.80% AE 2.52%) than in alendronate group (37.04% AE 8.00% and 19.50% AE 8.22%) (both P < 0.001). The BTMs and BMD were significantly greater in the teriparatide group than in the alendronate group. In teriparatide group, KA increment was negatively correlated with the change in PINP