Abstract Background Airway remodeling is a key feature of asthma, characterized by increased proliferation of airway smooth muscle cells (ASMCs). S100A8 is a calcium‑binding protein with a potential to regulate cell proliferation. Here, the effect of exogenous S100A8 protein on the proliferation of ASMCs induced by platelet‑derived growth factor (PDGF) and the underlying molecular mechanism was investigated. Methods Rat ASMCs were cultured with or without a neutralizing antibody to the receptor for advanced glycation end‑products (RAGE), a potential receptor for S100A8 protein. Purified recombinant rat S100A8 protein was then added into the cultured cells, and the proliferation of ASMCs induced by PDGF was detected by colorimetric‑based WST‑8 assay and ampedance‑based xCELLigence proliferation assay. The expression levels of RAGE in ASMCs were analyzed using western blotting assay. Results Results showed that exogenous S100A8 inhibited the PDGF‑induced proliferation of rat ASMCs in a dose‑ dependent manner with the maximal effect at 1 μg/ml in vitro. Furthermore, when ASMCs was pre‑treated with anti‑RAGE neutralizing antibody, the inhibitory effect of S100A8 on PDGF‑induced proliferation was significantly sup‑ pressed. In addition, neither the treatment with S100A8 or PDGF alone nor the pre‑treatment with rS100A8 followed by PDGF stimulation affected the expression levels of RAGE. Conclusions Our study demonstrated that S100A8 inhibits PDGF‑induced ASMCs proliferation in a manner depend‑ ent on membrane receptor RAGE.

BACKGROUND: BrdU is a commonly used reagent in cell proliferation assays, and WST-1 measurement is widely used to detect cell viability. However, no previous study has formally reported the combination of the two assays, which may be used to detect the proliferation and viability simultaneously. In this study, we examined the effect of adding BrdU 2 h prior to the WST-1 assay and tried to test the possibility of the combined detection using rat airway smooth muscle cells. RESULTS: The WST-1 measurements obtained from the combined detection were consistent with those obtained from the separate detection, which suggested that the addition of BrdU 2 h prior to the WST-1 analysis did not affect the WST-1 results. The BrdU measurements obtained from the combined detection also demonstrated the same trend as that obtained from the separate detection, and dosages of 200, 400 and 800 ng/ml testing reagent significantly inhibited the proliferation of rat airway smooth muscle cells. CONCLUSIONS: Our study suggests that the BrdU and WST-1 measurements can be applied simultaneously without mutual interference, which may increase the efficacy and consistency of these measurements to a certain extent.

PURPOSE: To systematically evaluate the clinical efficacy of reamed and nonreamed intramedullary nailing in treatment of closed tibial fractures with Cochrane systematic review methods. METHODS: According to the Cochrane systematic review methods, literatures were retrieved from Cochrane library, PubMed, EMbase and other database. Randomized controlled trials (RCTs) and quasi-randomized controlled clinical trials about reamed and nonreamed intramedullary nailing in the treatment of closed tibial fractures were collected and RevMan 5.0 was chosen for meta-analysis. RESULTS: A total of seven studies were included in this meta-analysis. Reamed intramedullary nailing was better than nonreamed intramedullary nailing in nonunion rate [P = 0.02, RR = 0.46, 95% CI: (0.24, 0.91)] and implant failure rate [P <0.0001, RR = 0.36, 95% CI: (0.22, 0.57)]. No statistically significant difference was observed in malunion rate, compartment syndrome rate, postoperative infection [P = 0.18, RR = 0.50, 95% CI: (0.18, 1.383); P = 0 43, RR = 0.77, 95% CI: (0.40, 1.48); P = 0.27, RR = 0.38, 95% CI: (0.01, 7.87)]. CONCLUSION: Compared with the nonreamed intramedullary nailing, reamed intramedullary nailing can lead to better outcome in the treatment of closed tibial fractures.