Radiographic diagnosis of distal fibula avulsion fractures: Comparison of ankle X-ray and three-dimensional reconstruction of CT / 北京大学学报(医学版)

OBJECTIVE@#To investigate the difference in sensitivity between X-ray and three-dimensional reconstruction of computed tomography (3D-CT) for the diagnosis of distal fibular avulsion fracture, and the radiographic presentation of the ossicle.@*METHODS@#From January to October 2018, 92 patients with distal fibular avulsion fracture were visited for surgical treatment in Department of Sports Medicine, Peking University Third Hospital, and 60 cases were finally enrolled according to the inclusion and exclusion criteria. Intraoperative detection was regarded as the gold standard, and the diagnostic sensitivity of preoperative ankle X-ray and 3D-CT for the distal fibular avulsion fractures was statistically determined. The ossicle maximum diameter as well as the degree of its displacement were also measured. On 3D-CT, the distance from the ossicle center point to the anterior fibular tuberosity (a), the distance to the fibular tip (b), and the a/b value was used to present the ossicle displacement.@*RESULTS@#Among the 60 patients, 36 and the 52 patients were correctly detected by X-ray and 3D-CT, respectively, and the sensitivities was 60.0% and 86.7%, respectively (P=0.004). The mean diameter of the ossicle on X-ray and 3D-CT was (9.2±3.9) mm and (10.5±3.2) mm, respectively. The mean distance from the ossicle center to the anterior fibular tuberosity (a) was (17.5±3.6) mm and the mean distance to the fibular tip (b) was (17.4±4.8) mm, with mean a/b values of 1.1±0.7. The intraclass correlation coefficients (ICC) for each measurement ranged from 0.891-0.998 with a high degree of consistency.@*CONCLUSION@#Compared with X-ray, 3D-CT has higher sensitivity in diagnosing distal fibular avulsion fractures, can help clinicians evaluate ossicle's location and choose surgical methods, and is recommended to be performed in patients with suspected distal fibula avulsion fractures in clinical practice.

Intermedin inhibits lipopolysaccharide-induced polarization of macrophages by activating AMPK signaling pathway / 中国药理学通报

Aim To evaluate the mechanism by which intermdin(IMD)inhibits lipopolysaccha ride(LPS)-induced polarization in RAW264.7 cells.Methods RAW264.7 cells were divided into control groups, LPS groups, LPS+IMD groups, LPS+IMD+Compound C groups.The mRNA expressions of tumor necrosis factor-α,(TNF-α,), CD86, inducible nitric oxide synthase(iNOS), Arginase-1(Arg-1)and CD206 were detected by Realtime-PCR.The protein expressions of p-AMPK, AMPK, TNF-α, intereukin-6(IL-6)and intereukin-10(IL-10)were detected by Western blot.The proportion of CD86+ M1 type cells was detected by Flow cytometry.In addition, the expression levels of supernatant cytokines, including IL-6 and TNF-α, were detected by ELISA.Results Compared with control and LPS groups, IMD treatment could up-regulate the expression level of p-AMPK and the ratio of p-AMPK/AMPK.LPS promoted M1 polarization, since the expressions of CD86, TNF-α and iNOS increased, while the expressions of CD206 and Arg-1 decreased by LPS induction.The proportion of M1 type cells increased and the secretion of TNF-α, IL-6 in the cell supernatant increased.And IMD treatment could inhibit the polarization of M1 induced by LPS.These effects were reversed by Compound C, an inhibitor of AMPK.Conclusion IMD can inhibit the M1-type polarization of LPS-induced macrophages by activating AMPK signaling pathway.

Molecular Pathway of Psoralidin-Induced Apoptosis in HepG2 Cell Line / 中国结合医学杂志

OBJECTIVE@#To test the role of psoralidin in human liver cancer HepG2 cells in vitro.@*METHODS@#Cell viability was assessed by methylthiazolyldiphenyl-tetrazolum bromide assay and apoptotic cells were labeled by annexin V then sorted by flow cytometry. Protein expressions of caspase-3, caspase-8, caspase-9, Bax, Bid, Bcl-2, Bcl-xL and p53 were examined by western blot while activity of caspase-3, -8 and -9 were also determined.@*RESULTS@#Psoralidin reduces cell viability greatly in a time dependent manner (64%, 40%, 21%, 12% at 2, 6, 24 and 48 h treatment with 64 μmol/L psoralidin respectively) and up-regulates activities of caspase-3, -8 and -9 in a concentration dependent manner (between 4 to 64 μmol/L). Psoralidin also increases the expression of pro-apoptosis genes Bax, Bid and p53 while decreases the expression of pro-survival genes Bcl-2 and Bcl-xL, both in a concentration dependent manner between 4 and 64 μmol/L (P<0.05 at 16 and 64 μmol/L). Caspase-3 inhibitor (Ac-DEVD-CHO at concentrations between 10 to 20 μmol/L), p53 inhibitor (pifithrin-α at 5 μmol/L) and cyclosporin A can attenuate the apoptotic effect of psoralidin.@*CONCLUSION@#The cytotoxic role of psoralidin might work through both intrinsic and extrinsic apoptotic pathway.