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Objective Plaque calcification and stent oversizing are two key factors contributing to in stent restenosis (ISR) following femoropopliteal stent angioplasty. This study aimed to explore a pre-operative quantitative assessment method of plaque calcification and rational parameters of stent oversizing in the femoropopliteal artery. Methods A total of 115 patients with atherosclerotic femoropopliteal arterial occlusive disease treated from January 2013 to January 2016 were included retrospectively. Computed tomography angiography (CTA) imaging was performed to analyse calcified plaque parameters (calcified plaque volume [CV], standard CV [SCV], burden of calcified plaque) and stent oversizing parameters at different vessel segments (distal oversizing, maximum oversizing, plaque oversizing). Optimal cut offs for the six parameters were determined by the maximum Youden's index. The relationship between calcified plaque, stent oversizing, and clinical outcomes were assessed by correlation analysis and multivariable Cox regression models. Results The one year primary patency rate was 77.4%; the rates of ISR, major amputation, target lesion revascularisation, and mortality were 40.9%, 8.7%, 17.4%, and 12.2%, respectively. For all six parameters, patients with values greater than the cut offs had a significantly higher incidence of ISR than those with values below the cut offs. ISR was positively correlated with all six calcification and oversizing parameters. Amputation and mortality were positively correlated with calcification parameters. Multivariable Cox regression analysis demonstrated that all six parameters were independent risk factors for ISR. All calcification parameters were identified as independent risk factors for amputation, while only CV and SCV were independent risk factors for mortality. Conclusion Calcified plaque in the femoropopliteal artery can be quantitatively analysed on pre-operative CTA images. High calcified plaque burden and excessive stent oversizing were associated with unfavourable outcomes following stent angioplasty.

Background The inhibition of glucocorticoid (GC) on osteoblastic differentiation of bone marrow stromal stem cells (BMSC) is an important pathway for GC to reduce bone formation. Recent studies implicated an important role of peroxisome proliferator-activated receptor-gamma (PPAR-γ) in GC-mediated cell proliferation and differentiation. Thus, our purpose is to investigate the role of PPAR-γ in regulating rat BMSC (rBMSC) osteoblastic differentiation. Methods The rBMSC treated with dexamethasone (Dex) was used to construct an in vitro cell model of GC-induced osteoporosis. The expressions of PPAR-γ, RUNX2, ALP, OPN and SFRP5 in cells were detected by RT-qPCR and western blot assays. Osteogenic differentiation of rBMSC was measured by Alizarin Red S (ARS) staining analysis. Lentivirus-delivered shRNA was used to knock down PPAR-γ or SFRP5, and lentivirus-delivered constructs were used to overexpress SFRP5 in rBMSC to verify the effect of PPAR-γ or SFRP5 on cell osteogenic differentiation. Results Dex significantly reduced rBMSC osteoblastic differentiation. The expression of PPAR-γ was enhanced in Dex treated rBMSC. PPAR-γ down-regulation improved Dex inhibition of rBMSC osteogenic differentiation. Moreover, PPAR-γ knockdown promoted protein levels of RUNX2, ALP, OPN and Dex-decreased rBMSC osteogenic differentiation. The expression of SFRP5 was reduced while Wnt and β-catenin were increased in PPAR-γ knockdown and Dex treated rBMSC. Moreover, the up-regulation of SFRP5 reversed the osteogenic differentiation of rBMSC induced by PPAR-γ knockdown. Conclusion These data indicated that in GC-induced osteoporosis, PPAR-γ/SFRP5 affects osteogenic differentiation by regulating the Wnt/β-catenin signaling pathway.

A general strategy for designing stable hypercarbon CB62−-based cluster-assembled compounds CpM(CB6)q− (M = Li, Na, K, Be, Mg, and Ca) is proposed. This approach takes advantage of (1) the extra st...