Objective The aim of this study was to evaluate the safety and efficacy of 135 cm Corsair microcatheter inpercutaneous coronary intervention (PCI) for coronary chronic total occlusion (CTO) with antegrade approach via radial artery. Methods From June 2010 to February 2014, a total of 81 patients with CTO lesions treated with 135cm Corsair microcatheter (Asahi Intec Co, Japan) and transradial antegrade approach was enrolled in this study. The success rate of CTO-PCI, the rate of Corsair microcatheter crossing the CTO lesions and the number of balloon catheters utilization were retrospectively analyzed. Unique complications related to the Corsair microcatheter were also documented. Results Success recanalization of CTO were achieved in 73 (90.1%) patients. Crossing the CTO body with Corsair microcatheter was found in 56(84.8%) patients. The number of balloon utilized after Corsair microcatheter crossing the CTO was much lower than that of patients who Corsair microcatheter failed to cross (1.3±0.6 per patient versus 2.8±1.2per patient, P < 0.05). The success recanalization rate of combined using Fielder XT guidewire with Corsair microcatheter was 51.5%. There was no complications related to Corsair microcatheter during the index procedure, no major adverse cardiac events during in-hospital clinical follow-up. Conclusions Corsair microcatheter was safe and effective in the recanalization for CTO with transradialantegrade approach. It can simplify the CTO-PCI procedure and reduce the number of balloon catheters.

OBJECTIVES: This research was performed to explore the effect of macrophage migration inhibitory factor (MIF) on the apoptosis of bone marrow mesenchymal stem cells (BMSCs) in ischemia and hypoxia environments. METHODS: The cell viability of BMSCs incubated under hypoxia/ischemia (H/I) conditions with or without pretreatment with MIF or triglycidyl isocyanurate (TGIC) was detected using cell counting kit-8 (CCK-8) analysis. Plasmids containing long noncoding RNA (lncRNA) maternally expressed gene 3 (MEG3) or β-catenin small interfering RNA (siRNA) were used to overexpress or downregulate the corresponding gene, and the p53 signaling pathway was activated by pretreatment with TGIC. The influences of MIF, overexpression of lncRNA MEG3, activation of the p53 signaling pathway, and silencing of β-catenin on H/I-induced apoptosis of BMSCs were revealed by western blotting, flow cytometry, and terminal deoxynucleotidyl transferase (TdT)-mediated dUTP nick-end labeling (TUNEL) staining. RESULTS: From the results of CCK-8 assay, western blotting, and flow cytometry, pretreatment with MIF significantly decreased the H/I-induced apoptosis of BMSCs. This effect was inhibited when lncRNA MEG3 was overexpressed by plasmids containing MEG3. The p53 signaling pathway was activated by TGIC, and β-catenin was silenced by siRNA. From western blot results, the expression levels of β-catenin in the nucleus and phosphorylated p53 (p-p53) were downregulated and upregulated, respectively, when the lncRNA MEG3 was overexpressed. Through flow cytometry, MIF was also shown to significantly alleviate the increased reactive oxygen species (ROS) level of BMSCs caused by H/I. CONCLUSIONS In summary, we conclude that MIF protected BMSCs from H/I-induced apoptosis by downregulating the lncRNA MEG3/p53 signaling pathway, activating the Wnt/β-catenin signaling pathway, and decreasing ROS levels.
Humans ; RNA, Long Noncoding/metabolism* ; Macrophage Migration-Inhibitory Factors/metabolism* ; beta Catenin/metabolism* ; Reactive Oxygen Species/metabolism* ; Sincalide/metabolism* ; Tumor Suppressor Protein p53/metabolism* ; Apoptosis ; Mesenchymal Stem Cells ; Wnt Signaling Pathway/genetics* ; RNA, Small Interfering/metabolism* ; Hypoxia/metabolism* ; Ischemia ; Bone Marrow Cells