Objective To design and test a device which is capable of accurately measuring and dynamically adjusting the axial pressure at the fracture end in real-time.Methods Upon completion of the design,the pressure measurement and adjustment device was implemented in a canine tibial fracture external fixation model.A pressure sensor was mounted at the fracture end,and the displayed values of the pressure sensor were used as the standard for comparison.The relationship between the displayed values of the measurement and adjustment device and the pressure sensor under identical conditions was examined.Results The device was utilized in external fixation models of tibial fractures in five beagles.A linear correlation was observed between the displayed values of the device and the pressure sensor at the fracture end.The measurement values from the device could be transformed into fracture end pressure through the application of coefficients,thereby facilitating accurate measurement and dynamic adjustment of the fracture end pressure.Conclusion The pressure measurement and adjustment device at the fracture end is easy to operate,enabling precise measurement and dynamic regulation of the pressure at the fracture end.It is well-suited for animal experiments aimed at investigating the impact of axial compression on fracture healing,demonstrating promising potential for experimental applications.

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.

Background::Hypothermia therapy has been suggested to attenuate myocardial necrosis; however, the clinical implementation as a valid therapeutic strategy has failed, and new approaches are needed to translate into clinical applications. This study aimed to assess the feasibility, safety, and efficacy of a novel selective intracoronary hypothermia (SICH) device in mitigating myocardial reperfusion injury.Methods::This study comprised two phases. The first phase of the SICH was performed in a normal porcine model for 30 minutes ( n = 5) to evaluate its feasibility. The second phase was conducted in a porcine myocardial infarction (MI) model of myocardial ischemia/reperfusion which was performed by balloon occlusion of the left anterior descending coronary artery for 60 minutes and maintained for 42 days. Pigs in the hypothermia group ( n = 8) received hypothermia intervention onset reperfusion for 30 minutes and controls ( n = 8) received no intervention. All animals were followed for 42 days. Cardiac magnetic resonance analysis (five and 42 days post-MI) and a series of biomarkers/histological studies were performed. Results::The average time to lower temperatures to a steady state was 4.8 ± 0.8 s. SICH had no impact on blood pressure or heart rate and was safely performed without complications by using a 3.9 F catheter. Interleukin-6 (IL-6), tumor necrosis factor-α, C-reactive protein (CRP), and brain natriuretic peptide (BNP) were lower at 60 min post perfusion in pigs that underwent SICH as compared with the control group. On day 5 post MI/R, edema, intramyocardial hemorrhage, and microvascular obstruction were reduced in the hypothermia group. On day 42 post MI/R, the infarct size, IL-6, CRP, BNP, and matrix metalloproteinase-9 were reduced, and the ejection fraction was improved in pigs that underwent SICH.Conclusions::The SICH device safely and effectively reduced the infarct size and improved heart function in a pig model of MI/R. These beneficial effects indicate the clinical potential of SICH for treatment of myocardial reperfusion injury.

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