Data involving combined mitral and aortic valve procedure via the right mini-thoracotomy approach are very limited. This single-center propensity-matching study aimed to evaluate early clinical outcomes of patients who underwent combined mitral and aortic valve procedure via right mini-thoracotomy versus full median sternotomy.From January 2013 to December 2016, 926 eligible patients in our center were identified for this study. After propensity score-matching, 91 pairs of patients were entered into a RT group (right mini-thoracotomy surgery) or a FS group (full median sternotomy surgery). In-hospital and follow-up clinical outcomes were investigated and analyzed.Patients in the RT group received similar surgical mortality as patients in the FS group (1.1% versus 2.2%, P > 0.05). Patients in the RT group as compared with the FS group were less likely to receive postoperative new onset of atrial fibrillation and red cell transfusion (11.0% versus 25.3%, P = 0.012; 17.6% versus 37.4%, P = 0.003, respectively), but they shared similar incidences of other major postoperative morbidity. Patients in the RT group as compared with the FS group experienced 6-minute longer aortic cross-clamping times and 9minute longer cardiopulmonary bypass times, but received shorter intensive care unit stay and postoperative hospitalization time. No repeat valve operation, peri-prosthetic leak, or moderate or severe mitral valve regurgitation following valvuloplasty were observed in either group before discharge and also within one year of surgery.In primary, isolated, combined mitral and aortic valve procedure, a right mini-thoracotomy approach may be utilized with accepted early clinical outcomes, and may be considered as a feasible alternative to the approach of full median sternotomy.(Int Heart J 2019; 60: 336-344)

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Growth and invasion of metastatic colorectal cancer (CRC) cells in the liver depend on microenvironment. Here, we showed that human hepatic sinusoidal endothelial cells (HHSECs) induce chemotaxis and outgrowth of CRC cells. Macrophage migration inhibitory factor (MIF), released by HHSECs, stimulated chemotaxis of CRC cells. MIF secreted by HHSECs, but not by CRC cells themselves, promoted migration and epithelial-mesenchymal transition (EMT) and facilitated proliferation and apoptotic resistance of CRC cells. In orthotopic implantation models in nude mice, exogenous MIF stimulated growth of CRC cells and metastasis. Furthermore, MIF accelerated mobility of CRC cells by suppressing F-actin depolymerization and phosphorylating cofilin. Noteworthy, MIF levels were correlated with the size of hepatic metastases. We suggest that HHSECs and paracrine MIF promote initial migration and proliferation of CRC cells in the hepatic sinusoids to generate liver metastases.