There are controversial reports about cardiac differentiation potential of mesenchymal stem cells (MSCs), and there is still no well-defined protocol for the induction of cardiac differentiation. The effects of retinoic acid (RA) and dimethyl sulfoxide (DMSO) on the proliferation and differentiation of human fetal liver-derived MSCs (HFMSCs) as well as the pluripotent state induced by 5-azacytidine (5-aza) in vitro were investigated. MSCs were isolated from fetal livers and cultured in accordance with previous reports. Cells were plated and were treated for 24 h by the combination of 5-aza, RA and DMSO in different doses. Different culture conditions were tested in our study, including temperature, oxygen content and medium. Three weeks later, cells were harvested for the certification of cardiac differentiation as well as the pluripotency, which indicated by cardiac markers and Oct4. It was found that the cardiac differentiation was only induced when HFMSCs were treated in the following conditions: in high-dose combination (5-aza 50 μM + RA 10(-1) μM + DMSO 1 %) in cardiac differentiation medium at 37 °C and 20 % O2. The results of immunohistochemistry and quantitative RT-PCR showed that about 40 % of the cells positively expressed Nkx2.5, desmin and cardiac troponin I, as well as Oct4. No beating cells were observed during the period. The combined treatment with RA, DMSO and 5-aza in high-dose could promote HFMSCs to differentiate into cardiomyocyte-like cells and possibly through the change of their pluripotent state.

The impact of heart failure (HF) on acute myocardial infarction (AMI) in patients from southwestern China remains unclear. The present study aimed to compare in-hospital cardiovascular events, mortality and clinical therapies in AMI patients with or without HF in southwestern China. In total, 591 patients with AMI hospitalized between February 2009 and December 2012 were examined; those with a history of HF were excluded. The patients were divided into four groups according to AMI type (ST-elevated or non-ST-elevated AMI) and the presence of HF during hospitalization. Clinical characteristics, in-hospital cardiovascular events, mortality, coronary angiography and treatment were compared. Clinical therapies, specifically evidence-based drug use were analyzed in patients with HF during hospitalization, including angiotensin converting enzyme inhibitors (ACEIs) and β-blockers (BBs). AMI patients with HF had a higher frequency of co-morbidities, lower left ventricular ejection fraction, longer length of hospital stay and a greater risk of in-hospital mortality compared with AMI patients without HF. AMI patients with HF were less likely to be examined by cardiac angiography or treated with reperfusion therapy or recommended medications. AMI patients with HF co-treated with ACEIs and BBs had a significantly higher survival rate (94.4 vs. 67.5%; P<0.001) compared with untreated patients or patients treated with either ACEIs or BBs alone. Logistic regression analysis revealed that HF and cardiogenic shock in patients with AMI were the strongest predictors of in-hospital mortality. AMI patients with HF were at a higher risk of adverse outcomes. Cardiac angiography and timely standard recommended medications were associated with improved clinical outcomes.

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Hemorrhagic fever with renal syndrome (HFRS) is an acute viral disease characterized by endothelial dysfunction. The cellular immune response, especially the virus-specific CD8+ T lymphocytes, is known to attack vascular endothelial cells (VEC) and to contribute to the diffuse damage and penetrability increasing of VEC. Lymphocyte function associated antigen 3 (LFA-3) is expressed on T lymphocytes and VEC, which is contributed to the activation of T lymphocytes. The expression of LFA-3 on the activated T lymphocytes and VEC is highly increased, which can exfoliate into plasma to increase the level of soluble LFA-3 (sLFA-3) in plasma. So the change of sLFA-3 levels is correlated with the activation of T lymphocytes. In this study we detected the levels of sLFA-3 in plasma of patients with HFRS. We examined the levels of sLFA-3 in plasma samples collected from 53 HFRS patients by double antibody sandwich ELISA. We found variable, but persistently elevated levels of sLFA-3 throughout the various phases and types of the HFRS disease, which suggest that sLFA-3 levels have correlation with disease stages. Moreover, elevated sLFA-3 levels are closely correlated to the severity of HFRS and the degree of kidney damage.