BACKGROUND: Recent trials and clinical studies have shown that intracoronary transplantation of bone marrow-derived mesenchymal stem cells (MSCs) improves cardiac function following acute myocardial infarction (AMI). However, whether homing of MSCs into the infarcted myocardium or not is still unknown.OBJECTIVE: To study the homing of MSCs intracoronary administration in porcine myocardial infarction model using in vivo magnetic resonance imaging tracking.METHODS: Porcine MSCs were isolated and cultured by the whole bone marrow method. Following labeling by superparamagnetic iron oxide (SPIO), MSCs were treated with trypsinization to adjust the concentration at 10~(10)/L. Myocardial infarction was induced in all 10 pigs. At one week after modeling, the labeled MSCs were delivered via intracoronary infusion with standard over-the-wire (OTW) balloon angioplasty catheters. Prussian blue staining was used to evaluate labeling efficiency, and double echo steady state was used to scan four-chamber and cor biloculare at long axis view, which was considered as locating phase to obtain image of left ventricle at short axis view. RESULTS AND CONCLUSION: MSCs could be efficiently and safely labeled with SPIO. Intracoronary transplantation of MSCs is able to home the sites of myocardial injury and the border between infarcted and normal tissue. MRI can track SPIO-labeled MSCs delivered through intracoronary and were confirmed on pathology. After 5 weeks the injected labeled cells could still be detected with MRI.

Objective To investigate the therapeutic effects and mechanism of Artemisia argyi ferment substance on systemic Candida albicans infection. Methods The model of systemic Candida albicans infection was established in immunosuppressed mice. The model mice were randomly divided into the model control,Artemisia argyi ferment substance( AAFS) at different doses(100,200,and 400 mg·kg-1 )and fluconazole group(20 mg·kg-1 ),30 mice in each. Mice in each treatment group were given therapeutic drugs by gavage for 5 consecutive days,twice daily. The survival of mice was determined 21 days after the model was set up. The serum levels of IFN-γand IL-2 were determined by ELISA. The proliferation activity of T lymphocyte in the spleen was detected by MTT assay. The number of living fungi in liver and kidney tissues was counted. Results Compared with the model control,AAFS at middle and high doses and fluconazole significantly increased the survival rate of mice,the serum levels of IFN-γand IL-2,and the proliferation activity of T lymphocyte in the spleen,but decreased the number of living fungi in tissues(P〈0. 01). Compared with low dose AAFS,middle and high doses of AAFS and fluconazole showed significantly different effect on each index(P〈0. 05 or P〈0. 01),but there was no difference among these groups(P〉0. 05). Conclusion AAFS at 200-400 mg·kg-1 has inhibitory effects on systemic Candida albicans infection in mice,the mechanism of which is related to increasing the proliferation of T lymphocyte in spleen and the levels of IFN-γand IL-2 in serum.

BACKGROUND:The use of mesenchymal stem cels in the field of tissue engineering for osteoarticular injury repair is a very promising tool since these cels are readily expandable and able to differentiate into chondrocytes. Abundant evidence suggests that microRNAs play critical roles in chondrogenic differentiation of mesenchymal stem cels.
OBJECTIVE:To observe the chondrogenic effect of human bone marrow mesenchymal stem cels transfected with lentiviral vectors bearing miR-221-3p/222-3p inhibition, thereby provding new strategies for cartilage injury.
METHODS: miRNA microarray technology was applied to detect microRNAs expression profiles at three different stages of chondrogenic differentiation induction after transforming growth factor-β3 treatment and verified by real-time fluorescence quantitative PCR (RT-qPCR). Human bone marrow mesenchymal stem cels were infected with lentivirus bearing miR-221-3p/222-3p inhibition. After co-suppressing the expression of miR-221/222-3p, cel counting kit-8 was used to determine the cel proliferation, the differentiation of bone marrow mesenchymal stem cels towards chondrocytes was verified by type II colagen protein expression through immunohistochemistry and glycosaminoglycan accumulation was also elevated by sarranine O staining. RT-PCR was used to detect type II colagen and aggrecan mRNA expression at 21 days of chondrogenic induction.
RESULTS AND CONCLUSION: The expression of miR-221-3p/222-3p was inhibited after Lv-miR221-3p/222-3p inhibition co-transfected into bone marrow mesenchymal stem cels. microRNA microarray and RT-qPCR results showed that the expression of miR-221-3p/222-3p was declined significantly at the anaphase of chondrogenic differentiation. The expression levels of chondrogenic markers, Aggrecan and type II colagen were significantly increased in the miR-221-3p/222-3p inhibition group and cel proliferation was also inhibited significantly compared with non-transduced cels or transduced with the empty lentiviral vector group. miR-221-3p/222-3p knockdown in bone marrow mesenchymal stem cels could inhibit proliferation but promote chondrogenic differentiation of bone marrow mesenchymal stem cels.

Objective:To observe the effect of berberine on leukemia drug-resistant cell strain K562/A02 to Adriamycin resistance and protein kinase C-alpha (PRKCA) and explore its possible mechanism.Methods:The leukemia K562 cells of human chronic myeloid and Adriamycin resistant strain K562/A02 were cultured in vitro with 2.5-50.0 μmol/L doxorubicin to treat thoese cells and drug resistance of K562 and K562/A02 to Adriamycin was detected, the 50% inhibitory concentration (IC 50) of the drug was calculatedthe resistance of K562 and K562/A02 to doxorubicin was detectd , and, K562/A02 cells were treated with doxorubicin solution at a final concentration of 5 μmol/L, and K562/A02 cells were divided into control group, inhibitor group (50 μmol/L PRKCA inhibitor), low dose berberine group, medium dose berberine group and high dose berberine group. Cell counting (CCK-8) method was used to detect the inhibition rate of cell proliferation, the apoptosis was detected by flow cytometry, real-time fluorescent quantitative PCR assay detects PRKCA, MRP, multidrug resistance related genes (MDR1) levels, and the protein expressions of protein kinase C-α (PRKCA), multidrug resistance related protein (MRP), P-glycoprotein (P-gp) were detected by Western blotting. Results:The IC 50 concentration of K562/A02 to Adriamycin was significantly higher than K562. Compared with the control group, the inhibition rate of cell proliferation and the apoptosis rate in the inhibitor group, low-dose berberine group, medium-dose berberine group, and high-dose berberine group were significantly increased ( P<0.05), the expression of PRKCA mRNA (0.45±0.08, 0.92±0.10, 0.57±0.05, 0.35±0.04 vs. 1.00±0.12), MDR1 gene (0.73±0.08, 0.87±0.09, 0.65±0.07, 0.41±0.05 vs. 1.00±0.11) and PRKCA (0.59±0.09, 0.78±0.12, 0.61±0.11, 0.42±0.07 vs. 0.96±0.14), MRP (0.62±0.08, 0.79±0.13, 0.62±0.10, 0.41±0.06 vs. 0.98±0.14), P-gp (0.55±0.08, 0.75±0.12, 0.59±0.09, 0.35±0.06 vs. 0.92±0.15) were significantly reduced ( P<0.05), and berberine was dose-dependent ( P<0.05); Overexpression of PRKCA can inhibit the effect of berberine on reversing the drug resistance of K562/A02 cells. Conclusion:Berberine may reverse the drug resistance of K562/A02 to Adriamycin by down-regulating PRKCA.

The medical-industrial fusion training model combines the knowledge and technology of medical and engineering disciplines in the training of oncology graduate students, which can help accurate diagnosis and treatment of tumors, promote cooperation and innovation in oncology research, as well as promote the cultivation and exchanges of composite and innovative medical talents in oncology, promote the innovation and development of oncology diagnostic and treatment technology, and improve the survival rate and quality of life of oncology patients. This paper discusses the application of medical-industrial fusion training model in the training of o ncology professionals, and explores the new teaching mode of medical-industrial fusion thinking in the cultivation of complex and innovative medical talents in oncology under the background of "new medical science".