ABSTRACT
Objective To investigate the feasibility of chemical exchange saturation transfer (CEST) imaging in the measurement of myocardial creatine (Cr) metabolites in phantom model using 3.0 T MR. Methods Five phantoms were made according to the volume percentage of Cr ranging from 10 to 50 mmol/L with an interval of 10 mmol/L. 3.0 T MR examinations with base protocol sequence,sequence with and without ECG were performed. Signal to noise,CrEST effect and Z spectra were analyzed. Comparison of signal noise ratio (SNR) among the three methods was performed using an analysis of variance. Bivariate correlations were obtained through Pearson analysis. Results Phantom studies demonstrated that different concentrations of Cr exhibited significant CEST effect with the three sequences. The SNR obtained by sequences with and without ECG were both higher than that of base sequence (both P<0.05). Moreover,no significance of SNR was found between sequences with and without ECG (P>0.05). There were positive correlation of MTR between sequences with ECG,sequences without ECG and base protocol sequence (r2= 0.974 and 0.997, both P<0.05). Conclusion Compared with base protocol sequence, the optimized sequence with ECG can acquire higher SNR CrEST images,indicating that myocardial CrEST imaging could be performed in clinical practice.
ABSTRACT
Objective:To study the effect of metformin on proliferation,cell cycle and apoptosis of U937 cells.Methods: U937 cells were treated with different concentrations of metformin,collected cells in 24,48 and 72 hours.Subsequently,cell proliferation was assessed by CCK-8 assay,and the cell cycle and apoptosis were analyzed by flow cytometry (FCM).The expression of Bcl-2,Bax,p-AMPK,p53 were determined by Western blot.Results: The proliferation of U937 cells was inhibited by metformin in a time-and dose-dependent manner.Metformin-treated cells were arrested at G0/G1 phase,the cell frequency at G0/G1 phase was increased in a time-and dose-dependent manner.Metformin also induced cell apoptosis in a dose-dependent manner.It showed that 20 mmol/L metformin induced cell apoptosis in a time-dependent manner.The expression of p-AMPK,p53,Bax was up-regulated while Bcl-2 expression was down-regulated after metformin treatment.Conclusion: Metformin could inhibit the U937 cell proliferation,block the cell cycle at G0/G1 phase,and induce cell apoptosis,which may partially be attribute to the up-regulation of Bax,down-regulation of Bcl-2,activation of AMPK/p53 signaling.