Enhanced external counterpulsation: A new method to alleviate contrast-induced acute kidney injury.

BACKGROUND: Contrast-induced acute kidney injury (CI-AKI) is a common complication after exposure to contrast media. Renal ischaemia occurs in the initial stage of CI-AKI, however, there are very few effective measures to improve renal perfusion. METHODS: A total of 114 patients with an estimated glomerular filtration rate (eGFR) of 60-89 ml/min/1.73m2 were randomly assigned to two groups: enhanced external counterpulsation (EECP) group (N = 57) and control group (N = 57). Two hours after contrast exposure, EECP group received EECP treatment for 1 h while no intervention was performed control group. The primary outcome was the incidence of serum cystatin C concentration to 10% above the baseline concentration at 24 h after contrast administration. The secondary outcomes were the incidence of CI-AKI (defined as an increase in serum creatinine concentration to ≥0.5 mg/dl or by 25% compare to the baseline after contrast exposure), contrast clearance and adverse clinical events. RESULTS: The primary outcome was observed in 26 patients (6 EECP and 20 control; 11% vs. 35%; P = 0.002). CI-AKI occurred in four patients (0 EECP and 4 control; 0% vs. 7%; P = 0.042). The clearance rate of iopromide in the initial 3 h was significantly different between EECP and control group (59.92 ± 8.84 vs 46.80 ± 9.26 ml/min/1.73 m2; P < 0.001). No adverse clinical events were observed in this study. CONCLUSIONS: This study demonstrates that EECP increases the contrast clearance and may have an effect in reducing the risk of CI-AKI. The study has been registered in Chinese Clinical Trial Registry (ChiCTR 2,000,039,190).

Mir-206 partially rescues myogenesis deficiency by inhibiting CUGBP1 accumulation in the cell models of myotonic dystrophy.

Objectives: In this study, we aim to determine how CUG-expansion and the abundance of Celf1 regulates normal myocyte differentiation and reveal the role ofmiR-206 in myotonic dystrohy and explore a possible gene therapy vector. Methods: we set up CUG-expansion and Celf1 overexpression C2C12 cell models to imitate the myocyte differentiation defects of DM1, then transfected AdvmiR-206 into cell models, tested the level of myogenic markers MyoD, MyoG, Mef2c, Celf1 by RT-PCRand Western Blotting, detected myotube formation by myosin heavy chain immunostaining. Result: 3'-UTR CUG-expansion leads to myotube defects and impaired myoblasts differentiation. Overexpression of Celf1 inhibits myoblast differentiation and impairs differentiation. Knockdown of Celf1 partially rescues differentiation defects of myoblasts harboring CUG-expansion. miR-206 incompletely reverses myoblast differentiation inhibition induced by CUG-expansion and partially recuses myoblast differentiation defects induced by Celf1 overexpression. Conclusions: Ectopic miR-206 mimicking the endogenous temporal patterns specifically drives a myocyte program that boosts myoblast lineages, likely by promoting the expression of MyoD to rectify the myogenic deficiency by stimulating the accumulation of Celf1. Abbreviations: DMPK: (dystrophia myotonica protein kinase); 3'-UTR: (3'-untranslated region); MBNL1: (muscleblind-like [Drosophila]); DM1: (myotonic dystrophy type 1); GFP: (green fluorescent protein); RT-PCR: (quantitative reverse transcriptase-polymerase chain reaction); shRNA: (short hairpin RNA).