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Prospective ECG-triggering DSCT angiography with a very low effective radiation dose allows the accurate diagnosis of anomalies in infants and children with complex CHD compared with TTE. It has great promise to become a commonly used second-line technique for complex CHD.

Single-cell impedance measurement is a label-free, noninvasive method for characterizing the electrical properties of single cells. At present, though widely used for impedance measurement, electric impedance flow cytometry (IFC) and electric impedance spectroscopy (EIS) are used alone for most microfluidic chips. In this paper, we present a microfluidic device combining the IFC and EIS techniques for single-cell electrical property measurement. The device uses hydrodynamic constriction to passively trap single cells and uses coplanar electrodes to obtain the impedance spectrum of the trapped cell via EIS and discrete impedance data points of the passing cells via IFC. Through experiment, we verified the individual functionality of IFC and EIS respectively, by revealing through IFC the impedance magnitude difference and quantifying through EIS the area-specific membrane capacitance and cytoplasm conductivity of the three types of cancer cells. We also demonstrated the complementarity of IFC and EIS, which holds for a wide range of the flow rate. We envision that the strategy of combining IFC and EIS provides a new thought in the efforts to enhancing the efficiency of electrical property measurement for single cells.

MicroRNA-25 (miR-25) has been reported to be a major miRNA marker in neural cells and is strongly expressed in ischemic brain tissues. However, the precise mechanism and effect of miR-25 in cerebral ischemia/reperfusion (I/R) injury needs further investigations. In the present study, the oxygen-glucose deprivation (OGD) model was constructed in human SH-SY5Y and IMR-32 cells to mimic I/R injury and to evaluate the role of miR-25 in regulating OGD/reperfusion (OGDR)-induced cell apoptosis. We found that miR-25 was downregulated in the OGDR model. Overexpression of miR-25 via miRNA-mimics transfection remarkably inhibited OGDR-induced cell apoptosis. Moreover, Fas was predicted as a target gene of miR-25 through bioinformatic analysis. The interaction between miR-25 and 3'-untranslated region (UTR) of Fas mRNA was confirmed by dual-luciferase reporter assay. Fas protein expression was downregulated by miR-25 overexpression in OGDR model. Subsequently, the small interfering RNA (siRNA)-mediated knockdown of Fas expression also inhibited cell apoptosis induced by OGDR model; in contrast, Fas overexpression abrogated the protective effects of miR-25 on OGDR-induced cells. Taken together, our results indicate that the upregulation of miR-25 inhibits cerebral I/R injury-induced apoptosis through downregulating Fas/FasL, which will provide a promising therapeutic target.

Recent studies have suggested that exercise may be beneficial for delaying or attenuating Alzheimer’s disease (AD). However, the underlying mechanisms were not clear. Microglia-mediated neuroinflammation is suggested to play an important role in the pathology of AD. The present study investigated the beneficial effects of treadmill exercise on amyloid-β (Aβ) deposition and cognitive function in amyloid precursor protein (APP)/PS1 mice in the early stage of AD progression and microglia-mediated neuroinflammation was mainly analyzed. The results demonstrated that 12 weeks of treadmill exercise preserved hippocampal cognitive function in APP/PS1 mice and substantially suppressed Aβ accumulation in the hippocampus. Treadmill exercise significantly inhibited neuroinflammation, which was characterized by a remarkably reduced expression of pro-inflammatory factors and increased expression of anti-inflammatory mediators in the hippocampus, resulting from a shift in activated microglia from the M1 to M2 phenotype. Treadmill exercise also attenuated oxidative stress presented by a marked reduction in methane dicarboxylic aldehyde (MDA) level and dramatically elevated SOD and Mn-SOD activities in the hippocampus. These findings suggest that treadmill exercise can effectively prevent the decrease in hippocampal-dependent cognitive function and Aβ deposits in early AD progression possibly via modulating microglia-mediated neuroinflammation and oxidative stress.

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