Fluid pumping by liquid metal droplet utilizing ac electric field.

We report a unique phenomenon in which liquid metal droplets (LMDs) under a pure ac electric field pump fluid. Unlike the directional pumping that occurs upon reversing the electric field polarity under a dc signal, this phenomenon allows the direction of fluid motion to be switched by simply shifting the position of the LMD within the cylindrical chamber. The physical mechanism behind this phenomenon has been termed Marangoni flow, caused by nonlinear electrocapillary stress. Under the influence of a localized, asymmetric ac electric field, the polarizable surface of the position-offset LMD produces a net time-averaged interfacial tension gradient that scales with twice the field strength, and thus pumps fluid unidirectionally. However, the traditional linear RC circuit polarization model of the LMD/electrolyte interface fails to capture the correct pump-flow direction when the thickness of the LMD oxide skin is non-negligible compared to the Debye length. Therefore, we developed a physical description by treating the oxide layer as a distributed capacitance with variable thickness and connected with the electric double layer. The flow profile is visualized via microparticle imaging velocimetry, and excellent consistency is found with simulation results obtained from the proposed nonlinear model. Furthermore, we investigate the effects of relevant parameters on fluid pumping and discuss a special phenomenon that does not exist in dc control systems. To our knowledge, no previous work addresses LMDs in this manner and uses a zero-mean ac electric field to achieve stable, adjustable directional pumping of a low-conductivity solution.

The role of Nrf2 in astragaloside IV-mediated antioxidative protection on heart failure.

CONTEXT: Heart failure is one of the most serious diseases worldwide. Astragaloside IV (ASI) is widely used in the treatment of cardiovascular diseases. OBJECTIVE: To elucidate the antioxidative mechanism of ASI in a rat model of left coronary artery ligation. MATERIALS AND METHODS: Left coronary artery of Sprague-Dawley rats was ligated to establish the model of heart failure, and then vehicle (saline) or ASI (1 mg/kg/day) was orally administered to the rats (n = 15) for 6 weeks. Echocardiography was used to evaluate the cardiac function. Myocardial infarct size was measured by triphenyltetrazolium chloride staining. Oxidative stress in the ventricular myocardium was determined. Molecular mechanisms were investigated by Western blot and chromatin immunoprecipitation. RESULTS: ASI improved the cardiac function, especially ejection fraction (75.27 ± 5.75% vs. 36.26 ± 4.14%) and fractional shortening (45.39 ± 3.66% vs. 17.88 ± 1.32%), and reduced the infarct size of left ventricle (20.69 ± 2.98% vs. 39.11 ± 3.97%). ASI maintained the levels of glutathione, catalase and superoxide dismutase and prevented the leakage of creatine kinase. In addition, ASI induced the protein expression of Nrf2 (1.97-fold) and HO-1 (2.79-fold), while reduced that of Keap-1 (0.77-fold) in the ventricular myocardium. In H9c2 cells, a rat cardiomyocyte cell line, ASI induced the translocation of Nrf2 from cytoplasm to nucleus, followed by transcriptional activation of NQO-1 (8.27-fold), SOD-2 (3.27-fold) and Txn-1 (9.83-fold) genes. DISCUSSION AND CONCLUSIONS: ASI prevented heart failure by counteracting oxidative stress through the Nrf2/HO-1 pathway. Application in clinical practice warrants further investigation.

Diabetes attenuates the inhibitory effects of endomorphin-2, but not endomorphin-1 on gastrointestinal transit in mice.

Diabetes affects the entire gastrointestinal tract from the esophagus to the anus. In the present study, the charcoal meal test was undertaken to evaluate and compare the effects of intracerebroventricular (i.c.v.) administration of endomorphins (EMs) on gastrointestinal transit in non-diabetic and diabetic mice. Significantly delayed gastrointestinal transit was found in both 4 and 8 weeks alloxan-induced diabetes compared to non-diabetes. Moreover, i.c.v. EM-1 and EM-2 dose-dependently delayed gastrointestinal transit in non-diabetes and diabetes. The EM-1-induced inhibitory effects of gastrointestinal transit in 4 weeks diabetes were qualitatively similar to those of non-diabetes. However, at higher doses, the EM-1-induced effects in 8 weeks diabetes were largely enhanced. Different to EM-1, the EM-2-induced inhibition of gastrointestinal transit in diabetic mice was significantly attenuated compared to non-diabetic mice. Moreover, these effects were further decreased in 8 weeks diabetes. The delayed gastrointestinal transit effects caused by EM-1 may be primarily mediated by µ2-opioid receptor in both non-diabetes and 4 weeks diabetes. Interestingly, in 8 weeks diabetes, these effects were mediated by µ2- and δ-receptors. However, the inhibitory effects of EM-2 were mediated by µ1-opioid receptor, which exerted a reduced function in diabetes. Also, poor blood glucose control might result in the attenuated effects of EM-2. Our present results demonstrated that diabetes attenuates the inhibitory effects of EM-2, but not EM-1 on gastrointestinal transit in mice. The different effects of EM-1 and EM-2 on gastrointestinal transit in diabetes may be due to changes of opioid receptor subtypes and their functional responses.

Characterization of opioid activities of endomorphin analogs with C-terminal amide to hydrazide conversion.

Previously, we have synthesized an endomorphin-2 (EM-2) analog with C-terminal amide to hydrazide conversion, exhibiting slightly lower µ-affinity than EM-2. In the present study, the influence of C-terminal amide group to hydrazide conversion on the in vitro and in vivo opioid activities of EMs was evaluated. Our results demonstrated that C-terminal amide to hydrazide conversion of EMs did not markedly change their µ-opioid receptor binding affinities. Nevertheless, EM-2-NHNH2 decreased guinea pig ileum (GPI) and mouse vas deferens (MVD) potencies by about 10- and 5-fold compared to the parent compound, respectively. It is noteworthy that EM-1-NHNH2 exhibited the highest antinociception after intracerebroventricular (i.c.v.) injection, about 1.5-fold more potent than EM-1, but with moderate colonic contractile and expulsive effects, comparable with EM-1. Additionally, though EM-2-NHNH2 showed a slightly lower antinociceptive effect than EM-2, at higher doses (i.c.v., 1.5 and 5 nmol/mouse) the inhibitory effects of colonic propulsion were significantly attenuated, which would be helpful in the development of suitable µ-opioid therapeutics, but without some undesirable side effects. Therefore, the present results gave the evidence that C-terminal amide to hydrazide conversion of EMs may play an important role in the regulation of opioid activities.