Depinning-Induced Capillary Wave during the Sliding of a Droplet on a Textured Surface

Surfaces covered with hydrophobic micro-/nanoscale textures can allow water droplets to slide easily because of low contact angle hysteresis. In contrast to the case of a droplet sliding on a smooth surface, when a droplet slides on a textured surface, it must recede from the textures at its rear edge and the resultant depinning events induce a capillary wave on the surface of the droplet. Although this depinning-induced capillary wave can be observed to some extent through high-speed imaging, important parameters of the wave, such as the wavelength and frequency, and the factors that determine these parameters are not fully understood. We report direct measurements of this depinning-induced capillary wave using microelectromechanical systems (MEMS)-based force sensors fabricated on a textured surface. Such sensor measurements reveal the frequency of the vibration occurring on the surface of the droplet, from which it is possible to calculate the wavelength of the capillary wave. We show that the frequency and wavelength of the depinning-induced capillary wave during the sliding of a water droplet on a micropillar array depend upon neither the size of the droplet nor its sliding velocity. However, the frequency (wavelength) decreases (increases) as the pitch of the micropillar array increases. We argue that the wavelength of the depinning-induced capillary wave is equal to the maximum length of the liquid bridges that develop at the micropillars before depinning. This hypothesis is confirmed by comparing the wavelengths obtained from the sensor measurements to the maximum liquid-bridge lengths calculated from observations using a high-speed camera

Visualization 1: Out-of-plane actuation with a sub-micron initial gap for reconfigurable terahertz micro-electro-mechanical systems metamaterials

Movie Originally published in Optics Express on 05 October 2015 (oe-23-20-26243

Depinning-Induced Capillary Wave during the Sliding of a Droplet on a Textured Surface

Surfaces covered with hydrophobic micro-/nanoscale textures can allow water droplets to slide easily because of low contact angle hysteresis. In contrast to the case of a droplet sliding on a smooth surface, when a droplet slides on a textured surface, it must recede from the textures at its rear edge and the resultant depinning events induce a capillary wave on the surface of the droplet. Although this depinning-induced capillary wave can be observed to some extent through high-speed imaging, important parameters of the wave, such as the wavelength and frequency, and the factors that determine these parameters are not fully understood. We report direct measurements of this depinning-induced capillary wave using microelectromechanical systems (MEMS)-based force sensors fabricated on a textured surface. Such sensor measurements reveal the frequency of the vibration occurring on the surface of the droplet, from which it is possible to calculate the wavelength of the capillary wave. We show that the frequency and wavelength of the depinning-induced capillary wave during the sliding of a water droplet on a micropillar array depend upon neither the size of the droplet nor its sliding velocity. However, the frequency (wavelength) decreases (increases) as the pitch of the micropillar array increases. We argue that the wavelength of the depinning-induced capillary wave is equal to the maximum length of the liquid bridges that develop at the micropillars before depinning. This hypothesis is confirmed by comparing the wavelengths obtained from the sensor measurements to the maximum liquid-bridge lengths calculated from observations using a high-speed camera

Nicorandil Prevents Gα_q-Induced Progressive Heart Failure and Ventricular Arrhythmias in Transgenic Mice

<div><h3>Background</h3><p>Beneficial effects of nicorandil on the treatment of hypertensive heart failure (HF) and ischemic heart disease have been suggested. However, whether nicorandil has inhibitory effects on HF and ventricular arrhythmias caused by the activation of G protein alpha q (Gα_q) -coupled receptor (GPCR) signaling still remains unknown. We investigated these inhibitory effects of nicorandil in transgenic mice with transient cardiac expression of activated Gα_q (Gα_q-TG).</p> <h3>Methodology/Principal Findings</h3><p>Nicorandil (6 mg/kg/day) or vehicle was chronically administered to Gα_q-TG from 8 to 32 weeks of age, and all experiments were performed in mice at the age of 32 weeks. Chronic nicorandil administration prevented the severe reduction of left ventricular fractional shortening and inhibited ventricular interstitial fibrosis in Gα_q-TG. SUR-2B and SERCA2 gene expression was decreased in vehicle-treated Gα_q-TG but not in nicorandil-treated Gα_q-TG. eNOS gene expression was also increased in nicorandil-treated Gα_q-TG compared with vehicle-treated Gα_q-TG. Electrocardiogram demonstrated that premature ventricular contraction (PVC) was frequently (more than 20 beats/min) observed in 7 of 10 vehicle-treated Gα_q-TG but in none of 10 nicorandil-treated Gα_q-TG. The QT interval was significantly shorter in nicorandil-treated Gα_q-TG than vehicle-treated Gα_q-TG. Acute nicorandil administration shortened ventricular monophasic action potential duration and reduced the number of PVCs in Langendorff-perfused Gα_q-TG mouse hearts. Moreover, HMR1098, a blocker of cardiac sarcolemmal K_ATP channels, significantly attenuated the shortening of MAP duration induced by nicorandil in the Gα_q-TG heart.</p> <h3>Conclusions/Significance</h3><p>These findings suggest that nicorandil can prevent the development of HF and ventricular arrhythmia caused by the activation of GPCR signaling through the shortening of the QT interval, action potential duration, the normalization of SERCA2 gene expression. Nicorandil may also improve the impaired coronary circulation during HF.</p> </div

Effects of nicorandil on the left ventricular fibrosis and on connective tissue growth factor (CTGF) and collagen type 1 gene expression.

<p>Panel A: Histology of the left ventricle stained with Masson’s trichrome in a WT, WT+nicorandil, Gα_q-TG, and Gα_qTG+nicorandil mouse. Original magnification: 40×. Panel B: Comparison of the fibrosis fraction in the left ventricle in WT, WT+nicorandil, Gα_q-TG, and Gα_qTG+nicorandil mice. Panel C: Quantitative analyses of CTGF and collagen type 1 gene expression by real-time real-time reverse transcriptase-polymerase chain reaction (RT-PCR) in WT, Gα_q-TG and Gα_q-TG+nicorandil hearts. Data for CTGF and collagen type 1 were normalized to those for ARPP0. Data are the mean ± SE obtained from 6 mice for each group. Panel D: Comparison of cardiomyocyte size in the left ventricle in WT, WT+nicorandil, Gα_q-TG, and Gα_qTG+nicorandil mice.</p

Echocardiographic parameters in WT, WT+nicorandil, Gα_q-TG, and Gα_q-TG+nicorandil mice.

<p>Data are the mean ± SE obtained from 6 mice for each group. ^ap<0.05, ^bp<0.01 vs. WT, +p<0.05, ^$p<0.01 vs. values in corresponding parameters of Gα_q-TG. LVEDd, left ventricular end-diastolic dimension; IVS, intraventricular septum.</p

Electrocardiographic parameters in WT, WT+nicorandil, Gα_q-TG, and Gα_q-TG+nicorandil mice.

<p>Data are the mean ± SE obtained from 6 mice for each group. ^ap<0.05, ^bp<0.01 vs. WT, +p<0.05 vs. values in corresponding parameters of vehicle-treated Gα_q-TG.</p

Quantitative analyses of Kir6.1 (A), Kir6.2 (A), SUR1 (B), SUR2A (B), SUR2B (B), eNOS (C), and iNOS (C) gene expression by real-time RT-PCR in WT, Gα_q-TG and Gα_q-TG+nicorandil hearts.

<p>Data for Kir6.1, Kir6.2, SUR1, SUR2A, SUR2B, eNOS, and iNOS were normalized to those for ARPP0. Data are the mean ± SE obtained from 6 mice for each group. SUR1, sulfonylurea receptor 1; SUR2A, sulfonylurea receptor 2A; SUR2B, sulfonylurea receptor 2B; eNOS, endothelial nitric oxide synthase; iNOS, inducible nitric oxide synthase; ARPP0, acidic ribosomal protein P0. Mice at the age of 32 weeks were used.</p

General parameters and the incidence of premature ventricular contraction (PVC) in WT, WT+nicorandil, Gα_q-TG, and Gα_q-TG+nicorandil mice.

<p>Data are the mean ± SE obtained from 10 mice for each group. ^ap<0.05, ^bp<0.01 vs. WT, +p<0.05, ^$p<0.01 vs. values in corresponding parameters of Gα_q-TG.</p

ECG lead II recordings from WT, WT+nicorandil, Gα_q-TG, and Gα_q+nicorandil mice.

<p>The upper 2 ECGs show premature ventricular contraction (PVC) and ventricular repetitive beats in anesthetized Gα_q-TG mice. The lower 3 ECGs recorded from a WT, WT+nicorandil, and Gα_q-TG+nicorandil mouse show P wave and QRS complex with a regular RR interval without any arrhythmia, indicating sinus rhythm. Mice at the age of 32 weeks were used. See text for details.</p