Coalescence of immiscible sessile droplets on a partial wetting surface

Droplet coalescence is a common phenomenon and plays an important role in multi-disciplinary applications. Previous studies mainly consider the coalescence of miscible liquid, even though the coalescence of immiscible droplets on a solid surface is a common process. In this study, we explore the coalescence of two immiscible droplets on a partial wetting surface experimentally and theoretically. We find that the coalescence process can be divided into three stages based on the timescales and force interactions involved, namely (I) the growth of the liquid bridge, (II) the oscillation of the coalescing sessile droplet, and (III) the formation of a partially-engulfed compound sessile droplet and the subsequent retraction. In stage I, the immiscible interface is found not to affect the scaling of the temporal evolution of the liquid bridge, which follows the same 2/3 power law as that of miscible droplets. In Stage II, by developing a new capillary timescale considering both surface and interfacial tensions, we show that the interfacial tension between the two immiscible liquids functions as a nonnegligible resistance to the oscillation which decreases the oscillation periods. In Stage III, a modified Ohnesorge number is developed to characterize the visco-capillary and inertia-capillary timescales involved during the displacement of water by oil; a new model based on energy balance is proposed to analyze the maximum retraction velocity, highlighting that the viscous resistance is concentrated in a region close to the contact line.Comment: 20 pages, 9 figure

Hierarchical PANI/NiCo-LDH core-shell composite networks on carbon cloth for high performance asymmetric supercapacitor

In this work, a facile two-step strategy is adopted to construct hierarchical polyaniline/ NiCo-layered double hydroxide (PANI/NiCo-LDH) core-shell composite nanofiber networks on carbon cloth (CC). Three-dimensional (3D) porous PANI nanofiber networks are firstly uniformly anchored on CC by in-situ oxidative polymerization, followed by growth of NiCo-LDH nanoflakes on the crosslinked PANI framework via electrochemical deposition. The morphology and electrochemical properties of PANI/NiCo-LDH composites are controlled by the deposition time of LDH. Benefiting from rapid electron transport and ion diffusion, the well-defined PANI/NiCo-LDH hierarchical composite with 200 s deposition of LDH delivers a large capacitance of 1845 F g -1 at 0.5 A g -1 and excellent cycling stability of 82% capacitance retention after 5000 cycles at a very high current density of 10.0 A g -1 . Furthermore, an asymmetric supercapacitor (ASC) assembled with PANI/NiCo-LDH as a positive electrode and activated carbon (AC) as a negative electrode exhibits a high capacitance of 147.2 F g -1 in a potential range from 0 to 1.5 V and superior energy density of 46.0 Wh kg -1 at a power density of 351.6W kg -1 . © 2019 by the authors. Licensee MDPI, Basel, Switzerland.National Key R&D Program of China [2016YFE0131200]; National Natural Science Foundation of China [51702098]; International Cooperation Project of Shanghai Municipal Science and Technology Committee [18520744400]; Ministry of Education, Youth, and Sports of the Czech Republic [LTACH17015

Dexmedetomidine Protects Rat Liver against Ischemia-Reperfusion Injury Partly by the α2A-Adrenoceptor Subtype and the Mechanism Is Associated with the TLR4/NF-κB Pathway

Toll-like receptor 4 (TLR4)/nuclear factor kappa B (NF-κB) signaling plays a dominant role in the pathogenesis of liver ischemia-reperfusion (IR) injury. Dexmedetomidine (Dex) protects the liver against IR injury via α2-adrenoceptor activation, but the contribution of TLR4 signaling remains unknown. The authors aimed to examine whether pretreatment with Dex produces hepatic protection and investigate the influence of Dex on TLR4/NF-κB signaling. Dex was given via intraperitoneal injection 30 min prior to orthotopic autologous liver transplantation (OALT) in rats, and three α2-adrenoceptor antagonists including atipamezole (a nonselective α2 receptor blocker), ARC-239 (a specific α2B/C blocker) and BRL-44408 (a specific α2A blocker) were injected intraperitoneally 10 min before Dex administration. Histopathologic evaluation of the liver and the measurement of serum alanine aminotransferase activity, TLR4/NF-κB expression in the liver, and pro-inflammatory factors (serum tumor necrosis factor-α, interleukin-1β and hepatic myeloperoxidase) concentrations were performed 8 h after OALT. Dex ameliorated liver injury after OALT probably by suppressing the TLR4/NF-κB pathway and decreasing inflammatory mediator levels. The protective effects of Dex were reversed by atipamezole and BRL-44408, but not by ARC-239, suggesting that these effects were mediated in part by the α2A subtype. In conclusion, Dex attenuates liver injury partly via the α2A-adrenoceptor subtype, and the mechanism is due to the suppression of the TLR4/NF-κB pathway

Downregulation of Lung Toll-Like Receptor 4 Could Effectively Attenuate Liver Transplantation-Induced Pulmonary Damage at the Early Stage of Reperfusion

Acute lung injury (ALI) is a severe complication of orthotopic liver transplantation (OLT) with unclear underline mechanism. Toll-like receptor 4 (TLR4) has been identified as a key receptor mediating inflammation. We hypothesized that TLR4-mediated pulmonary inflammation may contribute to development of ALI during OLT. Patients with or without ALI were observed for serum cytokines and expression of TLR4 on peripheral blood polymorphonuclear leukocytes (PMNs). Next, rats which underwent orthotopic autologous liver transplantation (OALT) were divided into sham and model groups. Pulmonary function and the level of TLR4 expression and cytokines were analyzed. Furthermore, the role of TLR4 in OALT-mediated ALI was assessed in rats treated with TLR4-siRNA before OALT. The PMNs TLR4 expression and the serum TNF-α and IL-β level were higher in patients with ALI than those with non-ALI. Interestingly, lung TLR4 expression was significantly increased after 8 hours of OALT with increased levels of TNF-α and IL-β, which lead to lung pathological damage and an increase of lung myeloperoxidase content. Moreover, knockdown of TLR4 reduced lung cytokines release and reversed the above pathologic changes after OALT and finally improved rats’ survival rate. In conclusion, TLR4 overexpression, potentially by stimulating proinflammatory cytokine overproduction, contributes to the development of ALI after OLT