Experimental investigations on drag-reduction characteristics of bionic surface with water-trapping microstructures of fish scales

Biological surfaces with unique wettability in nature have provided an enormous innovation for scientists and engineers. More specifically, materials possessing various wetting properties have drawn considerable attention owing to their promising application prospects. Recently, great efforts have been concentrated on the researches on wetting-induced drag-reduction materials inspired by biology because of their ability to save energy. In this work, the drag-reduction characteristics of the bionic surface with delicate water-trapping microstructures of fish Ctenopharyngodon idellus scales were explored by experimental method. Firstly, the resistance of smooth surface and bionic surface experimental sample at different speeds was carefully tested through the testing system for operation resistance. Then, the contact angle (CA) of fish scale surface was measured by means of the contact angle measuring instrument. It was discovered that the bionic surface created a rewarding drag-reduction effect at a low speed, and the drag-reduction rate significantly displayed a downward trend with the increase in flow speed. Thus, when the rate was 0.66 m/s, the drag-reduction effect was at the optimum level, and the maximum drag reduction rate was 2.805%, which was in concordance with the simulated one. Furthermore, a contact angle (CA) of 11.5° appeared on the fish scale surface, exhibiting fine hydrophilic property. It further manifested the spreading-wetting phenomenon and the higher surface energy for the area of apical of fish scales, which played an important role in drag-reduction performance. This work will have a great potential in the engineering and transportation field

The studies on gas adsorption properties of MIL-53 series MOFs materials

Molecular dynamics (MD), grand canonical Monte Carlo (GCMC) and ideal adsorbed solution theory (IAST) were used to study the structures and gas adsorption properties of MIL-53(M)[M=Cr, Fe, Sc, Al] metal organic framework (MOF) materials. The results show that the volumes of those MOF materials increase significantly at high temperature. By analyzing the adsorption isotherms, we found that the temperature had a paramount effect on the gas adsorption behaviors of these MOF materials. For MIL-53(Cr), the orders of the quantities of adsorbed gases were CH4>N2>CO2>H2S, CH4>H2S>CO2>N2 and CH4>CO2>H2S>N2 at 100K, 293K and 623K, respectively. We also calculated the adsorption of several combinations of two gases by MIL-53(Cr) at 293K, the results indicate that the material had selective adsorption of CH4 over CO2, H2S and N2. Our calculations provide microscopic insights into the gas adsorption performances of these MOFs and may further guide the practice of gas separation

Abnormal Downregulation of Caveolin-3 Mediates the Pro-Fibrotic Action of MicroRNA-22 in a Model of Myocardial Infarction

Background/Aims: Cardiac fibrosis is an important cardiac remodeling event that can ultimately lead to the development of severe arrhythmia and heart failure. MicroRNAs (miRNAs) are involved in the pathogenesis of many cardiovascular diseases. Here, we aimed to investigate the effects of caveolin-3 (Cav3) on the pathogenesis of cardiac fibrosis and the underlying molecular mechanisms. Methods: Cav3 expression was decreased in cardiac fibrosis in vivo and in vitro model. To investigate the role of Cav3 in cardiac fibrosis, we transfected cardiac fibroblasts (CFs) with the siRNA of Cav3 and Cav3-overexpressing plasmid. The collagen content and proliferation of CFs were detected by qRT-PCR, western blot, MTT, and immunofluorescence. A luciferase reporter gene assay and gain/loss of function were used to detect the relationship between miR-22 and Cav3. Results: Cav3 depletion in CFs induced an increase in collagen content, cell proliferation, and phenotypic conversion of fibroblasts to myofibroblasts. Conversely, Cav3 overexpression in CFs was shown to inhibit angiotensin II-mediated excessive collagen deposition through protein kinase C (PKC)ε inactivation. Cav3 was experimentally confirmed as a direct target of miR-22, containing two seed binding sites in its 3′-untranslated region, and miR-22 was demonstrated to be significantly upregulated in the ischemic border zone in mice after myocardial infarction and in neonatal rat CFs pretreated with angiotensin II. miR-22 overexpression increased CFs proliferation, and collagen and α-smooth muscle actin levels in CFs, while the knockdown of endogenous miR-22 decreased CFs numbers. Conclusions: Our findings demonstrate that miR-22 accelerates cardiac fibrosis through the miR-22-Cav3-PKCε pathway, which, therefore, may represent a new therapeutic target for treatment of excessive fibrosis-associated cardiac diseases