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This study presents a dielectrophoresis-based liquid metal (LM) droplet control microfluidic device. Six square liquid metal electrodes are fabricated beneath an LM droplet manipulation pool. By applying different voltages on the different electrodes, a non-uniform electric field is formed around the LM droplet, and charges are induced on the surface of the droplet accordingly, so that the droplet could be driven inside the electric field. With a voltage of ±1000 V applied on the electrodes, the LM droplets are driven with a velocity of 0.5 mm/s for the 2.0 mm diameter ones and 1.0 mm/s for the 1.0 mm diameter ones. The whole chip is made of PDMS, and microchannels are fabricated by laser ablation. In this device, the electrodes are not in direct contact with the working droplets; a thin PDMS film stays between the electrodes and the driven droplets, preventing Joule heat or bubble formation during the experiments. To enhance the flexibility of the chip design, a gallium-based alloy with melting point of 10.6 °C is used as electrode material in this device. This dielectrophoresis (DEP) device was able to successfully drive liquid metal droplets and is expected to be a flexible approach for liquid metal droplet control.Cutaneous melanoma is often resistant to therapy due to its high plasticity, as well as its ability to metabolise chemotherapeutic drugs. Sphingolipid signalling plays a pivotal role in its progression and metastasis. One of the ways melanoma alters sphingolipid rheostat is via over-expression of lysosomal acid ceramidase (AC), which catalyses the hydrolysis of pro-apoptotic long-chain ceramides into sphingosine and fatty acid. In this report, we examine the role of acid ceramidase in maintaining cellular homeostasis through the regulation of autophagy and mitochondrial activity in melanoma cell lines. We show that under baseline conditions, wild-type melanoma cells had 3-fold higher levels of the autophagy marker, microtubule-associated proteins 1A/1B light chain 3B (LC3 II), compared to AC-null cells. This difference was further magnified after cell starvation. Moreover, we noticed autophagy impairment in A375 AC-null cells, possibly due to local accumulation of non-metabolized ceramides. GSK2643943A in vivo Nonetheless, we observed that AC-null cells exhibited a significant increase in mitochondrial membrane potential compared to control cells. Consistent with this observation, we found that, after total starvation, ~30% of AC-null cells undergo apoptosis compared to ~6% of wild-type cells. As expected, AC transfection restored viability in A375 AC-null cells. Together, these findings suggest that AC-null melanoma cells change and adapt their metabolism to survive in the absence of AC, although in a way that does not allow them to cope with the stress of nutrient deprivation.By promoting atrial structural remodeling, atrial hypoxia contributes to the development of the atrial fibrillation substrate. Our study aimed to investigate the modulatory effect of hypoxia on profibrotic activity in cultured HL-1 cardiomyocytes and explore the possible signaling transduction mechanisms of profibrotic activity in vitro. Hypoxia (1% O2) significantly and time-dependently increased the expression of hypoxia-inducible factor (HIF)-1α and fibrotic marker proteins collagen I and III (COL1A and COL3A), transforming growth factor (TGF)-β1 and α-smooth muscle actin (SMA). Western blot or immunohistochemistry analysis showed that hypoxia-induced increase in COL1A and COL3A was significantly attenuated by the addition of SP600125 (a specific c-Jun N-terminal kinase [JNK] inhibitor) or expression of dominant-negative JNK before hypoxia treatment. The inhibition of hypoxia-activated phosphorylation of JNK signal components (JNK, MKK4, nuclear c-Jun and ATF-2) by pre-treatment with SP600125 could suppress hypoxia-stimulated HIF-1α upregulation and fibrotic marker proteins expression. Hypoxia significantly increased reactive oxygen species (ROS) production in cultured HL-1 atrial cells. Pre-treatment with N-acetylcysteine significantly abrogated the expression of nuclear HIF-1α, JNK transduction components and fibrotic marker proteins. Taken together, these findings indicated that the hypoxia-induced atrial profibrotic response occurs mainly via the ROS/JNK pathway, its downstream upregulation of HIF-1α and c-Jun/ATF2 phosphorylation and nuclear translocation to up-regulate the expression of fibrosis-related proteins (COL1A, COL3A, TGF-β1 and α-SMA). Our result suggests that suppression of ROS/JNK signaling pathway is a critical mechanism for developing a novel therapeutic strategy against atrial fibrillation.The response of fiber-reinforced polymer composites to an externally applied mechanical excitation is closely related to the microscopic stress transfer mechanisms taking place in the fiber-matrix interphasial region. In particular, in the case of viscoelastic responses, these mechanisms are time dependent. Defining the interphase thickness as the maximum radial distance from the fiber surface where a specific matrix property is affected by the fiber presence, it is important to study its variation with time. In the present investigation, the stress relaxation behavior of a glass fiber-reinforced polymer (GFRP) under flexural conditions was studied. Next, applying the hybrid viscoelastic interphase model (HVIM), developed by the first author, the interphase modulus and interphase thickness were both evaluated, and their variation with time during the stress relaxation test was plotted. It was found that the interphase modulus decreases with the radial distance, being always higher than the bulk matrix modulus. In addition, the interphase thickness increases with time, showing that during stress relaxation, fiber-matrix debonding takes place. Finally, the effect of fiber interaction on the interphase modulus was found. It is observed that fiber interaction depends on both the fiber-matrix degree of adhesion as well as the fiber volume fraction and the time-dependent interphase modulus.The COVID-19 pandemic has been accompanied by rapidly emerging evidence, changing guidance, and misinformation, which present new challenges for health literacy (HL) and digital health literacy (DHL) skills. This study explored whether COVID-19-related information access, attitudes, and behaviors were associated with health literacy and digital health literacy among college students in the United States. Self-reported measures of health literacy, along with items on pandemic-related attitudes, behaviors, information sources, and social networks, were collected online using a managed research panel. In July 2020, 256 responses were collected, which mirrored the racial/ethnic and gender diversity of U.S. colleges. Only 49% reported adequate HL, and 57% found DHL tasks easy overall. DHL did not vary by HL level. In multivariable models, both HL and DHL were independently associated with overall compliance with basic preventive practices. Higher DHL, but not HL, was significantly associated with greater willingness to get a COVID-19 vaccine and the belief that acquiring the disease would negatively impact their life.

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