Ultrafast Patterning Vertically Aligned Carbon Nanotube Forest on Al Foil and Si Substrate Using Chemical Vapor Deposition (CVD).

This study introduces a method of patterning carbon nanotube (CNTs) forests that is both fast and simple. We found that, as commercially available oil-based markers undergo nanotube synthesis, a thin film forms that prevents the catalyst, ferrocene, from coming into contact with the surface of the test sample. This, thus, blocks CNT growth. Through further deduction, we used styrene maleic anhydride (SMA) to conduct CNT patterning, in addition to analyzing the relationship between the weight percent concentration of the SMA and the extent to which it blocked CNT growth. We developed two separate methods for applying ink to soft and hard substrates: one method involved ink printing and the other laser stripping. In the CNT pattern we produced, a minimum line width of around 10 µm was attained.

Applying Aluminum⁻Vertically-Aligned Carbon Nanotube Forests Composites for Heat Dissipation.

Vertically-aligned carbon nanotube forests (VACNTs) with excellent axial heat dissipation properties were formed on aluminum foil to dissipate heat. In addition, the heat dissipation efficiency of aluminum-VACNTs composites in this work was compared with that of commercially available mainstream thermal sheets under the same natural cooling conditions. Chemical vapor deposition (CVD) was employed as a synthesis method using a three-segment high-temperature furnace. Subsequently, the temperature changes in a heating body with the aluminum-VACNTs composites was measured over time subject to natural cooling. In addition, the performance was compared with copper and pyrolytic graphite sheets. The experimental results revealed that the heat dissipation efficiency of the flexible aluminum-VACNTs composites was higher than that of clean aluminum foil, a copper sheet, and a pyrolytic graphite sheet by up to 56%, 40%, and 20%, respectively. Moreover, this work also verified the height of the carbon nanotube (CNT) did not influence the heat dissipation efficiency, indicating that the time cost of synthesis could be reduced.

Piezoelectric Sensor to Measure Soft and Hard Stiffness with High Sensitivity for Ultrasonic Transducers.

During dental sinus lift surgery, it is important to monitor the thickness of the remaining maxilla to avoid perforating the sinus membrane. Therefore, a sensor should be integrated into ultrasonic dental tools to prevent undesirable damage. This paper presents a piezoelectric (PZT) sensor installed in an ultrasonic transducer to measure the stiffness of high and low materials. Four design types using three PZT ring materials and a split PZT for actuator and sensor ring materials were studied. Three sensor locations were also examined. The voltage signals of the sensor and the displacement of the actuator were analyzed to distinguish the low and high stiffness. Using sensor type T1 made of the PZT-1 material and the front location A1 provided a high sensitivity of 2.47 Vm/kN. The experimental results demonstrated that our design can measure soft and hard stiffness.

miR-499 regulates mitochondrial dynamics by targeting calcineurin and dynamin-related protein-1.

Myocardial infarction is a leading cause of mortality worldwide. Here we report that modulation of microRNA-499 (miR-499) levels affects apoptosis and the severity of myocardial infarction and cardiac dysfunction induced by ischemia-reperfusion. We found that both the α- and ß-isoforms of the calcineurin catalytic subunit are direct targets of miR-499 and that miR-499 inhibits cardiomyocyte apoptosis through its suppression of calcineurin-mediated dephosphorylation of dynamin-related protein-1 (Drp1), thereby decreasing Drp1 accumulation in mitochondria and Drp1-mediated activation of the mitochondrial fission program. We also found that p53 transcriptionally downregulates miR-499 expression. Our data reveal a role for miR-499 in regulating the mitochondrial fission machinery and we suggest that modulation of miR-499 levels may provide a therapeutic approach for treating myocardial infarction.

[Properties of energy transfer in two host materials doped with Ir(ppy)3 and Rubrene].

The devices with phosphorescent material tris(2-phenylpyridine)iridium [Ir(ppy)3] and fluorescent material 5,6,11, 12-tetraphenylnaphthacene [Rubrene] as dopants in two kinds of host were constructed in the present study. Respectively, the two kinds of host are polyvinylcarbazole [PVK] and 4,4'-N,N-dicarbazole-biphenyl [CBP]. We studied the properties of energy transfer between host materials and dopants. Firstly, the absorption and photoluminescence spectra of PVK, CBP, Ir(ppy)3 and Rubrene were measured. The spectral overlap between the photoluminescence of PVK and the absorption spectrum of Ir(ppy)3 is larger than that of Rubrene. The result of the spectral overlap for CBP is the same as PVK. It was shown that the energy transfer from the two host materials to Ir(ppy)3 is stronger than that to Rubrene. In addition, the energy transfer from Ir(ppy)3 to Rubrene is possible according to their absorption and photoluminescence spectra. We compared the electroluminescence properties of different devices. In devicel of ITO/PVK : Rubrene : Ir(ppy)3 (100 : 5 : x)/BCP(10 nm)/Alq3 (20 nm)/Al and device 2 ITO/CBP : Rubrene : Ir(ppy)3 (100 : 5 : x)/BCP(10 nm)/Alq3 (20 nm)/Al(x = 0, 3), under the same DC bias, the electroluminescence results show that energy transfer from host to Rubrene through Ir(ppy)3 is the main mechanism. And energy transfer is much more efficient in CBP as host than in PVK. In addition, at the same voltage, the light power of the device doped with Ir(ppy)3 and Rubrene is obviously stronger than that of the device doped with Rubrene only. When the concentration of Ir(ppy)3 increases, the light power decreases at the same voltage, and the effect of concentration quenching is enhanced.

Novel cardiac apoptotic pathway: the dephosphorylation of apoptosis repressor with caspase recruitment domain by calcineurin.

BACKGROUND: Apoptosis repressor with caspase recruitment domain (ARC) is abundantly expressed in cardiomyocytes. Protein kinase CK2 can phosphorylate ARC at threonine-149, thereby enabling ARC to antagonize apoptosis. ARC phosphorylation occurs in a constitutive manner. Nevertheless, cardiomyocytes still undergo apoptosis that is related to cardiac diseases such as myocardial infarction and heart failure. Whether the occurrence of apoptosis is related to the loss of protection by ARC under pathological conditions remains unknown. METHODS AND RESULTS: ARC phosphorylation levels are decreased in cardiomyocytes treated with isoproterenol or aldosterone. We explored the molecular mechanism by which ARC phosphorylation levels are decreased. Our results reveal that either direct incubation or coexpression with calcineurin leads to a decrease in ARC phosphorylation levels. Inhibition of calcineurin can attenuate the reduction in ARC phosphorylation levels on treatment with isoproterenol or aldosterone. These data indicate that the reduction in ARC phosphorylation levels is related to its dephosphorylation by calcineurin. Our results further reveal that ARC can prevent isoproterenol- and aldosterone-induced apoptosis, but this function depends on its phosphorylation status. Isoproterenol and aldosterone upregulate Fas ligand expression, and Fas ligand and caspase-8 are required for isoproterenol and aldosterone to induce apoptosis. However, phosphorylated but not dephosphorylated ARC is able to inhibit caspase-8-mediated apoptosis. Phosphorylated ARC exerts its effects against caspase-8 by directly associating with procaspase-8 and inhibiting its interaction with Fas-associated protein with death domain. CONCLUSIONS: Our study identifies a novel cardiac apoptotic pathway in which ARC is dephosphorylated by calcineurin. This pathway could be a component in the cardiac apoptotic machinery.