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Polypropylene has been widely used as dielectric material in organic thin-film capacitors due to their high breakdown strength, low dielectric loss and self-healing capability. However, polypropylene’s energy density is relatively low. Increasing the energy density of polypropylene by adding materials with a high dielectric constant is commonly used. Still, it often leads to an increase in dielectric loss, lower dielectric strength and other shortcomings. In this study, a thin 2D platelet of mica/graphene oxide composite material was made from exfoliated mica as a substrate and attached by graphene oxide. The mica/graphene oxide platelets were added to polypropylene to make a plastic dielectric composite. The non-conductive flat inorganic additive can increase the dielectric constant and dielectric strength of the composite without increasing dielectric loss. The tiny mica/graphene oxide platelets can significantly improve the dielectric properties of polypropylene. The results show that by adding a small amount (less than 1 wt%) mica/graphene oxide, the relative dielectric constant of polypropylene can increase to more than 3.7 without causing an increase in dielectric loss and the dielectric strength of polypropylene can also enhance.

High-quality GaN films grown on 4H-SiC (0001) substrate with 4° of miscutting orientation have been done by plasma-assisted molecular beam epitaxy with different N/Ga flux ratio. The effect of N/Ga flux ratio on the surface morphology, chemical composition, structural and optical properties was systematically investigated. The observations of in-situ reflective high-energy electron diffraction demonstrated the special surface of SiC substrate and GaN growth transition from two-to three-dimension depending on N/Ga flux ratio. In the Ga-rich condition for epitaxy, Ga droplets formed and the root mean square value of surface roughness increased by the characterizations of scanning electron microscopy and atomic force microscopy which also related to the formation of the pits on the surface due to the accumulation of excess Ga on the surface. The better growth parameter of GaN films in the work is N/Ga flux ratio of 28 at substrate temperature 700 °C. Its surface oxide and charge-compensated surface state associated with defects are minimized from the surface composition analysis of X-ray photoelectron spectroscopy. In the structural characterization of high-resolution X-ray diffraction, the value of full width at half maximum and density of threading dislocation are lower to prove the high-quality structure of GaN film grown at N/Ga flux ratio of 28. Finally, the photoluminescence analysis performed the narrow near-band-edge peak and yellow band, corresponding to the better quality of GaN films. In this report, high-quality GaN films on 4H-SiC (0001) with 4° of miscutting orientation have been demonstrated by the reduction of defect states via the different N/Ga flux ratio. N/Ga flux ratio not only influences the growth mechanism and surface morphology, but also the surface chemical composition, crystal quality and optical properties of GaN compound semiconductors.

GaN films were deposited by plasma-assisted molecular beam epitaxy on different substrates, i.e. Si (111), Sapphire (0001) and 4H-SiC (0001) with 4 ° of miscutting orientation. Due to the lattice mismatch between GaN films and substrates, the substrates profoundly affect the growth mechanism of GaN films on them during the epitaxy. The smooth and complete GaN films can be obtained on 4H-SiC substrates based on the analyses of reflection high energy electron diffraction, scanning electron microscopy and atomic force microscopy. Higher quality of GaN films on 4H-SiC was also confirmed by high resolution X-ray diffraction. Photoluminescence measurements show that the compress stress existed in GaN films grown on sapphire, but tensile stress was observed in the films grown on 4H-SiC and Si. Meanwhile, in-situ annealing treatment of post expitxy can remove Ga droplets on GaN films and decrease the surface roughness and defect density of GaN films; however, thermal decomposition on the surface of GaN films was observed in the characterizations of X-ray photoelectron spectroscopy.

Polyetheretherketone (PEEK) is a high-performance, semi-crystalline thermal polymer with medical advantages such as biocompatibility and radiolucency. PEEK has an elastic modulus comparable to that of human cortical bone, so it can effectively reduce the stress shielding effect caused by the mismatch between the mechanical properties of an implant and human bone tissue. However, PEEK is biologically inert, and its use typically relies on a variety of surface modification methods, such as surface coatings of bio-ceramic materials, enhancing the surface bioactivity, and osseointegration. Compared to thermal spray or plasma spray technologies, the cold spray is carried out at relatively low temperatures, retaining the original properties of the material. This research establishes an open-source three-dimensional printer compatible with PEEK and also develops a powder-spray module based on the cold spray technology that can coat the surfaces of PEEK printings with hydroxyapatite (HA) to improve its bioactivity. This paper discusses the best parameter selection for PEEK printing, a thermal history analysis of the printing process, and the adhesion of HA powder coated on PEEK specimens with different porosities. Finally, the PEEK implant is printed to measure its performance under a vertical load.

In this study, we propose a mass production-able and low-cost method to fabricate the anodes of Li-ion battery. Carbonaceous anodes, integrated with thin amorphous silicon layers by plasma enhanced chemical vapor deposition, can improve the performance of specific capacity and coulombic efficiency for Li-ion battery. Three different thicknesses of a-Si layers (320, 640, and 960 nm), less than 0.1 wt% of anode electrode, were deposited on carbonaceous electrodes at low temperature 200 °C. Around 30 mg of a-Si by plasma enhanced chemical vapor deposition (PECVD) can improve the specific capacity ~42%, and keep coulombic efficiency of the half Li-ion cells higher than 85% after first cycle charge-discharge test. For the thirty cyclic performance and rate capability, capacitance retention can maintain above 96%. The thicker a-Si layers on carbon anodes, the better electrochemical performance of anodes with silicon-carbon composites we get. The traditional carbonaceous electrodes can be deposited a-Si layers easily by plasma enhanced chemical vapor deposition, which is a method with high potential for industrialization.

Observations of nerve axons in vivo reveal that electrical activity increases the number and speed of transported mitochondria, showing how sudden increases in energy demand may be satisfied., Matching energy supply and demand is critical in the bioenergetic homeostasis of all cells. This is a special problem in neurons where high levels of energy expenditure may occur at sites remote from the cell body, given the remarkable length of axons and enormous variability of impulse activity over time. Positioning mitochondria at areas with high energy requirements is an essential solution to this problem, but it is not known how this is related to impulse conduction in vivo. Therefore, to study mitochondrial trafficking along resting and electrically active adult axons in vivo, confocal imaging of saphenous nerves in anaesthetised mice was combined with electrical and pharmacological stimulation of myelinated and unmyelinated axons, respectively. We show that low frequency activity induced by electrical stimulation significantly increases anterograde and retrograde mitochondrial traffic in comparison with silent axons. Higher frequency conduction within a physiological range (50 Hz) dramatically further increased anterograde, but not retrograde, mitochondrial traffic, by rapidly increasing the number of mobile mitochondria and gradually increasing their velocity. Similarly, topical application of capsaicin to skin innervated by the saphenous nerve increased mitochondrial traffic in both myelinated and unmyelinated axons. In addition, stationary mitochondria in axons conducting at higher frequency become shorter, thus supplying additional mitochondria to the trafficking population, presumably through enhanced fission. Mitochondria recruited to the mobile population do not accumulate near Nodes of Ranvier, but continue to travel anterogradely. This pattern of mitochondrial redistribution suggests that the peripheral terminals of sensory axons represent sites of particularly high metabolic demand during physiological high frequency conduction. As the majority of mitochondrial biogenesis occurs at the cell body, increased anterograde mitochondrial traffic may represent a mechanism that ensures a uniform increase in mitochondrial density along the length of axons during high impulse load, supporting the increased metabolic demand imposed by sustained conduction., Author Summary As mitochondria are the main power source for most cells, their correct localization is vital for cellular homeostasis. The morphological and functional complexity of neurons, and the unpredictability of energy demand resulting from sustained impulse activity, means that correct mitochondrial function and location is particularly important for these cells. However, it is unclear how mitochondrial transport responds to the wide range of physiological conduction frequencies experienced by an intact nervous system. Here we image mitochondria moving along mouse saphenous nerve axons in vivo and observe the effects of sustained trains of impulses, evoked either by electrical stimulation of myelinated axons at physiological frequencies (1 and 50 Hz), or chemical stimulation (cutaneous capsaicin) in unmyelinated axons. We find that the number and speed of mitochondria moving towards the peripheral sensory terminals dramatically increases in active axons. The increased numbers of mobile mitochondria seem to originate from “pinched off” segments of stationary mitochondria (mitochondrial fission), and from recruitment of small stationary mitochondria. The transported mitochondria appear to accumulate in sensory nerve terminals in the skin. This study suggests that mitochondrial fission is involved in rapidly supplying mobile mitochondria to aid their re-distribution to regions of increased metabolic demand along axons.

International audience; Measurements of the practical adhesion of screen-printed Ag films on BaTiO(3) substrates have been completed, showing that the interfacial crack propagation energy decreases rapidly with increasing silver volume porosity. A geometrical model is proposed to estimate the interface porosity, which is relevant for adhesion concerns, in function of the volume porosity of the sintered silver layer. Experimental results present more consistent tendencies after this transcripti

Traumatic brain injury (TBI) triggers a series of neuroinflammatory processes that contribute to evolution of neuronal injury. The present study investigated the neuroprotective effects and anti-inflammatory actions of berberine, an isoquinoline alkaloid, in both in vitro and in vivo TBI models. Mice subjected to controlled cortical impact injury were injected with berberine (10 mg·kg(-1)) or vehicle 10 min after injury. In addition to behavioral studies and histology analysis, blood-brain barrier (BBB) permeability and brain water content were determined. Expression of PI3K/Akt and Erk signaling and inflammatory mediators were also analyzed. The protective effect of berberine was also investigated in cultured neurons either subjected to stretch injury or exposed to conditioned media with activated microglia. Berberine significantly attenuated functional deficits and brain damage associated with TBI up to day 28 post-injury. Berberine also reduced neuronal death, apoptosis, BBB permeability, and brain edema at day 1 post-injury. These changes coincided with a marked reduction in leukocyte infiltration, microglial activation, matrix metalloproteinase-9 activity, and expression of inflammatory mediators. Berberine had no effect on Akt or Erk 1/2 phosphorylation. In mixed glial cultures, berberine reduced TLR4/MyD88/NF-κB signaling. Berberine also attenuated neuronal death induced by microglial conditioned media; however, it did not directly protect cultured neurons subjected to stretch injury. Moreover, administration of berberine at 3 h post-injury also reduced TBI-induced neuronal damage, apoptosis and inflammation in vivo. Berberine reduces TBI-induced brain damage by limiting the production of inflammatory mediators by glial cells, rather than by a direct neuroprotective effect.

Background Traumatic brain injury (TBI) induces a complex sequence of apopototic cascades that contribute to secondary tissue damage. The aim of this study was to investigate the effects of salidroside, a phenolic glycoside with potent anti-apoptotic properties, on behavioral and histological outcomes, brain edema, and apoptosis following experimental TBI and the possible involvement of the phosphoinositide 3-kinase/protein kinase B (PI3K)/Akt signaling pathway. Methodology/Principal Findings Mice subjected to controlled cortical impact injury received intraperitoneal salidroside (20, or 50 mg/kg) or vehicle injection 10 min after injury. Behavioral studies, histology analysis and brain water content assessment were performed. Levels of PI3K/Akt signaling-related molecules, apoptosis-related proteins, cytochrome C (CytoC), and Smac/DIABLO were also analyzed. LY294002, a PI3K inhibitor, was administered to examine the mechanism of protection. The protective effect of salidroside was also investigated in primary cultured neurons subjected to stretch injury. Treatment with 20 mg/kg salidroside_significantly improved functional recovery and reduced brain tissue damage up to post-injury day 28. Salidroside_also significantly reduced neuronal death, apoptosis, and brain edema at day 1. These changes were associated with significant decreases in cleaved caspase-3, CytoC, and Smac/DIABLO at days 1 and 3. Salidroside increased phosphorylation of Akt on Ser473 and the mitochondrial Bcl-2/Bax ratio at day 1, and enhanced phosphorylation of Akt on Thr308 at day 3. This beneficial effect was abolished by pre-injection of LY294002. Moreover, delayed administration of salidroside at 3 or 6 h post-injury reduced neuronal damage at day 1. Salidroside treatment also decreased neuronal vulnerability to stretch-induced injury in vitro. Conclusions/Significance Post-injury salidroside improved long-term behavioral and histological outcomes and reduced brain edema and apoptosis following TBI, at least partially via the PI3K/Akt signaling pathway.