The Electronic Conductive Adhesive (ECA) is a promising material as a substitute of traditional tin-lead solder, with many advantages outperforming tin-lead containing solder such as environmentally friendly, requiring much lower processing temperature and a much finer pitch. However, one critical problem related to ECA application is that the contact resistance increases significantly during an aging test, particularly at 85°C/85% relative humidity (RH) when ECA is bonded onto non-noble metal surfaces due to galvanic corrosion. Recently, it has been reported that graphene has an interesting and wonderful property, impermeability; it can prohibit most molecules from going through due to the fact that graphene is one of the most impermeable barrier materials, and it has become a potential candidate for anti-corrosion applications. Some papers studying the application of graphene for anti-corrosion of steel and other metals have already been published. In this paper, graphene film [12] barriers were introduced between the ECA and metal pad to alleviate the galvanic corrosion problem, which can lead to the deterioration of contact resistance, then the aging test @85°C/85% was performed for 500 hours. It was found that the contact resistance increased quickly during the first 200 hours of aging test for samples without graphene film barriers, while the contact resistance for samples with graphene barrier remained stable. Samples with graphene film barriers showed a smaller shift of the contact resistance than those without graphene barrier. The results indicated that the graphene film barrier can be used to improve ECA's reliability, especially @85°C/85% conditions.
Non-invasive brain tissue stimulation with a magnetic coil provides several irreplaceable advantages over that with an implanted electrode, in altering neural activities under pathological situations. We reviewed clinical cases that utilized time-varying magnetic fields for the treatment of epilepsy, and the safety issues related to this practice. Animal models have been developed to foster understanding of the cellular/molecular mechanisms underlying magnetic control of epileptic activity. These mechanisms include (but are not limited to) (1) direct membrane polarization by the magnetic field, (2) depolarization blockade by the deactivation of ion channels, (3) alteration in synaptic transmission, and (4) interruption of ephaptic interaction and cellular synchronization. Clinical translation of this technology could be improved through the advancement of magnetic design, optimization of stimulation protocols, and evaluation of the long-term safety. Cellular and molecular studies focusing on the mechanisms of magnetic stimulation are of great value in facilitating this translation.
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Pituitary adenylate cyclase-activating polypeptide (PACAP) is an endogenous peptide with neuroprotective effects on retinal neurons, but the precise mechanism underlying these effects remains unknown. Considering the abundance of mitochondria in retinal ganglion cells (RGCs), we postulate that the protective effect of PACAP is associated with the regulation of mitochondrial function. RGC-5 cells were subjected to serum deprivation for 48 hours to induce apoptosis in the presence or absence of 100 nM PACAP. As revealed with the Cell Counting Kit-8 assay, PACAP at different concentrations significantly increased the viability of RGC-5 cells. PACAP also inhibited the excessive generation of reactive oxygen species in RGC-5 cells subjected to serum deprivation. We also showed by flow cytometry that PACAP inhibited serum deprivation-induced apoptosis in RGC-5 cells. The proportions of apoptotic cells and cells with mitochondria depolarization were significantly decreased with PACAP treatment. Western blot assays demonstrated that PACAP increased the levels of Bcl-2 and inhibited the compensatory increase of PAC1. Together, these data indicate protective effects of PACAP against serum deprivation-induced apoptosis in RGCs, and that the mechanism of this action is associated with maintaining mitochondrial function.
Background: Reduction of the production of amyloid-β (Aβ) species has been intensively investigated as potential therapeutic approaches for Alzheimer’s disease (AD). However, the degradation of Aβ species, another potential beneficial approach, has been far less explored. Objective: To investigate the potential of multi-copper oxidases (MCOs) in degrading Aβ peptides and their potential benefits for AD treatment. Methods: We investigated the degradation efficiency of MCOs by using electrophoresis and validated the ceruloplasmin (CP)-Aβ interaction using total internal reflection fluorescence microscopy, fluorescence photometer, and fluorescence polarization measurement. We also investigated the therapeutic effect of ascorbate oxidase (AO) by using induced pluripotent stem (iPS) neuron cells and electrophysiological analysis with brain slices. Results: We discovered that CP, an important MCO in human blood, could degrade Aβ peptides. We also found that other MCOs could induce Aβ degradation as well. Remarkably, we revealed that AO had the strongest degrading effect among the tested MCOs. Using iPS neuron cells, we observed that AO could rescue neuron toxicity which induced by Aβ oligomers. In addition, our electrophysiological analysis with brain slices suggested that AO could prevent an Aβ-induced deficit in synaptic transmission in the hippocampus. Conclusions: To the best of our knowledge, our report is the first to demonstrate that MCOs have a degrading function for peptides/proteins. Further investigations are warranted to explore the possible benefits of MCOs for future AD treatment.
The novel micromagnetic stimulation (μMS) technology aims to provide high resolution on neuronal targets. However, consistency of neural activation could be compromised by a lack of surgical accuracy, biological variation, and human errors in operation. We have recently modeled the activation of an unmyelinated axon by a circular micro-coil. Although the coil could activate the axon, its performance sometimes lacked focality and consistency. The site of axonal activation could shift by several experimental factors, including the reversal of the coil current, displacement of the coil, and changes in the intensity of the stimulation. Current clinical practice with transcranial magnetic stimulation (TMS) has suggested that figure-eight coils could provide better performance in magnetic stimulation than circular coils. Here, we estimate the performance of μMS by a figure-eight micro-coil, by exploring the impact of the same experimental factors on its focality and consistency in axonal activation. We derived the analytical expression of the electric field and activating function generated by the figure-eight micro-coil, and estimated the location of axonal activation. Using NEURON modeling of an unmyelinated axon, we found two different types (A and B) of axon activation by the figure-eight micro-coil, mediated by coil currents of reversed direction. Type A activation is triggered by membrane hyperpolarization followed by depolarization; Type B activation is triggered by direct membrane depolarization. Consequently, the two types of stimulation are governed by distinct ion channel mechanisms. In comparison to the circular micro-coil, the figure-eight micro-coil requires significantly less current for axonal activation. Under figure-eight micro-coil stimulation, the site of axonal activation does not change with the reversal of the coil current, displacement of the coil, or changes in the intensity of the stimulation. Ultimately, the figure-eight micro-coil provides a more efficient and consistent site of activation than the circular micro-coil in μMS.
Abstract Background When a cell is exposed to a time-varying magnetic field, this leads to an induced voltage on the cytoplasmic membrane, as well as on the membranes of the internal organelles, such as mitochondria. These potential changes in the organelles could have a significant impact on their functionality. However, a quantitative analysis on the magnetically-induced membrane potential on the internal organelles has not been performed. Methods Using a two-shell model, we provided the first analytical solution for the transmembrane potential in the organelle membrane induced by a time-varying magnetic field. We then analyzed factors that impact on the polarization of the organelle, including the frequency of the magnetic field, the presence of the outer cytoplasmic membrane, and electrical and geometrical parameters of the cytoplasmic membrane and the organelle membrane. Results The amount of polarization in the organelle was less than its counterpart in the cytoplasmic membrane. This was largely due to the presence of the cell membrane, which "shielded" the internal organelle from excessive polarization by the field. Organelle polarization was largely dependent on the frequency of the magnetic field, and its polarization was not significant under the low frequency band used for transcranial magnetic stimulation (TMS). Both the properties of the cytoplasmic and the organelle membranes affect the polarization of the internal organelle in a frequency-dependent manner. Conclusions The work provided a theoretical framework and insights into factors affecting mitochondrial function under time-varying magnetic stimulation, and provided evidence that TMS does not affect normal mitochondrial functionality by altering its membrane potential.
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