Transient Breakdown Research Articles

Dynamic Gain Analysis Reveals Encoding Deficiencies in Cortical Neurons That Recover from Hypoxia-Induced Spreading Depolarizations.

Cortical regions that are damaged by insults, such as ischemia, hypoxia, and trauma, frequently generate spreading depolarization (SD). At the neuronal level, SDs entail complete breakdown of ionic gradients, persisting for seconds to minutes. It is unclear whether these transient events have a more lasting influence on neuronal function. Here, we describe electrophysiological changes in cortical neurons after recovery from hypoxia-induced SD. When examined with standard measures of neuronal excitability several hours after recovery from SD, layer 5 pyramidal neurons in brain slices from mice of either sex appear surprisingly normal. However, we here introduce an additional parameter, dynamic gain, which characterizes the bandwidth of action potential encoding by a neuron, and thereby reflects its potential efficiency in a multineuronal circuit. We find that the ability of neurons that recover from SD to track high-frequency inputs is markedly curtailed; exposure to hypoxia did not have this effect when SD was prevented pharmacologically. Staining for Ankyrin G revealed at least a fourfold decrease in the number of intact axon initial segments in post-SD slices. Since this effect, along with the effect on encoding, was blocked by an inhibitor of the Ca2+-dependent enzyme, calpain, we conclude that both effects were mediated by the SD-induced rise in intracellular Ca2+ Although effects of calpain activation were detected in the axon initial segment, changes in soma-dendritic compartments may also be involved. Whatever the precise molecular mechanism, our findings indicate that in the context of cortical circuit function, effectiveness of neurons that survive SD may be limited.SIGNIFICANCE STATEMENT Spreading depolarization, which commonly accompanies cortical injury, entails transient massive breakdown of neuronal ionic gradients. The function of cortical neurons that recover from hypoxia-induced spreading depolarization is not obviously abnormal when tested for usual measures of neuronal excitability. However, we now demonstrate that they have a reduced bandwidth, reflecting a significant impairment of their ability to precisely encode high-frequency components of their synaptic input in output spike trains. Thus, neurons that recover from spreading depolarizations are less able to function normally as elements in the multineuronal cortical circuitry. These changes are correlated with activation of the calcium-dependent enzyme, calpain.

Transition in channel flow with streamwise magnetic field

Abstract Transition to turbulence in a magnetohydrodynamic channel flow is studied numerically under a uniform and constant streamwise magnetic field. The laminar–turbulence transition can be triggered with transient growth and subsequent breakdown of linear optimal perturbations in different forms: streamwise mode, a single oblique mode and a pair of symmetric oblique modes. The nonlinear evolution of optimal modes is analyzed via a series of direct numerical simulations at a single subcritical Reynolds number R e = 5000 and different Hartmann numbers H a ranged from 10 to 70. It is found that, the superposition of symmetric oblique modes can trigger the transition most efficiently even with a lower perturbation energy level. The streamwise mode is less efficient and transition can be observed only after adding three dimensional random noise at the moment of strongest energy amplification. The magnetic damping effect is significant at high Hartmann number and no transition is found under a sufficiently strong magnetic field with H a larger than approximately 70. This critical value can be predicted straightforwardly from the linear relationship of friction coefficient of channel flow and magnetic interaction parameter.

A Deeper Look at Bottom-up Copper Deposition in High Aspect Ratio through Silicon Vias

Superconformal copper electrodeposition in larger features, as in smaller features, is influenced by both suppressor and chloride in the copper electrolyte. Different behaviors are observed in electroanalytical measurements of low and high chloride electrolytes. One significant difference is the dependence of suppression breakdown and associated S-shaped negative differential resistance (S-NDR) on transport assessed using a rotating disk electrode. Superconformal filling of 56 μm tall, annular Through Silicon Vias (TSVs) from the electrolytes can exhibit the bottom-up evolution previously noted for the Cu system as well as transient or steady-state passivation breakdown along the TSV sidewall, with uniform deposition below, previously demonstrated with Au, Ni and Co S-NDR systems. As both filling geometries are predicted by S-NDR based models, I will discuss the factors that we believe determine the experimental filling geometry.

Clamping system for series connected IGBTs to avoid transient breakdown voltages

IGBTs (Insulated Gate Bipolar Transistor) can be used for power DC-DC converters at higher voltages. A series connection is needed due to the blockingcapability limit of 6500V. The voltage must be shared among the IGBTs both dynamic when switching and blocking mode. A non-synchronized switching creates transient voltage that might damage the IGBT. The non-synchronized switching comes from different delays in the gate drivers and deviation in the IGBT parameters. This paper investigates in theory and practice a solutioncontains of clamp circuit, dynamic and static circuit. Turning on process of the stack of three IGBTs are in focus in a buck converter design. An operatingvoltage closer to the IGBT limit is used in order to press the system. For the simulations (Pspice) and experimental tests, fast IGBTs (1200V /30A IXYH40N120C3) are used to show the good dynamic of the chosen solution. The Lab tests also show that because of the deviation in parameters preadjustment of the gate signals is needed. The experimental tests have been carried out in different clamp voltage to finally have clamp voltage close tothe blocking voltage of the IGBTs and maximum 2A as output current. Examples of wave forms for voltages are given and discussed.

Abstract 5215: Time dependent blood-brain barrier modulation by vascular endothelial growth factor to improve CNS drug delivery

Abstract Introduction: Efforts to transiently increase blood brain barrier permeability would facilitate improved CNS delivery of chemotherapy agents. Previous studies demonstrated that vascular endothelial factor (VEGF) increases permeability in traumatic brain injury and ischemic brain disease. Exogenously administered VEGF increases barrier permeability in the non-diseased CNS. In our study, we investigated the role for exogenous VEGF therapy to modulate blood-brain barrier permeability Methods: For in vitro studies, confluent mouse brain endothelial cells (BEND.3) were treated with VEGF165. Trans-endothelial electrical resistance measured cell impedance changes and immunofluorescence was used to assess qualitative expression of tight and adherens junction proteins at key time points. Western blotting and qPCR were done to evaluate the effect of VEGF on expression of protein and RNA associated with tight and adherens junctions. Results: Confluent endothelial cells treated with rVEGF165 (200ng/mL) evaluated by TEER show a significant drop in cell impedance approximately 6 hours post treatment, compared to control (more than 10-fold) reflecting increased permeability of the monolayer. Treatment with progressively higher doses of VEGF (200, 400, and 600ng/mL) showed a progressively greater drop in cell impedance. Immunofluorescence of endothelial cells treated with rVEGF165 (200ng/mL) shows disassembly of both tight junctions and adherens junctions between 4 and 8 hours post-treatment compared to controls. Western blots and qPCR demonstrate that rVEGF165 treatment induces down-regulation of genes associated with tight junctions, such as Claudin5, beginning as early as 4 hours post treatment and continuing up to 24 hours post treatment. Conclusion: Our results suggest that VEGF is capable of inducing transient breakdown of the blood-brain barrier, which may facilitate improved CNS delivery of chemotherapeutic agents. Our in vitro data warrants further investigations of the applicability of VEGF therapy to induce endothelial cell permeability in animal tumor models, potentially improving delivery of chemotherapeutic drugs. Citation Format: Matthew McCord. Time dependent blood-brain barrier modulation by vascular endothelial growth factor to improve CNS drug delivery [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2017; 2017 Apr 1-5; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2017;77(13 Suppl):Abstract nr 5215. doi:10.1158/1538-7445.AM2017-5215

Temporal assessment of nanoparticle accumulation after experimental brain injury: Effect of particle size

Nanoparticle (NP) based therapeutic and theranostic agents have been developed for various diseases, yet application to neural disease/injury is restricted by the blood-brain-barrier (BBB). Traumatic brain injury (TBI) results in a host of pathological alterations, including transient breakdown of the BBB, thus opening a window for NP delivery to the injured brain tissue. This study focused on investigating the spatiotemporal accumulation of different sized NPs after TBI. Specifically, animal cohorts sustaining a controlled cortical impact injury received an intravenous injection of PEGylated NP cocktail (20, 40, 100, and 500 nm, each with a unique fluorophore) immediately (0 h), 2 h, 5 h, 12 h, or 23 h after injury. NPs were allowed to circulate for 1 h before perfusion and brain harvest. Confocal microscopy demonstrated peak NP accumulation within the injury penumbra 1 h post-injury. An inverse relationship was found between NP size and their continued accumulation within the penumbra. NP accumulation preferentially occurred in the primary motor and somatosensory areas of the injury penumbra as compared to the parietal association and visual area. Thus, we characterized the accumulation of particles up to 500 nm at different times acutely after injury, indicating the potential of NP-based TBI theranostics in the acute period after injury.

Grainyhead-like 2 inhibits the coactivator p300, suppressing tubulogenesis and the epithelial-mesenchymal transition.

Developmental morphogenesis and tumor progression require a transient or stable breakdown of epithelial junctional complexes to permit programmed migration, invasion, and anoikis resistance, characteristics endowed by the epithelial-mesenchymal transition (EMT). The epithelial master-regulatory transcription factor Grainyhead-like 2 (GRHL2) suppresses and reverses EMT, causing a mesenchymal-epithelial transition to the default epithelial phenotype. Here we investigated the role of GRHL2 in tubulogenesis of Madin-Darby canine kidney cells, a process requiring transient, partial EMT. GRHL2 was required for cystogenesis, but it suppressed tubulogenesis in response to hepatocyte growth factor. Surprisingly, GRHL2 suppressed this process by inhibiting the histone acetyltransferase coactivator p300, preventing the induction of matrix metalloproteases and other p300-dependent genes required for tubulogenesis. A 13-amino acid region of GRHL2 was necessary for inhibition of p300, suppression of tubulogenesis, and interference with EMT. The results demonstrate that p300 is required for partial or complete EMT occurring in tubulogenesis or tumor progression and that GRHL2 suppresses EMT in both contexts through inhibition of p300.

Proteome of Plasmopara viticola-infected Vitis vinifera provides insights into grapevine Rpv1/Rpv3 pyramided resistance to downy mildew

Grapevine is one of the major fruit crops worldwide and requires phytochemical use due to susceptibility to numerous pests, including downy mildew. The pyramiding of previous identified QTL resistance regions allows selection of genotypes with combined resistance loci in order to build up sustainable resistance. This study investigates resistance response of pyramided plants containing Rpv1 and Rpv3 loci to Plasmopara viticola infection process. Phenotypic characterization showed complete resistance and lack of necrotic hypersensitive response spots. Principal Component Analysis revealed infected 96hpi (hours post-inoculation) samples with the most distant proteomes of the entire dataset, followed by the proteome of infected 48hpi samples. Quantitative and qualitative protein differences observed using 2-DE gels coupled to nanoHPLC-ESI-MS/MS analysis showed a lack of transient breakdown in defense responses (biphasic modulation) accompanying the onset of disease. Forty-one proteins were identified, which were mainly included into functional categories of redox and energy metabolism. l-ascorbate degradation pathway was the major altered pathway and suggests up-regulation of anti-oxidant metabolism in response to apoplastic oxidative burst after infection. Overall, these data provide new insights into molecular basis of this incompatible interaction and suggests several targets that could potentially be exploited to develop new protection strategies against this pathogen. Biological significanceThis study provide new insights into the molecular basis of incompatible interaction between Plasmopara viticola and pyramided Rpv1/Rpv3 grapevine and suggests several targets that could potentially be exploited to develop new protection strategies against this pathogen. This is the first proteomic characterization of resistant grapevine available in the literature and it presents contrasting proteomic profiles of that of susceptible plants. The resistance against downy mildew in grapevine has been a long sought and the availability of resistance loci is of major importance. This is the first molecular characterization of resistance provided by Rpv1 and Rpv3 genes.

An Unexpected Transient Breakdown of the Blood Brain Barrier Triggers Passage of Large Intravenously Administered Nanoparticles.

The highly restrictive blood-brain barrier (BBB) plays a critically important role in maintaining brain homeostasis and is pivotal for proper neuronal function. The BBB is currently considered the main limiting factor restricting the passage of large (up to 200 nm) intravenously administered nanoparticles to the brain. Breakdown of the barrier occurs as a consequence of cerebrovascular diseases and traumatic brain injury. In this article, we report that remote injuries in the CNS are also associated with BBB dysfunction. In particular, we show that a focal partial transection of the optic nerve triggers a previously unknown transient opening of the mammalian BBB that occurs in the visual centres. Importantly, we demonstrate that this transient BBB breakdown results in a dramatic change in the biodistribution of intravenously administered large polymeric nanoparticles which were previously deemed as BBB-impermeable.

A Dioxobilin-Type Fluorescent Chlorophyll Catabolite as a Transient Early Intermediate of the Dioxobilin-Branch of Chlorophyll Breakdown in Arabidopsis thaliana.

Chlorophyll breakdown in higher plants occurs by the so called “PaO/phyllobilin” path. It generates two major types of phyllobilins, the characteristic 1-formyl-19-oxobilins and the more recently discovered 1,19-dioxobilins. The hypothetical branching point at which the original 1-formyl-19-oxobilins are transformed into 1,19-dioxobilins is still elusive. Here, we clarify this hypothetical crucial transition on the basis of the identification of the first natural 1,19-dioxobilin-type fluorescent chlorophyll catabolite (DFCC). This transient chlorophyll breakdown intermediate was isolated from leaf extracts of Arabidopsis thaliana at an early stage of senescence. The fleetingly existent DFCC was then shown to represent the direct precursor of the major nonfluorescent 1,19-dioxobilin that accumulated in fully senescent leaves.

Experimental study of rotating Hagen-Poiseuille flow discharging into a 1:8 sudden expansion

In this paper, we present experimental evidence for the five different states that result from rotating Hagen-Poiseuille flow when it discharges into a 1:8 sudden expansion, namely: stable, convectively unstable, unstable shear layer, stable and unstable vortex breakdowns. Sanmiguel-Rojas et al. [“Three-dimensional structure of confined swirling jets at moderately large Reynolds numbers,” Phys. Fluids 20, 044104 (2008)] numerically predicted four of these five states and mapped the transition from one state to another. Our main objective is to study the onset of instabilities and vortex breakdown in these states experimentally. For this purpose, we visualize the flow at the inlet of the expansion for several values of moderately large Reynolds numbers, Re, and of swirl parameters, S. We analyze the inner region of the state that corresponds to the unstable shear layer in the sudden expansion and find two different states that share the same character, although they have different non-dimensional frequencies. The first relates to an oscillating structure near the axis, which arises at a small value of the swirl parameter, as well as to a generation of vortices that move downstream. The second shows, for greater values of the swirl parameter, vortices interacting with the boundary layer located on the wall of the static container that is perpendicular to the flow direction. In addition, we find a transition from stable to unstable vortex breakdown when perturbations become absolutely unstable inside the rotating pipe flow. Therefore, the most remarkable experimental finding is a new state, namely, unstable or transient vortex breakdown that takes place for the same pair of values (Rea, Sa) at which the onset of the absolute instability curve appears and intersects the region of stable vortex breakdown.

Redistribution of neural phase coherence reflects establishment of feedforward map in speech motor adaptation.

Despite recent progress in our understanding of sensorimotor integration in speech learning, a comprehensive framework to investigate its neural basis is lacking at behaviorally relevant timescales. Structural and functional imaging studies in humans have helped us identify brain networks that support speech but fail to capture the precise spatiotemporal coordination within the networks that takes place during speech learning. Here we use neuronal oscillations to investigate interactions within speech motor networks in a paradigm of speech motor adaptation under altered feedback with continuous recording of EEG in which subjects adapted to the real-time auditory perturbation of a target vowel sound. As subjects adapted to the task, concurrent changes were observed in the theta-gamma phase coherence during speech planning at several distinct scalp regions that is consistent with the establishment of a feedforward map. In particular, there was an increase in coherence over the central region and a decrease over the fronto-temporal regions, revealing a redistribution of coherence over an interacting network of brain regions that could be a general feature of error-based motor learning in general. Our findings have implications for understanding the neural basis of speech motor learning and could elucidate how transient breakdown of neuronal communication within speech networks relates to speech disorders.

“You Shall Not Pass”—tight junctions of the blood brain barrier

The structure and function of the barrier layers restricting the free diffusion of substances between the central nervous system (brain and spinal cord) and the systemic circulation is of great medical interest as various pathological conditions often lead to their impairment. Excessive leakage of blood-borne molecules into the parenchyma and the concomitant fluctuations in the microenvironment following a transient breakdown of the blood-brain barrier (BBB) during ischemic/hypoxic conditions or because of an autoimmune disease are detrimental to the physiological functioning of nervous tissue. On the other hand, the treatment of neurological disorders is often hampered as only minimal amounts of therapeutic agents are able to penetrate a fully functional BBB or blood cerebrospinal fluid barrier. An in-depth understanding of the molecular machinery governing the establishment and maintenance of these barriers is necessary to develop rational strategies allowing a controlled delivery of appropriate drugs to the CNS. At the basis of such tissue barriers are intimate cell-cell contacts (zonulae occludentes, tight junctions) which are present in all polarized epithelia and endothelia. By creating a paracellular diffusion constraint TJs enable the vectorial transport across cell monolayers. More recent findings indicate that functional barriers are already established during development, protecting the fetal brain. As an understanding of the biogenesis of TJs might reveal the underlying mechanisms of barrier formation during ontogenic development numerous in vitro systems have been developed to study the assembly and disassembly of TJs. In addition, monitoring the stage-specific expression of TJ-associated proteins during development has brought much insight into the “developmental tightening” of tissue barriers. Over the last two decades a detailed molecular map of transmembrane and cytoplasmic TJ-proteins has been identified. These proteins not only form a cell-cell adhesion structure, but integrate various signaling pathways, thereby directly or indirectly impacting upon processes such as cell-cell adhesion, cytoskeletal rearrangement, and transcriptional control. This review will provide a brief overview on the establishment of the BBB during embryonic development in mammals and a detailed description of the ultrastructure, biogenesis, and molecular composition of epithelial and endothelial TJs will be given.

Assessment of Retinal Alterations after Intravitreal Ocriplasmin with Spectral-Domain Optical Coherence Tomography

Assessment of Retinal Alterations after Intravitreal Ocriplasmin with Spectral-Domain Optical Coherence Tomography

Transgressions of compartment boundaries and cell reprogramming during regeneration in Drosophila

Animals have developed mechanisms to reconstruct lost or damaged tissues. To regenerate those tissues the cells implicated have to undergo developmental reprogramming. The imaginal discs of Drosophila are subdivided into distinct compartments, which derive from different genetic programs. This feature makes them a convenient system to study reprogramming during regeneration. We find that massive damage inflicted to the posterior or the dorsal compartment of the wing disc causes a transient breakdown of compartment boundaries, which are quickly reconstructed. The cells involved in the reconstruction often modify their original identity, visualized by changes in the expression of developmental genes like engrailed or cubitus interruptus. This reprogramming is mediated by up regulation of the JNK pathway and transient debilitation of the epigenetic control mechanism. Our results also show that the local developmental context plays a role in the acquisition of new cell identities: cells expressing engrailed induce engrailed expression in neighbor cells. DOI: http://dx.doi.org/10.7554/eLife.01831.001.

Characterization of electroporation for unbiased delivery of small molecules in high throughput screening applications (654.13)

In cell‐based high throughput screening applications, the assumption is typically made that all molecules have equal and complete access to the target of interest. In the case of intracellular targets, this is most likely not the case, as the molecules in a diverse screening library will exhibit varying degrees of cell permeability, or even lack thereof. This is likely to result in in false negatives.Electroporation is the use of brief electric pulses to overcome the barrier of the cell membrane. By the application of external electric fields, transient and reversible breakdown of the membrane can be induced. This transient state can be used to load cells with a variety of different molecules. Initially developed for gene transfer, electroporation can be used for delivery of a variety of other molecules ranging from ions to drugs, dyes, tracers and antibodies. Electroporation has proven useful both in vitro, in vivo and in patients, where drug delivery to tumors has been performed.In this work, we have explored the use of a high throughput electroporation platform, Cellaxess Elektra, for unbiased delivery of small molecules into cells in a cell‐based assay. The molecules selected were fluorescent and were representative of those that can be found in a small molecule library. The cell permeability with and without electroporation was characterized by means of fluorescence microscopy, and in the selected collection of ~400 compounds, 20 exhibited low or no cell permeability which could be enhanced by means of electroporation. We believe that this could prove to be a valuable tool in identifying families of new leads previously undiscovered.

DNS of bypass transition in entrance channel flow induced by boundary layer interaction

Developing entrance flows are of interest in a large number of application areas. They have been widely studied in the past, but many aspects of these flows are not yet fully understood. One of the questions concerns the stability and turbulent transition in the entrance region of a channel. The present study investigates by direct numerical simulation (DNS) the laminar–turbulent transition induced by boundary layer interaction in a spatially developing flow near the entrance of a channel, where the laminar flow is linearly stable. For uniform inlet flow conditions and at sufficiently high Reynolds number, the turbulent transition actually takes place inside the boundary layers and well before the fully developed regime. The transition of one of the two boundary layers is triggered near the entry section by small amplitude perturbations, such as the ones created by small isolated obstacles distributed on the wall. These generate elongated streaks, and their transient growth and breakdown lead to the turbulent transition of the boundary layer near the entrance region. The transition of the second boundary layer is induced by the interaction with the first further downstream. After the transition of the second boundary layer, turbulence occupies the whole channel width and a turbulent channel flow develops. The transition is analyzed with the help of an orthogonal decomposition of the solenoidal velocity field. The observed transition scenario differs from existing simulations of streak breakdown where the perturbation is optimized for a transition to occur in a region far away from the entry section. In our simulations, the perturbation setup generates a significant nonlinear growth of the streaks that are pushed away from the wall. Transient varicose instabilities, followed by sinuous instabilities induce the development of mushroom-shaped transitional structures in the outer region of the laminar boundary layer, that further break down downstream. The second boundary-layer transition resembles the one occurring under free-stream turbulence, with the generation of finite-length streaks and turbulent spots.

Electromagnetic-pulse-induced activation of p38 MAPK pathway and disruption of blood–retinal barrier

The blood–retinal barrier (BRB) is critical for maintaining retina homeostasis and low permeability. In this study, we evaluated the effects of electromagnetic pulse (EMP) exposure on the permeability of BRB, alterations of tight junction (TJ) proteins of BRB and if any, involvement of mitogen-activated protein kinase (MAPK) pathway. Male Sprague–Dawley (SD) rats and RF/6A cells which were pretreated with or without MAPKs inhibitors were sham exposed or exposed to EMP at 200kV/m for 200 pulses. The alteration of BRB permeability was examined through fluorescence microscope and quantitatively assessed using Evans blue (EB) and endogenous albumin as tracers. The expressions of TJ proteins and some signaling molecules of MAPK pathway were measured by Western blots. The observations were that EMP exposure resulted in increased BRB permeability concurrent with the decreased expressions of occludin and claudin-5, which were correlated with the increased expressions of phospho-p38, phospho-JNK and phospho-ERK and could be blocked when pretreated with p38 MAPK inhibitor. Thus, the results suggested that the alterations of occludin and claudin-5 may play an important role in the disruption of TJs, which may lead to the transient breakdown of BRB after EMP exposure with the involvement of p38 MAPK pathway through phosphorylation of signaling molecules.

Staged management of pectus carinatum

AimThe aim was to report the treatment of pectus carinatum with a novel Argentine brace and operation. MethodsThe bracing and clinical data of 137 consenting pectus carinatum patients treated between October 2008 and December 2011 were reviewed for outcome. Institutional approval was obtained. Data are reported as median (range). ResultsMedian age 122 bracing patients was 14 (10–28)years with 67 (55%) progressing under active treatment. Five patients (4%) were lost to follow-up, and thirteen (11%) failed treatment. Thirty-seven patients (30%) exhibited flattening of the sternum after 6 (1–24)months without surgery. After flattening, patients then wore the brace for progressively fewer hours each day as a “retainer” for 5 (3–19)months. Five patients (4%) experienced recurrence 5 (3–7)months after brace treatment was discontinued. Complications were limited to transient skin breakdown in nine patients. Three of the 13 Argentine brace failures and 15 other pectus carinatum patients were treated surgically. Thirteen underwent Abramson's minimally invasive operation and five an open repair, all with good initial correction. For Abramson repairs, seven patients have had bars removed, with results rated as excellent (n=4), good (n=2), and failure (n=1, converted to open with excellent result later). In three patients with stiff chests, costal cartilage was resected thoracoscopically during the Abramson repair with measurably improving compliance. ConclusionStaged treatment of pectus carinatum allows most teenagers to be managed non-operatively. For patients who fail bracing or are not amenable to bracing, minimally invasive surgical treatment for pectus carinatum is a viable option.

Anomalous Currents in Low Voltage Polymer Tantalum Capacitors

Low voltage Polymer Ta capacitors fabricated with porous Ta anodes, anodic oxide films of Ta as a dielectric, and poly(3,4-ethylenedioxythiophene) (PEDOT) cathodes were investigated. The polymer cathodes were formed by either pure in-situ polymerization or hybrid polymerization, with in-situ PEDOT inside the porous anodes and a pre-polymerized PEDOT cathode on the external surface of the anodes. Anomalous transient current, DC leakage, and breakdown voltage were observed and investigated at normal and reverse polarities in a broad range of temperatures and voltages. Anomalously high transient current in the ampere range was observed when a pulse of rated voltage at normal polarity (+ on the Ta anode) was applied to the capacitors, and anomalous DC current was observed when rated voltage was applied at low temperature. This effect was significantly more pronounced in the hybrid devices, but significantly decreased in all cases with humidification. The anomalous currents were explained by the presence of dipoles, charged polymer chains, in the conducting polymer cathode at its interface with the dielectric.