Active Channel Research Articles

Overcoming volumetric capacitance-rate performance tradeoff with 0D/2D conductive carbon nitride/phosphorene heterostructure for flexible supercapacitor

Few-layer black phosphorus (FL-BP) is considered a rising star 2D material for flexible supercapacitors (FSCs) due to its exceptional properties, including mechanical flexibility and high active surface area. However, the disordered deposition of FL-BP nanoflakes often leads to face-to-face restacking, which diminishes the effective active area and ion transport channels. This poses a huge challenge in simultaneously achieving high volumetric capacitance and rate capability. To address this, a 3D porous 0D/2D FL-BP/conductive carbon nitride (FL-BP/c-CN) film has been developed. The introduction of 0D c-CN nanoparticles effectively prevents the restacking of FL-BP nanoflakes and expands the nanofluidic channels, thus facilitating charge transport and ions diffusion. Additionally, the highly conductive c-CN nanoparticles embedded into the FL-BP layers significantly improve overall conductivity. As a result, the FL-BP/c-CN film-based FSC demonstrates a remarkable rate performance, retaining 70% capacitance as the scan rate increases from 10 to 100 mV/s. Moreover, the incorporation of 0D c-CN nanoparticles increases the available space for charge accumulation, yielding a volumetric capacitance of 28.5 F/cm3 at a scan rate of 10 mV/s, which is three times higher than that of a pure FL-BP film electrode (9.2 F/cm3). This work presents an innovative approach for developing high-performance FL-BP-based FSCs.

In Vivo Expression of an SCA27A-linked FGF14 Mutation Results in Haploinsufficiency and Impaired Firing of Cerebellar Purkinje Neurons.

Autosomal dominant mutations in FGF14 , which encodes intracellular fibroblast growth factor 14 (iFGF14), underlie spinocerebellar ataxia type 27A (SCA27A), a devastating multisystem disorder resulting in progressive deficits in motor coordination and cognitive function. Mice lacking iFGF14 ( Fgf14 -/- ) exhibit similar phenotypes, which have been linked to iFGF14-mediated modulation of the voltage-gated sodium (Nav) channels that control the high frequency repetitive firing of Purkinje neurons, the main output neurons of the cerebellar cortex. To investigate the pathophysiological mechanisms underlying SCA27A, we developed a targeted knock-in strategy to introduce the first point mutation identified in FGF14 into the mouse Fgf14 locus ( Fgf14 F145S ), we determined the impact of in vivo expression of the mutant Fgf14 F145S allele on the motor performance of adult animals and on the firing properties of mature Purkinje neurons in acute cerebellar slices. Electrophysiological experiments revealed that repetitive firing rates are attenuated in adult Fgf14 F145S/+ cerebellar Purkinje neurons, attributed to a hyperpolarizing shift in the voltage-dependence of steady-state inactivation of Nav channels. More severe effects on firing properties and Nav channel inactivation were observed in homozygous Fgf14 F145S/F145S Purkinje neurons. Interestingly, the electrophysiological phenotypes identified in adult Fgf14 F145S/+ and Fgf14 F145S/F145S cerebellar Purkinje neurons mirror those observed in heterozygous Fgf14 +/- and homozygous Fgf14 -/- Purkinje neurons, respectively, suggesting that the mutation results in the loss of the iFGF14 protein. Western blot analysis of lysates from adult heterozygous Fgf14 F145S/+ and homozygous Fgf14 F145S/F145S animals revealed reduced or undetectable, respectively, iFGF14 expression, supporting the hypothesis that the mutant allele results in loss of the iFGF14 protein and that haploinsufficiency underlies SCA27A neurological phenotypes.

Devising a method for detecting an aerial object by radar with an additional channel of passive reception

The object of this paper is the process of detecting an aerial object by a radar with active and passive reception channels. The main hypothesis of the study assumed that the introduction of an additional channel of passive reception would increase the conditional probability of correct detection at a fixed value of the conditional probability of false alarms. When detecting an aerial object, it was considered that the signals from aerial object represent a reflected signal after being emitted by the active radar channel elemitted own radio signals. A radar with active and passive reception channels assumes the presence of two channels. The active location channel provides reception of signals reflected from an aerial object, their processing and detection according to the Neumann-Pearson criterion. The passive location channel functions according to the principle of panoramic spectral analysis based on windowed Fourier transforms. The information combining device is intended for the compatible combining of information from active and passive channels of radar reception. At the output of the passive location channel, an output signal is formed, and the coordinates of the aerial object are measured. To ensure the functioning of the radar with active and passive reception channels, it is necessary to ensure the time synchronization of the reception channels. The quality of detection of aerial objects by radar with active and passive signal reception channels was evaluated. The quality indicator defines the conditional probability of correct detection. The dependences of the conditional probability of correct detection are given for a radar with only an active reception channel and a radar with active and passive reception channels. It was established that the introduction of an additional channel of passive reception to the radar increases the conditional probability of correct detection by an average of (20–40) %, depending on the signal-to-noise ratio.

Transmembrane Serine Protease 2 and Proteolytic Activation of the Epithelial Sodium Channel in Mouse Kidney.

The renal epithelial sodium channel (ENaC) is essential for sodium balance and blood pressure control. ENaC undergoes complex proteolytic activation by not yet clearly identified tubular proteases. Here, we examined a potential role of transmembrane serine protease 2 (TMPRSS2). Murine ENaC and TMPRSS2 were (co-)expressed in Xenopus laevis oocytes. ENaC cleavage and function were studied in TMPRSS2-deficient murine cortical collecting duct (mCCDcl1) cells and TMPRSS2-knockout (Tmprss2-/-) mice. Short-circuit currents (ISC) were measured to assess ENaC-mediated transepithelial sodium transport of mCCDcl1 cells. The mCCDcl1 cell transcriptome was studied using RNA sequencing. The effect of low-sodium diet with or without high potassium were compared in Tmprss2-/- and wildtype mice using metabolic cages. ENaC-mediated whole-cell currents were recorded from microdissected tubules of Tmprss2-/- and wildtype mice. In oocytes, co-expression of murine TMPRSS2 and ENaC resulted in fully cleaved γ-ENaC and ∼2-fold stimulation of ENaC currents. High baseline expression of TMPRSS2 was detected in mCCDcl1 cells without a stimulatory effect of aldosterone on its function or transcription. TMPRSS2 knockout in mCCDcl1 cells compromised γ-ENaC cleavage and reduced baseline and aldosterone-stimulated ISC which could be rescued by chymotrypsin. A compensatory transcriptional upregulation of other proteases was not observed. Tmprss2-/- mice kept on standard diet exhibited no apparent phenotype, but renal γ-ENaC cleavage was altered. In response to a low-salt diet, particularly with high potassium intake, Tmprss2-/- mice increased plasma aldosterone significantly more than wildtype mice to achieve a similar reduction of renal sodium excretion. Importantly, the stimulatory effect of trypsin on renal tubular ENaC currents was much more pronounced in Tmprss2-/- mice than that in wildtype mice. This indicated the presence of incompletely cleaved and less active channels at the cell surface of TMPRSS2-deficient tubular epithelial cells. TMPRSS2 contributes to proteolytic ENaC activation in mouse kidney in vivo.

Relations of magnetic and electrochemical anti-corrosion properties of (Zr, Ti)-doped NdCeFeB magnets with Ti content

Zr and Ti were co-doped into NdCeFeB sintered magnets to improve the magnetic and electrochemical anti-corrosion properties. Both performance are found closely associated with Ti content. At 0.15 wt%Ti, the sample shows higher coercivity without energy product loss compared to the Ti-free sample and other Ti additions, due to the matrix-phases refinement and optimized distribution of RE-rich phases. For this sample, its corrosion current density and charge transfer resistance are 1.94 μA/cm2 and 1734 Ω•cm2 in NaCl solution respectively, which exhibits obviously improved corrosion resistance in comparison with the Ti-free magnet. The charge transfer resistance has been increased by 45.6 %. The apparently improved corrosion resistance is mainly attributed to the decreased amount of active reaction channels and the enhanced protective effect of TiO2, arising from the increment of Ti-rich precipitates. When the content of Ti dopant exceeds 0.5 wt%, the beneficial effects of Ti are overshadowed by the harmful effect of the density reduction on anti-corrosion performance, and the charge transfer resistance decreased with further increasing the dopant content. The new findings provide a theoretical basis for improving physicochemical properties of NdCeFeB magnet.

The Initial Experience of Eslicarbazepine in Children at Three Canadian Tertiary Pediatric Care Centers.

Eslicarbazepine (ESL) is a once-daily, third-generation antiseizure medication for focal-onset seizures. The primary mechanism of action is enhancing the slow inactivation of voltage-gated sodium channels. The study objective was to review real-world experience regarding retention rate, efficacy, and tolerability of eslicarbazepine, soon after it became available for children in Canada. A retrospective review was performed on all patients prescribed eslicarbazepine from September 2017 to June 2020, with at least 3 years of follow-up data, at 3 Canadian tertiary care pediatric centers. Fifty patients were identified, and the mean age of eslicarbazepine initiation was 12.4 years (range 3-19 years). Most patients had drug-resistant epilepsy, trying a mean of 5.04 (range 0-14) antiseizure medications before the initiation of eslicarbazepine. Twenty-four patients (48.0%) experienced adverse effects, including dizziness (n = 10), drowsiness (n = 6), dizziness and drowsiness (n = 1), nausea and abdominal pain (n = 4), transient unsteadiness and diplopia (n = 1), and negative mood changes (n = 2). None had serious adverse effects, including rash. The retention rate of eslicarbazepine at last follow-up was 70%. Fifteen (30%) had ≥50% seizure reduction, with 2 of these patients becoming seizure free. Ten (20%) had 25% to 50% reduction, 2 (4%) had worsening of seizures, and 17 (34%) had no change in seizure frequency. The study results support the long-term effectiveness and tolerability of eslicarbazepine in a cohort of children with predominantly drug-resistant epilepsy in a real-life setting from 3 Canadian centers with initial use after approval. Adverse effects were nonserious, infrequently leading to eslicarbazepine discontinuation.

Inactivation induced by pathogenic Cav1.3 L-type Ca2+-channel variants enhances sensitivity for dihydropyridine Ca2+ channel blockers.

Pathogenic gain-of-function mutations in Cav1.3 L-type voltage-gated Ca2+-channels (CACNA1D) cause neurodevelopmental disorders with or without endocrine symptoms. We aimed to confirm a pathogenic gain-of function phenotype of CACNA1D de novo missense mutations A749T and L271H, and investigated the molecular mechanism causing their enhanced sensitivity for the Ca2+-channel blocker isradipine, a potential therapeutic for affected patients. Wildtype and mutant channels were expressed in tsA-201 cells and their gating analysed using whole-cell and single-channel patch-clamp recordings. The voltage-dependence of isradipine action was quantified using protocols inducing variable fractions of inactivated channels. The molecular basis for altered channel gating in the mutants was investigated using in silico modelling and molecular dynamics simulations. Both mutations were confirmed pathogenic due to characteristic shifts of voltage-dependent activation and inactivation towards negative potentials (~20 mV). At negative holding potentials both mutations showed significantly higher isradipine sensitivity compared to wildtype. The affinity for wildtype and mutant channels increased with channel inactivation as predicted by the modulated receptor hypothesis (30- to 40-fold). The IC50 was indistinguishable for wildtype and mutants when >50% of channels were inactivated. Mutations A749T and L271H induce pathogenic gating changes. Like wildtype, isradipine inhibition is strongly voltage-dependent. Our data explains their apparent higher drug sensitivity at a given negative voltage by the availability of more inactivated channels due to their more negative inactivation voltage range. Low nanomolar isradipine concentrations will only inhibit Cav1.3 channels in neurons during prolonged depolarized states without selectivity for mutant channels.

Chemical mapping of the surface interactome of PIEZO1 identifies CADM1 as a modulator of channel inactivation

The propeller-shaped blades of the PIEZO1 and PIEZO2 ion channels partition into the plasma membrane and respond to indentation or stretching of the lipid bilayer, thus converting mechanical forces into signals that can be interpreted by cells, in the form of calcium flux and changes in membrane potential. While PIEZO channels participate in diverse physiological processes, from sensing the shear stress of blood flow in the vasculature to detecting touch through mechanoreceptors in the skin, the molecular details that enable these mechanosensors to tune their responses over a vast dynamic range of forces remain largely uncharacterized. To survey the molecular landscape surrounding PIEZO channels at the cell surface, we employed a mass spectrometry-based proteomic approach to capture and identify extracellularly exposed proteins in the vicinity of PIEZO1. This PIEZO1-proximal interactome was enriched in surface proteins localized to cell junctions and signaling hubs within the plasma membrane. Functional screening of these interaction candidates by calcium imaging and electrophysiology in an overexpression system identified the adhesion molecule CADM1/SynCAM that slows the inactivation kinetics of PIEZO1 with little effect on PIEZO2. Conversely, we found that CADM1 knockdown accelerates inactivation of endogenous PIEZO1 in Neuro-2a cells. Systematic deletion of CADM1 domains indicates that the transmembrane region is critical for the observed effects on PIEZO1, suggesting that modulation of inactivation is mediated by interactions in or near the lipid bilayer.

A Novel De Novo Gain-of-Function CACNA1D Variant in Neurodevelopmental Disease With Congenital Tremor, Seizures, and Hypotonia.

De novo gain-of-function variants in the CACNA1D gene, encoding the L-type voltage-gated Ca2+ channel CaV1.3, cause a multifaceted syndrome. Patients show variable degrees of autism spectrum disorder, developmental delay, epilepsy, and other neurologic and endocrine abnormalities (primary aldosteronism and/or hyperinsulinemic hypoglycemia). We study here a novel variant [c.3506G>A, NM_000720.4, p.(G1169D)] in 2 children with the same CACNA1D mutation but different disease severity. The clinical data of the study patients were collected. After molecular analysis and cloning by site-directed mutagenesis, patch-clamp recordings of transfected tsA201 cells were conducted in whole-cell configuration. The functional effects of wild-type and mutated channels were analyzed. One child is a severely affected boy with a novel de novo CACNA1D variant with additional clinical symptoms including prenatal-onset tremor, congenital respiratory insufficiency requiring continuous positive airway pressure ventilation, and sensorineural deafness. Despite episodes of hypoglycemia, insulin levels were normal. Aldosterone:renin ratios as a screening parameter for primary aldosteronism were variable. In the second patient, putative mosaicism of the p.(G1169D) variant was associated with a less severe phenotype. Patch-clamp electrophysiology of the p.(G1169D) variant in a heterologous expression system revealed pronounced activity-enhancing gating changes, including a shift of channel activation and inactivation to more hyperpolarized potentials, as well as impaired channel inactivation and deactivation. Despite retained sensitivity to the Ca2+ channel blocker isradipine in vitro, no beneficial effects of isradipine or nifedipine treatment were observed in the index case. Through this report, we expand the knowledge about the disease presentation in patients with CACNA1D variants and show the novel variant's modulatory effects on CaV1.3 gating.

Sediment Source Partitioning and Budgeting Over Historical Timescales in a Glacierized, Mountain Catchment

AbstractManaging and living with geohazards is especially challenging in mountain landscapes and requires an understanding of catchment‐scale sediment dynamics and internal system functioning. While sediment budgeting is a valuable framework, challenges remain including partitioning sediment yield by source and grain size and addressing scale issues. This study advances our understanding of bed material dynamics in glacierized mountain catchments by applying a range of complementary techniques to measure sediment transfers in the Fitzsimmons Creek watershed. First, we measured the historical bed material yield using field surveys and historical air photo analysis, revealing an average specific sediment yield of 210 Mg km−2 yr−1, that varied by a factor of 17 over the 76‐year record. Hydro‐meteorological and historical analyses suggest that gravel extraction had the largest impact over the past three decades, while an extreme landslide and flood event produced the highest recorded sediment yield. Second, we constructed a detailed sediment budget along the river system using high‐resolution, multi‐temporal lidar and geomorphic mapping data. Sediment source partitioning indicates that landslide, active channel, and floodplain sources each contributed about one‐third of the total sediment supply. Net degradation occurred along the valley bottom upstream of the fan‐delta, resulting in steadily increasing downstream sediment yield. This trend is punctuated by chronic landsliding near the outlet, driven by postglacial incision through glaciogenic sediments at a hanging valley step. Contemporary glacial and proglacial sources were not measured directly but surprisingly contributed minimally. These findings provide insight into the sediment dynamics of glacierized mountain catchments and their potential controls.

Dual S-Scheme g-C3N4/Ag3PO4/g-C3N5 photocatalysts for removal of tetracycline pollutants through enhanced molecular oxygen activation

A dual S-scheme g-C3N4/Ag3PO4/g-C3N5 heterojunction was prepared by decomposition methods, and it displayed enhanced performance to degrade tetracycline hydrochloride with the ideal stability under different water substrates and ions. Comparing with three single components, as g-C3N4, g-C3N5, and Ag3PO4, the dual S-scheme g-C3N4/Ag3PO4/g-C3N5 heterojunction displayed 4.4-, 3.4-, and 2.5-times enhancements in the tetracycline hydrochloride removal. Based on the dynamics analyses for charge carriers and band structure calculations, two channels of molecular oxygen activation (MOA) between Ag3PO4 and g-C3N4 (and g-C3N5) were confirmed. More importantly, according to this double consumption process of excited electrons, dual S-scheme g-C3N4/Ag3PO4/g-C3N5 could suppress the charge recombination, which was the key point to boosting photocatalytic activity. Moreover, the determination of intermediates also supported the vital role of MOA during these photocatalytic reactions. this report of two reactive sites in MOA that generate reactive oxygen species in a “V” type band structure. The electronic dynamic in the reaction was also testified by several detections, indicating the enhanced charge separation and migration from internal field effect and electron trapping from dual S-scheme mechanism. This work provides a new research direction for the design and mechanism analysis of dual S-scheme photocatalysts

Hierarchical MTC User Activity Detection and Channel Estimation With Unknown Spatial Covariance

Hierarchical MTC User Activity Detection and Channel Estimation With Unknown Spatial Covariance

Study on Action and Mechanism of Potentilla discolor Bunge using Patch-Clamp to Explore the Effect of the Main Components of Potentilla discolor Bunge on Myocardial Cell Membranes

Background Potentilla discolor Bunge (PDB) is a plant of the Rosaceae family. A wide range of pharmacological activities, such as antibacterial, hypoglycemic, and others, can be achieved through its chemical components, which include terpenes, steroids, polyphenols, and flavonoids. However, the effects of the herb on the heart are unclear. Purpose To explore the effect of the main components of PDB on myocardial cell membranes. Materials and Methods We investigated the role of different concentrations of PDB in cardiomyocytes by evaluating myocardial electrical activity. We used high-performance liquid chromatography to analyze the components. Patch-clamp experiments were conducted to detect the drugs’ impact on the ion channels of cardiomyocytes. Results PDB regulated 14 potential metabolites in mice. Interestingly, quercetin exerts certain effects on the heart by acting on the inositol phosphate metabolism pathway. Quercetin is a monomer compound that can enhance the activity of IK1 on the myocardium membrane. Conclusion This study showed that monomeric compounds of PDB can significantly enhance IK1 activity and influence ion channels in a concentration-dependent manner.

Discovery of E0199: A novel compound targeting both peripheral NaV and KV7 channels to alleviate neuropathic pain

This research study focuses on addressing the limitations of current neuropathic pain (NP) treatments by developing a novel dual-target modulator, E0199, targeting both NaV1.7, NaV1.8, and NaV1.9 and KV7 channels, a crucial regulator in controlling NP symptoms. The objective of the study was to synthesize a compound capable of modulating these channels to alleviate NP. Through an experimental design involving both in vitro and in vivo methods, E0199 was tested for its efficacy on ion channels and its therapeutic potential in a chronic constriction injury (CCI) mouse model. The results demonstrated that E0199 significantly inhibited NaV1.7, NaV1.8, and NaV1.9 channels with a particularly low half maximal inhibitory concentration (IC50) for NaV1.9 by promoting sodium channel inactivation, and also effectively increased KV7.2/7.3, KV7.2, and KV7.5 channels, excluding KV7.1 by promoting potassium channel activation. This dual action significantly reduced the excitability of dorsal root ganglion neurons and alleviated pain hypersensitivity in mice at low doses, indicating a potent analgesic effect without affecting heart and skeletal muscle ion channels critically. The safety of E0199 was supported by neurobehavioral evaluations. Conclusively, E0199 represents a ground-breaking approach in NP treatment, showcasing the potential of dual-target small-molecule compounds in providing a more effective and safe therapeutic option for NP. This study introduces a promising direction for the future development of NP therapeutics.

Wearable and Multiplexed Biosensors based on Oxide Field-Effect Transistors.

Wearable sensors designed for continuous, non-invasive monitoring of physicochemical signals are important for portable healthcare. Oxide field-effect transistor (FET)-type biosensors provide high sensitivity and scalability. However, they face challenges in mechanical flexibility, multiplexed sensing of different modules, and the absence of integrated on-site signal processing and wireless transmission functionalities for wearable sensing. In this work, a fully integrated wearable oxide FET-based biosensor array is developed to facilitate the multiplexed and simultaneous measurement of ion concentrations (H+, Na+, K+) and temperature. The FET-sensor array is achieved by utilizing a solution-processed ultrathin (≈6nm thick) In2O3 active channel layer, exhibiting high compatibility with standard semiconductor technology, good mechanical flexibility, high uniformity, and low operational voltage of 0.005V. This work provides an effective method to enable oxide FET-based biosensors for the fusion of multiplexed physicochemical information and wearable health monitoring applications.

Assessing the effectiveness of “River Morphodynamic Corridors” for flood hazard mapping

In dynamic rivers the assessment of flood hazard related to geomorphological dynamics assumes crucial importance. Recently, some geomorphological approaches have been developed to assess channel dynamics in response to floods. In this study we explore the River Morphodynamic Corridors which include the current active channel and areas of the alluvial plain that may be (re)activated by channel dynamics during floods. In order to assess the effectiveness of such corridors for mapping flood hazard, we delineated the morphodynamic corridors along a river network of 74 km in the Cordevole River catchment (Italy) and compared the corridors with the channel changes that were triggered by a high-magnitude event (Vaia Storm) that hit the study area in October 2018. We observed that the morphodynamic corridors are capable to define areas where channel dynamics are most likely to occur and have proven satisfactorily effective in predicting channel widenings triggered by a severe flood. The results show that it is crucial to adopt different procedures for corridor delineation based on channel width, i.e., for small streams (width < 30 m) a more precautionary approach should be adopted that considers the entire alluvial plain as an area potentially affected by channel dynamics. The study highlighted an inherent limitation of the approach, since erosion that can affect valley slopes or fluvial terraces (i.e., widening of the alluvial plain) is not taken into account. This application represents the first validation of the River Morphodynamic Corridors approach through comparison with observed flood channel changes. Through this analysis, it can be inferred that, notwithstanding its relatively simple procedure, the approach allows a robust mapping and delineation of flood hazard due to river channel dynamics. The River Morphodynamic Corridors, when applied jointly with hydraulic model for assessing inundation processes, allow an overall assessment of flood hazard, particularly in dynamic river contexts.

Geopolitical risk and energy price crash risk

This paper explores the link between geopolitical risks and energy prices crash risk. Studying energy price crashes is important given the sharp fall in oil prices in 2008 and 2014. The analysis focuses on three energy markets: natural gas, oil, and coal, while it employs two measures: the negative coefficient of skewness and the down-to-up volatility, to construct proxies for crash risks. The period of examination is January 2000 to December 2023, whereas that for coal is January 2010 to December 2023. The study employs a modified version of the smooth transition autoregressive model. The results show that, within the modelling framework, coal and oil crash risks are driven by the cyclical behavior of geopolitical acts, whereas natural gas crash risks by geopolitical threats. Causality tests confirm the prediction that geopolitical tensions cause crash risks in energy markets. The results also confirm that the “Economic Activity Channel” is only valid for energy markets driven by geopolitical threats. Energy market regulators should be concerned about crash risks, given that the energy supply shows cyclical boom and bust cycles in prices and production. Crash risks could also potentially cause a fall in investments required to enhance energy efficiency.

Design of different oxygen content and high performance bilayer In2O3 thin-film transistors at room temperature for flexible electronics

In this study, homojunction bilayer In2O3thin film transistors (TFTs) were prepared by RF-magnetron sputtering at room temperature. Herein, an active channel of bilayer In2O3TFTs are consist of the front channel with lower (poor) oxygen content and the back channel with higher (rich) oxygen content. Therefore, optimizedbilayer In2O3TFT was fabricatedandaμFE of 32.5 cm2/Vs and a small SS of 280 mV/decade, a small VTH of 0.3 Vwere achieved. In addition, small VTH shifts of 0.7 (−1.0) and 0.4 (−1.2) V under gate bias and light illumination stress tests were obtained. Through XPS band structure analysis indicated that the formation of band bending between the channel layers leads to electron injection from the back channel into the front channel, resulting in accumulation of forming carriers near the interface of the bilayer, resulting in increase the μFE of In2O3TFTs. Furthermore, XPS and LFN measurement demonstrate that control the oxygen content can reduced the oxygen-related defects and bulk/interface trap density while controlling the Ne and carrier transport in the bilayer In2O3 film,which enhance the stability of In2O3TFTs. Overall, the high-performance bilayer In2O3TFTshave opena new method to obtaine the flexible electronic devices.

Structural basis for the rescue of hyperexcitable cells by the amyotrophic lateral sclerosis drug Riluzole

Neuronal hyperexcitability is a key element of many neurodegenerative disorders including the motor neuron disease Amyotrophic Lateral Sclerosis (ALS), where it occurs associated with elevated late sodium current (INaL). INaL results from incomplete inactivation of voltage-gated sodium channels (VGSCs) after their opening and shapes physiological membrane excitability. However, dysfunctional increases can cause hyperexcitability-associated diseases. Here we reveal the atypical binding mechanism which explains how the neuroprotective ALS-treatment drug riluzole stabilises VGSCs in their inactivated state to cause the suppression of INaL that leads to reversed cellular overexcitability. Riluzole accumulates in the membrane and enters VGSCs through openings to their membrane-accessible fenestrations. Riluzole binds within these fenestrations to stabilise the inactivated channel state, allowing for the selective allosteric inhibition of INaL without the physical block of Na+ conduction associated with traditional channel pore binding VGSC drugs. We further demonstrate that riluzole can reproduce these effects on a disease variant of the non-neuronal VGSC isoform Nav1.4, where pathologically increased INaL is caused directly by mutation. Overall, we identify a model for VGSC inhibition that produces effects consistent with the inhibitory action of riluzole observed in models of ALS. Our findings will aid future drug design and supports research directed towards riluzole repurposing.

An adaptive approach for integrating primary user behavior in compressive spectrum sensing

Compressive sensing (CS) has been widely used to sense the wideband spectrum with fewer measurements by taking advantage of radio spectrum underutilization. As new smart devices, such as IoT devices, smart home devices, and wearables, use batteries and have limited memory, more research is needed to reduce the overuse of cognitive radio (CR) resources through spectrum sensing. To reduce the number of compressive measurements required for spectrum recovery, researchers proposed approaches like weighted and sequential compressive sensing. In this paper, we estimate the primary user’s (PU) behavior statistics and use the estimated information in a novel weighted sequential compressive spectrum sensing approach. Our proposed approach can reduce and adapt the number of measurements and the sensing time to the changing number of active channels in a dynamically changing wideband spectrum.