Membrane Channels Research Articles

Building high-speed facilitated transport channels in Pebax membranes with montmorillonite for efficient CO2/N2 separation

ABSTRACT Development of high-performance mixed matrix membranes (MMMs) is of great significance for CO2 separation membrane technology, in order to improve the commercial competitiveness and practical applications. Montmorillonite (MMT) was developed as a dopant to fabricate Polyether block amide (Pebax1074)-based MMMs for strengthening the CO2/N2 separation. The morphology, chemical groups, microstructure, and thermal properties of MMMs were characterised by scanning electron microscope, FTIR spectroscopy, X-ray diffraction and thermal analysis, respectively. The effects of MMT contents, permeation pressure and permeation temperature on the gas separation performance of the Pebax/MMT MMMs were investigated. The results show that the uniformly dispersed dopants MMT in the membrane matrix significantly influence the thermal stability and the structural compactness of MMMs. Moreover, the CO2 permeability monotonously increases in spite of the CO2/N2 selectivity first increasing and then decreasing with the MMT content elevating from 0% to 10% in MMMs. The highest CO2/N2 selectivity could reach to 120.3, along with the CO2 permeability of 130.6 Barrer for the MMMs made by MMT content of 6%.

TolC and EmrA1 contribute to Francisella novicida multidrug resistance and modulation of host cell death.

Francisella tularensis is a Gram-negative intracellular bacterial pathogen and causative agent of tularemia. We previously identified the outer membrane channel protein TolC as contributing to antimicrobial resistance and subversion of host responses by F. tularensis. To advance understanding of TolC function in Francisella and to identify components that might work together with TolC, we took advantage of a transposon mutant library in F. novicida, a model species that causes a tularemia-like disease in mice. Our findings identify TolC and the membrane fusion protein EmrA1 as important for both antimicrobial resistance and suppression of macrophage cell death. This study also revealed differences in cell death pathways triggered by F. novicida versus F. tularensis infection that may relate to differences in virulence.

Electrochemical identification and quantification of through‐plane proton channels in graphene oxide membranes

Stacked graphene oxide (GO) proton membranes are promising candidates for use in energy devices due to their proton conductivity. Identification of through‐plane channels in these membranes is critical but challenging due to their anisotropic nature. Here, we present an electrochemical reduction method for identifying and quantifying through‐plane proton channels in GO membranes. The simplicity lies in the operando optical observation of the change in contrast as GO is electrochemically reduced. Here, we find three proton‐dominated three‐phase interfaces, which are critical for the reduction reactions of GO membranes. Based on these findings, a method is proposed to identify and quantify through‐plane channels in stacked GO proton membranes using a simple three‐electrode device in combination with real‐time imaging of the membrane surface.

Electrochemical identification and quantification of through-plane proton channels in graphene oxide membranes.

Stacked graphene oxide (GO) proton membranes are promising candidates for use in energy devices due to their proton conductivity. Identification of through-plane channels in these membranes is critical but challenging due to their anisotropic nature. Here, we present an electrochemical reduction method for identifying and quantifying through-plane proton channels in GO membranes. The simplicity lies in the operando optical observation of the change in contrast as GO is electrochemically reduced. Here, we find three proton-dominated three-phase interfaces, which are critical for the reduction reactions of GO membranes. Based on these findings, a method is proposed to identify and quantify through-plane channels in stacked GO proton membranes using a simple three-electrode device in combination with real-time imaging of the membrane surface.

Dual role for pannexin 1 at synapses: regulating functional and morphological plasticity.

Pannexin 1 (PANX1) is an ion and metabolite membrane channel and scaffold protein enriched in synaptic compartments of neurons in the central nervous system. In addition to a well-established link between PANX1 and synaptic plasticity, we recently identified a role for PANX1 in the regulation of dendritic spine stability. Notably, PANX1 and its interacting proteins are linked to neurological conditions involving dendritic spine loss. Understanding the dual role of PANX1 in synaptic function and morphology may help to shed light on these links. We explore potential mechanisms, including PANX1's interactions with postsynaptic receptors and cytoskeleton regulating proteins. Finally, we contextualize PANX1's dual role within neurological diseases involving dendritic spine and synapse dysfunction.

In-situ visualization and structure optimization of the flow channel of proton exchange membrane fuel cells

In-situ visualization and structure optimization of the flow channel of proton exchange membrane fuel cells

Epidermal secretion-purified biosensing patch with hydrogel sebum filtering membrane and unidirectional flow microfluidic channels

The development of biosensing electronics for real-time sweat analysis has attracted increasing research interest due to their promising applications for non-invasive health monitoring. However, one of the critical challenges lies in the sebum interference that largely limits the sensing reliability in practical scenarios. Herein, we report a flexible epidermal secretion-purified biosensing patch with a hydrogel filtering membrane that can effectively eliminate the impact of sebum and sebum-soluble substances. The as-prepared sebum filtering membranes feature a dual-layer sebum-resistant structure based on the poly(hydroxyethyl methacrylate) hydrogel functionalized with nano-brush structured poly(sulfobetaine) to eliminate interferences and provide self-cleaning capability. Furthermore, the unidirectional flow microfluidic channels design based on the Tesla valve was incorporated into the biosensing patch to prevent external sebum contamination and allow effective sweat refreshing for reliable sensing. By seamlessly combining these components, the epidermal secretion-purified biosensing patch enables continuous monitoring of sweat uric acid, pH, and sodium ions with significantly improved accuracy of up to 12 %. The proposed strategy for enhanced sweat sensing reliability without sebum interference shows desirable compatibility for different types of biosensors and would inspire the advances of flexible and wearable devices for non-invasive healthcare.

MicroRNA maintains nutrient homeostasis in the symbiont-host interaction.

Endosymbionts provide essential nutrients for hosts, promoting growth, development, and reproduction. However, the molecular regulation of nutrient transport from endosymbiont to host is not well understood. Here, we used bioinformatic analysis, RNA-Sequencing, luciferase assays, RNA immunoprecipitation, and in situ hybridization to show that a bacteriocyte-distributed MRP4 gene (multidrug resistance-associated protein 4) is negatively regulated by a host (aphid)-specific microRNA (miR-3024). Targeted metabolomics, microbiome analysis, vitamin B6 (VB6) supplements, 3D modeling/molecular docking, in vitro binding assays (voltage clamp recording and microscale thermophoresis), and functional complementation of Escherichia coli were jointly used to show that the miR-3024/MRP4 axis controls endosymbiont (Serratia)-produced VB6 transport to the host. The supplementation of miR-3024 increased the mortality of aphids, but partial rescue was achieved by providing an external source of VB6. The use of miR-3024 as part of a sustainable aphid pest-control strategy was evaluated by safety assessments in nontarget organisms (pollinators, predators, and entomopathogenic fungi) using virus-induced gene silencing assays and the expression of miR-3024 in transgenic tobacco. The supplementation of miR-3024 suppresses MRP4 expression, restricting the number of membrane channels, inhibiting VB6 transport, and ultimately killing the host. Under aphids facing stress conditions, the endosymbiont titer is decreased, and the VB6 production is also down-regulated, while the aphid's autonomous inhibition of miR-3024 enhances the expression of MRP4 and then increases the VB6 transport which finally ensures the VB6 homeostasis. The results confirm that miR-3024 regulates nutrient transport in the endosymbiont-host system and is a suitable target for sustainable pest control.

Study on heat transfer performance of cooling channels in proton exchange membrane fuel cells based on topology optimization

Based on topology optimization method, a dual-objective function topology optimization model containing minimum average temperature and minimum flow power dissipation was established in this study. Coupled with the uneven heat generation model of proton exchange membrane fuel cells, the optimal layout scheme under the target operating conditions was adaptively obtained. The effects of volume fraction, objective function weight, and parabolic inlet velocity on the flow channel structure and cooling performance of topological cooling plates were studied. The results indicate that with the increase of volume fraction, the area of fluid region increases, the average temperature and the pressure drop of cooling plate gradually decrease. At the volume fraction of 0.5, the cooling plate has the best cooling performance. The temperature difference and maximum temperature reach the minimum values of 5.45 K and 347.58 K, respectively. When the volume fraction increases from 0.4 to 0.6, the pressure difference decreases by 67.64 %. With the increase of temperature weight coefficient, the area of high-temperature area gradually decreases, and the temperature uniformity is significantly improved. When the inlet velocity of coolant is 0.025 m/s and the temperature weight coefficient is 0.9, the average and maximum temperatures of cooling plate reach the lowest values, which are 343.53 K and 344.51 K, respectively. The maximum temperature of cooling plate under parabolic inlet velocity is of 347.87 K, which is 0.29 K higher than that under uniform inlet velocity. Non-uniform coolant inlet velocity will lead to a decrease in heat transfer capacity of cooling plate and an increase in coolant power consumption.

Sub-nanometer size level regulation of biomimetic channels in porous membrane for high-capacity removal of toxic dye contaminants

Organic dyes are an important chemical with a market demand of millions of tons. However, their massive emissions, especially alkaline dye contaminants, have caused serious disruption of the ecosystem and even cancers. Inspired by bionic mass transfer, several amino acid fragments (carboxylic acid, γ-aminobutyric acid, and glutamic acid) are introduced into the 2.5 nm-pore size cavity through in-situ polymerization. The flexible amino acid chains facilitate the transport of guest molecules into the channels, accelerating their movement within the porous framework. These flexible chains are implanted into a 2.5 nm pore cavity, forming a 0.8–1.5 nano-meter-sized confinement space, bringing about the strong absorption capability for alkaline contaminants. Notably, LNU-74-glutamic acid achieves an ultra-fast absorption rate for toxic dye contaminants (4.74 g g−1h−1), as well as the highest capacity per unit area among all reported porous adsorbents, including porous carbons, metal–organic frameworks, porous polymers. After encapsulation in commercial polymer, the mixed-matrix membrane reveals (LNU-74-glutamic acid@MMM) a rejection rate greater than 98 % in various real water environments at permeation flux of ∼320 L m−2h−1, including strong acid/alkali, river water, and seawater.

Expression and prognostic impact of VDAC3 in colorectal adenocarcinoma.

Colorectal adenocarcinoma (COAD) is a malignant tumor with high mortality and low 5-year survival rate. Voltage-dependent anion channel 3 (VDAC3) is the least understood isoform of voltage-dependent anion-selective channels in the mitochondrial outer membrane. In this thesis, we aimed to investigate the prognostic value of VDAC3 and provide new insights into colon adenocarcinoma. We utilized The Cancer Genome Atlas (TCGA) database, Gene Expression Omnibus (GEO) database, Human Protein Atlas online database, and the University of ALabama at Birmingham CANcer data analysis Portal (UALCAN) database to analyze VDAC3 expression in COAD and assess patient survival rates. Univariate and multivariate Cox regression analyses were employed to evaluate VDAC3's prognostic significance for COAD. Gene set variation analysis (GSVA) was utilized to explore COAD-related signaling pathways associated with VDAC3. Additionally, we predicted the relationship between VDAC3 expression and anticancer drug sensitivity using the CellMiner database. In the TCGA database, VDAC3 demonstrated elevated expression levels in COAD, which was further validated by findings from the GEO database. Survival analysis conducted using Kaplan-Meier (K-M) curves highlighted that the patients with decreased VDAC3 expression exhibited significantly shorter overall survival durations. VDAC3 expression demonstrated correlation with COAD pathological stage. VDAC3 gene mutation was linked to COAD outcomes. Cox regression analysis showed that VDAC3 was an independent predictor. In addition, GSVA analysis showed that VDAC3 was closely related to mitochondria-related biological processes and involved in the occurrence and development of mitochondria-related diseases. Finally, analysis of the CellMiner database predicted that VDAC3 expression was positively correlated with chelerythrine and cladribine, but negatively correlated with Ergenyl. Our study suggests that VDAC3 may be a potential biomarker for early diagnosis, prognosis, and treatment of COAD.

Resting human trabecular meshwork cells experience tonic cation influx.

The trabecular meshwork (TM) regulates intraocular pressure (IOP) by converting biochemical and biomechanical stimuli into intracellular signals. Recent electrophysiological studies demonstrated that this process is mediated by pressure sensing ion channels in the TM plasma membrane while the molecular and functional properties of channels that underpin ionic homeostasis in resting cells remain largely unknown. Here, we demonstrate that the TM resting potential is subserved by a powerful cationic conductance that disappears following Na+ removal and substitution with choline or NMDG+. Its insensitivity to TTX, verapamil, phenamil methanesulfonate and amiloride indicates it does not involve voltage-operated Na+, Ca2+ and epithelial Na+ (ENaC) channels or Na+/H+ exchange while a modest hyperpolarization induced by SEA-0440 indicates residual contribution from reversed Na+/Ca2+ exchange. Tonic cationic influx was inhibited by Gd3+ and Ruthenium Red but not GsMTx4, indicating involvement of TRP-like but not Piezo channels. Transcriptional analysis detected expression of most TRP genes, with the canonical transcriptome pool dominated by TRPC1 followed by the expression ofTRPV1, TRPC3 and TRPC5. TRPC3 antagonist Pyr3 and TRPC1,4,5 antagonist Pico1,4,5 did not affect the standing current, whereas the TRPC blocker SKF96365 promoted rather than suppressed, Na+ influx. TM cells thus maintain the resting membrane potential, control Na+ homeostasis, and balance K+ efflux through a novel constitutive monovalent cation leak current with properties not unlike those of TRP channels. Yet to be identified at the molecular level, this novel channel sets the homeostatic steady-state and controls the magnitude of pressure-induced transmembrane signals.

Characterization of human aquaporin ion channels in a yeast expression system as a tool for novel ion channel discovery.

Aquaporin (AQP) channels found in all domains of life are transmembrane proteins which mediate passive transport of water, glycerol, signaling molecules, metabolites, and charged solutes. Discovery of new classes of ion-conducting AQP channels has been slow, likely reflecting time- and labor-intensive methods required for traditional electrophysiology. Work here defines a sensitive mass-throughput system for detecting AQP ion channels, identified by rescue of cell growth in the K+-transport-defective yeast strain CY162 following genetic complementation with heterologously expressed cation-permeable channels, using the well characterized human AQP1 channel for proof of concept. Results showed AQP1 conferred transmembrane permeability to cations which rescued survival in CY162 yeast. Comprehensive testing showed that growth response properties fully recapitulated AQP1 pharmacological agonist and antagonist profiles for activation, inhibition, dose-dependence, and structure-function relationships, demonstrating validity of the yeast screening tool for AQP channel identification and drug discovery efforts. This method also provided new information on divalent cation blockers of AQP1, pH sensitivity of antagonists, and ion permeability of human AQP6. Site-directed mutagenesis of AQP1 channel regulatory domains confirmed that yeast growth rescue was mediated by the introduced channels. Optical monitoring with a lithium-sensitive photoswitchable probe in living cells independently demonstrated monovalent cation permeability of AQP1 channels in yeast plasma membrane. Ion channel properties of AQP1 expressed in yeast were consistent with those of AQP1 expressed in Xenopus laevis oocyte and K+-transport defective Escherichia coli. Outcomes here establish a powerful new approach for efficient screening of phylogenetically diverse AQPs for yet untested functions as cation channels.

Localization of Piezo 1 and Piezo 2 in Lateral Line System and Inner Ear of Zebrafish (Danio rerio).

Piezo proteins have been identified as mechanosensitive ion channels involved in mechanotransduction. Several ion channel dysfunctions may be associated with diseases (including deafness and pain); thus, studying them is critical to understand their role in mechanosensitive disorders and to establish new therapeutic strategies. The current study investigated for the first time the expression patterns of Piezo proteins in zebrafish octavolateralis mechanosensory organs. Piezo 1 and 2 were immunoreactive in the sensory epithelia of the lateral line system and the inner ear. Piezo 1 (28.7 ± 1.55 cells) and Piezo 2 (28.8 ± 3.31 cells) immunopositive neuromast cells were identified based on their ultrastructural features, and their overlapping immunoreactivity to the s100p specific marker (28.6 ± 1.62 cells), as sensory cells. These findings are in favor of Piezo proteins' potential role in sensory cell activation, while their expression on mantle cells reflects their implication in the maintenance and regeneration of the neuromast during cell turnover. In the inner ear, Piezo proteins' colocalization with BDNF introduces their potential implication in neuronal plasticity and regenerative events, typical of zebrafish mechanosensory epithelia. Assessing these proteins in zebrafish could open up new scenarios for the roles of these important ionic membrane channels, for example in treating impairments of sensory systems.

Purinergic control of apical ion conductance by luminal ATP in rat colonic epithelium

ATP, released e.g. after cell damage or during inflammation, can alter ion transport across the intestinal mucosa via stimulation of purinergic receptors in the basolateral as well as in the apical membrane of epithelial cells. When ATP acts from the serosal side, it induces an increase in short-circuit current (Isc) via Cl− secretion across the colonic epithelium. In contrast, mucosal ATP or its derivative, BzATP, predominantly stimulating ionotropic P2X4 and P2X7 receptors, evoke an increase in Isc, which could not be explained by Cl− secretion. The underlying ion currents after stimulation of apical purinergic receptors in rat distal colon are still unclear and were investigated in the present study.Ussing chamber experiments revealed that the Isc induced by mucosal ATP was dependent on the presence of mucosal Ca2+ and inhibited by the K+ channel blocker, Ba2+, indicating the involvement of Ca2+-dependent K+ channels. Blockade of the transepithelial Isc by lanthanides (La3+, Gd3+) suggests that Ca2+ enters the epithelium via nonselective cation channels. Experiments with basolaterally depolarized epithelia confirmed the activation of apical lanthanide-sensitive Na+- and Ca2+-permeable cation channels by ATP. Putative candidates might be TRP channels, from which several subtypes were detected in colonic tissue in RT-PCR experiments. In addition, the activation of an apical Cl− conductance was observed when suitable Cl− concentration gradients were applied. Consequently, mucosal ATP, acting as ‘danger signal’, stimulates cation and anion channels in the apical membrane to induce a secretory response as part of the local defence mechanism in the intestinal epithelium.

Microporous membrane with ionized sub-nanochannels enabling highly selective monovalent and divalent anion separation

Membranes tailored for selective ion transport represent a promising avenue toward enhancing sustainability across various fields including water treatment, resource recovery, and energy conversion and storage. While nanochannels formed by polymers of intrinsic microporosity (PIM) offer a compelling solution with their uniform and durable nanometer-sized pores, their effectiveness is hindered by limited interactions between ions and nanochannel. Herein, we introduce the randomly twisted V-shaped structure of Tröger’s Base unit and quaternary ammonium groups to construct ionized sub-nanochannel with a window size of 5.89–6.54 Å between anion hydration and Stokes diameter, which enhanced the dehydrated monovalent ion transport. Combining the size sieving and electrostatic interaction effects, sub-nanochannel membranes achieved exceptional ion selectivity of 106 for Cl-/CO32- and 82 for Cl-/SO42-, significantly surpassing the state-of-the-art membranes. This work provides an efficient template for creating functionalized sub-nanometer channels in PIM membranes, and paves the way for the development of precise ion separation applications.

In-situ observation and quantification of membrane deformation in reverse osmosis, using optical coherence tomography

Deformation of the membrane can seriously hamper the performance of a reverse osmosis process. Currently, the most used approach to obtain detailed information on membrane deformation is by conducting membrane autopsy. However, ex-situ analysis can only observe irreversible deformation. In this study, optical coherence tomography (OCT) was introduced as method for in-situ 3D visualization and quantification of membrane and feed channel deformation during operation with varying transmembrane pressure (0–55 bar). In-situ monitoring of membrane surface geometry in a lab-scale flow-cell revealed the formation of specific patterns with ridges and valleys. The deformation became more pronounced with increasing applied pressure, due to membrane intrusion into the permeate spacer. The asymmetric structure of the permeate spacer causes a clear distinction in spatial distribution of ridges and valleys, depending on which side faces the membrane. Interestingly, membrane surface displacement increased linearly with TMP, with slope depending on spacer orientation (A vs B) and type (BW vs SW). Under pressure, we found the following displacements: Ridge – BW-A 1.7 ± 0.1 μm/bar, BW-B 1.9 ± 0.1 μm/bar, SW-A&B 1.5 ± 0.3 μm/bar; Valley – BW-A 3.2 ± 0.1 μm/bar, BW-B 2.7 ± 0.1 μm/bar, SW-A 1.7 ± 0.2 μm/bar, SW-B 1.8 ± 0.3 μm/bar. Measuring the membrane position under pressure revealed that the displacement involves the whole membrane-permeate spacer structure, i.e., the permeate spacer is also deformed. By alternating high and low feed pressure, we could distinguish between reversible and irreversible deformation. In-situ measurement of membrane deformation can contribute to understanding of pressure related performance and can serve as input for advanced modeling.

Plasmodesmata Function and Callose Deposition in Plant Disease Defense.

Callose, found in the cell walls of higher plants such as β-1,3-glucan with β-1,6 branches, is pivotal for both plant development and responses to biotic and abiotic stressors. Plasmodesmata (PD), membranous channels linking the cytoplasm, plasma membrane, and endoplasmic reticulum of adjacent cells, facilitate molecular transport, crucial for developmental and physiological processes. The regulation of both the structural and transport functions of PD is intricate. The accumulation of callose in the PD neck is particularly significant for the regulation of PD permeability. This callose deposition, occurring at a specific site of pathogenic incursion, decelerates the invasion and proliferation of pathogens by reducing the PD pore size. Scholarly investigations over the past two decades have illuminated pathogen-induced callose deposition and the ensuing PD regulation. This gradual understanding reveals the complex regulatory interactions governing defense-related callose accumulation and protein-mediated PD regulation, underscoring its role in plant defense. This review systematically outlines callose accumulation mechanisms and enzymatic regulation in plant defense and discusses PD's varied participation against viral, fungal, and bacterial infestations. It scrutinizes callose-induced structural changes in PD, highlighting their implications for plant immunity. This review emphasizes dynamic callose calibration in PD constrictions and elucidates the implications and potential challenges of this intricate defense mechanism, integral to the plant's immune system.

Taurine modulates host cell responses to Helicobacter pylori VacA toxin.

Colonization of the human stomach with Helicobacter pylori strains producing active forms of the secreted toxin VacA is associated with an increased risk of peptic ulcer disease and gastric cancer, compared with colonization with strains producing hypoactive forms of VacA. Previous studies have shown that active s1m1 forms of VacA cause cell vacuolation and mitochondrial dysfunction. In this study, we sought to define the cellular metabolic consequences of VacA intoxication. Untargeted metabolomic analyses revealed that several hundred metabolites were significantly altered in VacA-treated gastroduodenal cells (AGS and AZ-521) compared with control cells. Pathway analysis suggested that VacA caused alterations in taurine and hypotaurine metabolism. Treatment of cells with the purified active s1m1 form of VacA, but not hypoactive s2m1 or Δ6-27 VacA-mutant proteins (defective in membrane channel formation), caused reductions in intracellular taurine and hypotaurine concentrations. Supplementation of the tissue culture medium with taurine or hypotaurine protected AZ-521 cells against VacA-induced cell death. Untargeted global metabolomics of VacA-treated AZ-521 cells or AGS cells in the presence or absence of extracellular taurine showed that taurine was the main intracellular metabolite significantly altered by extracellular taurine supplementation. These results indicate that VacA causes alterations in cellular taurine metabolism and that repletion of taurine is sufficient to attenuate VacA-induced cell death. We discuss these results in the context of previous literature showing the important role of taurine in cell physiology and the pathophysiology or treatment of multiple pathologic conditions, including gastric ulcers, cardiovascular disease, malignancy, inflammatory diseases, and other aging-related disorders.

Biochemical Approach of Acid-Base Disturbances: Diagnosis Algorithm

Context: The biochemical approach to acid-base balance classifies disturbances in two categories based on cellular mechanisms. The first one being cellular respiration (ATP), which presents high anion gap and changes in carbon dioxide levels, and the second one, cellular metabolism (ion transport through membrane channels), which evidences normal anion gap and changes in other cations and anions. Objective: To present a new diagnostic algorithm for acid-base disturbances, based on the biochemical approach. Method: Original research with systematic analysis and data organization, following biochemical processes that affect acid-base balance. Results: A simple, three-step algorithm which classifies information in a diagnostic table that connects blood gas analysis results (pH, anion gap or base excess, bicarbonate, carbon dioxide and unmeasured anions) with the biochemical cause and most probable clinical findings. Conclusions: The biochemical approach is considered the new model to understand, explain and diagnose acid-base balance and disturbances. All high anion gap disturbances occur in cellular respiration, while all normal anion gap disturbances occur in membrane channel function. The diagnosis algorithm simplifies and organizes the information to describe medical conditions with data from a blood gas analysis. This approach is the first model to establish a linear correlation between lab results, biochemical cause, and clinical findings of acid-base disturbances.