Lung influenza virus specific memory CD4 T cell location and optimal cytokine production are dependent on interactions with lung antigen-presenting cells.

Influenza A virus (IAV) infection leads to the formation of mucosal memory CD4 T cells that can protect the host. An in-depth understanding of the signals that shape memory cell development is required for more effective vaccine design. We have examined the formation of memory CD4 T cells in the lung following IAV infection of mice, characterising changes to the lung landscape and immune cell composition. IAV-specific CD4 T cells were found throughout the lung at both primary and memory time points. These cells were found near lung airways and in close contact with a range of immune cells including macrophages, dendritic cells, and B cells. Interactions between lung IAV-specific CD4 T cells and MHCII+ cells during the primary immune response were important in shaping the subsequent memory pool. Treatment with an anti-MHCII blocking antibody increased the proportion of memory CD4 T cells found at lung airways but reduced interferon-γ expression by IAV-specific immunodominant memory CD4 T cells. The immunodominant CD4 T cells expressed higher levels of PD1 than other IAV-specific CD4 T cells and PD1+ memory CD4 T cells were located further away from MHCII+ cells than their PD1-low counterparts. This distinction in location was lost in mice treated with anti-MHCII antibody. These data suggest that sustained antigen presentation in the lung impacts on the formation of memory CD4 T cells by regulating their cytokine production and location.

Molecularly Imprinted Polymer Biosensor Based on Nitrogen-Doped Electrochemically Exfoliated Graphene/Ti3 CNTX MXene Nanocomposite for Metabolites Detection.

Rapid and accurate quantification of metabolites in different bodily fluids is crucial for a precise health evaluation. However, conventional metabolite sensing methods, confined to centralized laboratory settings, suffer from time-consuming processes, complex procedures, and costly instrumentation. Introducing the MXene/nitrogen-doped electrochemically exfoliated graphene (MXene@N-EEG) nanocomposite as a novel biosensing platform in this work addresses the challenges associated with conventional methods, leveraging the concept of molecularly imprinted polymers (MIP) enables the highly sensitive, specific, and reliable detection of metabolites. To validate our biosensing technology, we utilize agmatine as a significant biologically active metabolite. The MIP biosensor incorporates electrodeposited Prussian blue nanoparticles as a redox probe, facilitating the direct electrical signaling of agmatine binding in the polymeric matrix. The MXene@N-EEG nanocomposite, with excellent metal conductivity and a large electroactive specific surface area, effectively stabilizes the electrodeposited Prussian blue nanoparticles. Furthermore, increasing the content of agmatine-imprinted cavities on the electrode enhances the sensitivity of the MIP biosensor. Evaluation of the designed MIP biosensor in buffer solution and plasma samples reveals a wide linear concentration range of 1.0 nM-100.0 µM (R2 = 0.9934) and a detection limit of 0.1 nM. Notably, the developed microfluidic biosensor offers low cost, rapid response time to the target molecule (10 min of sample incubation), good recovery results for detecting agmatine in plasma samples, and acceptable autonomous performance for on-chip detection. Moreover, its high reliability and sensitivity position this MIP-based biosensor as a promising candidate for miniaturized microfluidic devices with the potential for scalable production for point-of-care applications.

Electrochemical Regeneration of Highly Stable and Sustainable Cellulose/Graphene Adsorbent Saturated with Dissolved Organic Dye.

Electrochemical regeneration of adsorbents presents a cost-effective and environmentally friendly approach. Yet, its application to 3D structured adsorbents such as cellulose/graphene-based aerogels remains largely unexplored. This study introduces a method for producing these aerogels, highlighting their significant adsorption capacity for dissolved organic pollutants and resilience during electrochemical regeneration. By adjusting the ratio of hydrophobized cellulose nanofibers to graphene, the aerogels demonstrate a tunable adsorption capacity, ranging from 56 to 228 mg/g. Hydrophobization using oleic acid is vital for maintaining the aerogels' structural stability in water. Notably, the aerogels maintain structural integrity and efficiency over at least 18 electrochemical regeneration cycles, underscoring their potential for long-term environmental applications. The increase in adsorption capacity observed after regeneration cycles, approximately 10-20% by the fifth cycle, is attributed to electrochemical surface roughening and the creation of new adsorption sites. The tunability and durability of these aerogels offer a sustainable solution for adsorption with electrochemical regeneration technology.

Mitochondrial DNA mutations drive aerobic glycolysis to enhance checkpoint blockade response in melanoma.

The mitochondrial genome (mtDNA) encodes essential machinery for oxidative phosphorylation and metabolic homeostasis. Tumor mtDNA is among the most somatically mutated regions of the cancer genome, but whether these mutations impact tumor biology is debated. We engineered truncating mutations of the mtDNA-encoded complex I gene, Mt-Nd5, into several murine models of melanoma. These mutations promoted a Warburg-like metabolic shift that reshaped tumor microenvironments in both mice and humans, consistently eliciting an anti-tumor immune response characterized by loss of resident neutrophils. Tumors bearing mtDNA mutations were sensitized to checkpoint blockade in a neutrophil-dependent manner, with induction of redox imbalance being sufficient to induce this effect in mtDNA wild-type tumors. Patient lesions bearing >50% mtDNA mutation heteroplasmy demonstrated a response rate to checkpoint blockade that was improved by ~2.5-fold over mtDNA wild-type cancer. These data nominate mtDNA mutations as functional regulators of cancer metabolism and tumor biology, with potential for therapeutic exploitation and treatment stratification.

Opposing Effects on Descending Control of Nociception by µ and κ Opioid Receptors in the Anterior Cingulate Cortex.

BACKGROUND: The efficiency of descending pain modulation, commonly assessed with the conditioned pain modulation procedure, is diminished in patients with chronic pain. The authors hypothesized that the efficiency of pain modulation is controlled by cortical opioid circuits. METHODS: This study evaluated the effects of µ opioid receptor activation in the anterior cingulate cortex on descending control of nociception, a preclinical correlate of conditioned pain modulation, in male Sprague-Dawley rats with spinal nerve ligation-induced chronic pain or in sham-operated controls. Additionally, the study explored the consequences of respective activation or inhibition of κ opioid receptor in the anterior cingulate cortex of naive rats or animals with neuropathic pain. Descending control of nociception was measured as the hind paw withdrawal response to noxious pressure (test stimulus) in the absence or presence of capsaicin injection in the forepaw (conditioning stimulus). RESULTS: Descending control of nociception was diminished in the ipsilateral, but not contralateral, hind paw of rats with spinal nerve ligation. Bilateral administration of morphine in the anterior cingulate cortex had no effect in shams but restored diminished descending control of nociception without altering hypersensitivity in rats with neuropathic pain. Bilateral anterior cingulate cortex microinjection of κ opioid receptor antagonists, including nor-binaltorphimine and navacaprant, also re-established descending control of nociception in rats with neuropathic pain without altering hypersensitivity and with no effect in shams. Conversely, bilateral injection of a κ opioid receptor agonist, U69,593, in the anterior cingulate cortex of naive rats inhibited descending control of nociception without altering withdrawal thresholds. CONCLUSIONS: Anterior cingulate cortex κ opioid receptor activation therefore diminishes descending control of nociception both in naive animals and as an adaptive response to chronic pain, likely by enhancing net descending facilitation. Descending control of nociception can be restored by activation of µ opioid receptors in the anterior cingulate cortex, but also by κ opioid receptor antagonists, providing a nonaddictive alternative to opioid analgesics. Navacaprant is now in advanced clinical trials.

Lung extracellular matrix modulates KRT5+ basal cell activity in pulmonary fibrosis.

Aberrant expansion of KRT5+ basal cells in the distal lung accompanies progressive alveolar epithelial cell loss and tissue remodelling during fibrogenesis in idiopathic pulmonary fibrosis (IPF). The mechanisms determining activity of KRT5+ cells in IPF have not been delineated. Here, we reveal a potential mechanism by which KRT5+ cells migrate within the fibrotic lung, navigating regional differences in collagen topography. In vitro, KRT5+ cell migratory characteristics and expression of remodelling genes are modulated by extracellular matrix (ECM) composition and organisation. Mass spectrometry- based proteomics revealed compositional differences in ECM components secreted by primary human lung fibroblasts (HLF) from IPF patients compared to controls. Over-expression of ECM glycoprotein, Secreted Protein Acidic and Cysteine Rich (SPARC) in the IPF HLF matrix restricts KRT5+ cell migration in vitro. Together, our findings demonstrate how changes to the ECM in IPF directly influence KRT5+ cell behaviour and function contributing to remodelling events in the fibrotic niche.

Electrode Materials for Enhancing the Performance and Cycling Stability of Zinc Iodide Flow Batteries at High Current Densities.

Aqueous redox flow battery systems that use a zinc negative electrode have a relatively high energy density. However, high current densities can lead to zinc dendrite growth and electrode polarization, which limit the battery's high power density and cyclability. In this study, a perforated copper foil with a high electrical conductivity was used on the negative side, combined with an electrocatalyst on the positive electrode in a zinc iodide flow battery. A significant improvement in the energy efficiency (ca. 10% vs using graphite felt on both sides) and cycling stability at a high current density of 40 mA cm-2 was observed. A long cycling stability with a high areal capacity of 222 mA h cm-2 is obtained in this study, which is the highest reported areal capacity for zinc-iodide aqueous flow batteries operating at high current density, in comparison to previous studies. Additionally, the use of a perforated copper foil anode in combination with a novel flow mode was discovered to achieve consistent cycling at exceedingly high current densities of >100 mA cm-2. In situ and ex situ characterization techniques, including in situ atomic force microscopy coupled with in situ optical microscopy and X-ray diffraction, are applied to clarify the relationship between zinc deposition morphology on the perforated copper foil and battery performance in two different flow field conditions. With a portion of the flow going through the perforations, a significantly more uniform and compact zinc deposition was observed compared to the case where all of the flow passed over the surface of the electrode. Results from modeling and simulation support the conclusion that the flow of a fraction of electrolyte through the electrode enhances mass transport, enabling a more compact deposit.

Mechanistic Insight into Electrode Processes by Operando Visualization of Interfacial pH Using Fluorescent Nanosensors.

Operando visualization of interfacial pH is crucial, yet challenging in electrochemical processes. Herein, we report the fabrication and utilization of ratiometric, fluorescent pH-sensitive nanosensors for operando quantification of fast-dynamic, interfacial pH changes in electrochemical processes and environments where unprotected fluorescent dyes would be degraded. Spatio-temporal pH changes were detected using an electrochemically coupled laser scanning confocal microscope (EC-LSCM) during the electrocoagulation treatment of model and field samples of oil-sands-produced water. Operando visualization of interfacial pH provided new insights into the electrode processes, including ion speciation, electrode fouling, and Faradaic efficiency. We provide compelling evidence that formed metal complexes precipitate at the edge of the pH boundary layer and that there is a strong coupling between the thickness of the interfacial pH layer and the electrode fouling. Furthermore, these findings provide a powerful pathway for optimizing the operating conditions, minimizing electrode passivation, and enhancing the efficiency of electrochemical processes, e.g., electrocoagulation, flow batteries, capacitive deionization, and electrolyzes.

Effect of polarity reversal on floc formation and rheological properties of a sludge formed by the electrocoagulation process.

Anode fouling is one of the key limiting factors to the widespread application of electrocoagulation (EC) for treatment of different types of contaminated water. Promising mitigation strategy to fouling is to operate the process under polarity reversal (PR) instead of direct current (DC). However, the PR operation comes at the cost of process complexity due to the alternation of electrochemical and chemical reactions. In this study, we systematically investigated the link between evolving fouling layer during DC and PR close to iron and aluminum electrodes and morphological and rheological properties of the formed sludge. By operando visualization of EC process, we demonstrate that during PR operation, precipitation of the iron and aluminum species occurs close to the anode interface, resulting in flocs with higher porosity and lower density than those formed under DC conditions. However, rheological investigation revealed that the PR conditions resulted in a sludge with more pronounced solid-like signature, but this enhancement in its viscoelastic properties is closely related to a period of the current's polarity reversal. We attribute this unexpected result to higher shear rate and collision of particles during PR conditions.

De novo priming: driver of immunotherapy responses or epiphenomenon?

The introduction of immunotherapy, in particular immune checkpoint inhibition, has revolutionised the treatment of a range of tumours; however, only a minority of patients respond to these therapies. Understanding the mechanisms by which different immune checkpoint inhibitors work will be critical for both predicting patients who will respond and to developing rational combination therapies to extend these benefits further. The initiation and maintenance of anti-tumour T cell responses is a complicated process split between both the tumour microenvironment and the tumour draining lymph node. As understanding of this process has increased, it has become apparent that immune checkpoint inhibitors can act both within the tumour and in the draining lymph node and that they can target both already activated T cells as well as stimulating the priming of novel T cell clones. Currently, it seems likely that immune checkpoint inhibition acts both within the tumour and in the tumour draining lymph node both reinvigorating existing clones and driving further de novo priming of novel clones. The relative contributions of these sites and targets may depend on the type of model being used and the timeline of the response. Shorter models emphasise the effect of reinvigoration in the absence of recruitment of new clones but studies spanning longer time periods examining T cell clones in patients demonstrate clonal replacement. Ultimately, further work is needed to determine which of the diverse effects of immune checkpoint inhibitors are the fundamental drivers of anti-tumour responses in patients.

Tumour mitochondrial DNA mutations drive aerobic glycolysis to enhance checkpoint blockade.

The mitochondrial genome encodes essential machinery for respiration and metabolic homeostasis but is paradoxically among the most common targets of somatic mutation in the cancer genome, with truncating mutations in respiratory complex I genes being most over-represented1. While mitochondrial DNA (mtDNA) mutations have been associated with both improved and worsened prognoses in several tumour lineages1-3, whether these mutations are drivers or exert any functional effect on tumour biology remains controversial. Here we discovered that complex I-encoding mtDNA mutations are sufficient to remodel the tumour immune landscape and therapeutic resistance to immune checkpoint blockade. Using mtDNA base editing technology4 we engineered recurrent truncating mutations in the mtDNA-encoded complex I gene, Mt-Nd5, into murine models of melanoma. Mechanistically, these mutations promoted utilisation of pyruvate as a terminal electron acceptor and increased glycolytic flux without major effects on oxygen consumption, driven by an over-reduced NAD pool and NADH shuttling between GAPDH and MDH1, mediating a Warburg-like metabolic shift. In turn, without modifying tumour growth, this altered cancer cell-intrinsic metabolism reshaped the tumour microenvironment in both mice and humans, promoting an anti-tumour immune response characterised by loss of resident neutrophils. This subsequently sensitised tumours bearing high mtDNA mutant heteroplasmy to immune checkpoint blockade, with phenocopy of key metabolic changes being sufficient to mediate this effect. Strikingly, patient lesions bearing >50% mtDNA mutation heteroplasmy also demonstrated a >2.5-fold improved response rate to checkpoint inhibitor blockade. Taken together these data nominate mtDNA mutations as functional regulators of cancer metabolism and tumour biology, with potential for therapeutic exploitation and treatment stratification.

Superinfection exclusion creates spatially distinct influenza virus populations.

Interactions between viruses during coinfections can influence viral fitness and population diversity, as seen in the generation of reassortant pandemic influenza A virus (IAV) strains. However, opportunities for interactions between closely related viruses are limited by a process known as superinfection exclusion (SIE), which blocks coinfection shortly after primary infection. Using IAVs, we asked whether SIE, an effect which occurs at the level of individual cells, could limit interactions between populations of viruses as they spread across multiple cells within a host. To address this, we first measured the kinetics of SIE in individual cells by infecting them sequentially with 2 isogenic IAVs, each encoding a different fluorophore. By varying the interval between addition of the 2 IAVs, we showed that early in infection SIE does not prevent coinfection, but that after this initial lag phase the potential for coinfection decreases exponentially. We then asked how the kinetics of SIE onset controlled coinfections as IAVs spread asynchronously across monolayers of cells. We observed that viruses at individual coinfected foci continued to coinfect cells as they spread, because all new infections were of cells that had not yet established SIE. In contrast, viruses spreading towards each other from separately infected foci could only establish minimal regions of coinfection before reaching cells where coinfection was blocked. This created a pattern of separate foci of infection, which was recapitulated in the lungs of infected mice, and which is likely to be applicable to many other viruses that induce SIE. We conclude that the kinetics of SIE onset segregate spreading viral infections into discrete regions, within which interactions between virus populations can occur freely, and between which they are blocked.

Fluorogenic Granzyme A Substrates Enable Real-Time Imaging of Adaptive Immune Cell Activity.

Cytotoxic immune cells, including T lymphocytes (CTLs) and natural killer (NK) cells, are essential components of the host response against tumors. CTLs and NK cells secrete granzyme A (GzmA) upon recognition of cancer cells; however, there are very few tools that can detect physiological levels of active GzmA with high spatiotemporal resolution. Herein, we report the rational design of the near-infrared fluorogenic substrates for human GzmA and mouse GzmA. These activity-based probes display very high catalytic efficiency and selectivity over other granzymes, as shown in tissue lysates from wild-type and GzmA knock-out mice. Furthermore, we demonstrate that the probes can image how adaptive immune cells respond to antigen-driven recognition of cancer cells in real time.

Fluorogenic Granzyme A Substrates Enable Real-Time Imaging of Adaptive Immune Cell Activity.

Cytotoxic immune cells, including T lymphocytes (CTLs) and natural killer (NK) cells, are essential components of the host response against tumors. CTLs and NK cells secrete granzyme A (GzmA) upon recognition of cancer cells; however, there are very few tools that can detect physiological levels of active GzmA with high spatiotemporal resolution. Herein, we report the rational design of the near-infrared fluorogenic substrates for human GzmA and mouse GzmA. These activity-based probes display very high catalytic efficiency and selectivity over other granzymes, as shown in tissue lysates from wild-type and GzmA knock-out mice. Furthermore, we demonstrate that the probes can image how adaptive immune cells respond to antigen-driven recognition of cancer cells in real time.

Impact of protein identity on tumor-associated antigen uptake into infiltrating immune cells: A comparison of different fluorescent proteins as model antigens.

Effective immune responses depend on efficient antigen uptake in the periphery, transport of those antigens to, and presentation in draining lymph nodes (LNs). These processes have been studied intensively using stable fluorescent proteins (FPs) as model antigens. To date, ZsGreen is the only FP that can be tracked efficiently towards LNs, hence, it is difficult to compare studies using alternated tracking proteins. Here, we systematically compared six different FPs. We included ZsGreen, ZsYellow, DsRed, AsRed, mCherry, and mRFP based on sequence homology and/or origin species, and generated FP-expressing tumor cell lines. Stability of fluorescent signal was assessed in vitro over time, across different pH environments, and in vivo through FP antigen uptake and transfer to immune cells isolated from tumors and tumor-draining LNs. ZsGreen could be detected in high percentages of all analyzed tumor-infiltrating immune cells, with highest amounts in tumor-associated macrophages (TAMs) and type 2 conventional dendritic cells (cDC2s). ZsYellow, AsRed, and DsRed followed a similar pattern, but percentages of FP-containing immune cells in the tumor were lower than for ZsGreen. Strikingly, mRFP and mCherry demonstrated a 'non-canonical' antigen uptake pattern where percentages of FP-positive tumor-infiltrating immune cells were highest for cDC1s not TAMs and cDC2s despite comparable stabilities and localization of all FPs. Analysis of antigen-containing cells in the LN was hindered by intracellular degradation of FPs. Only ZsGreen could be efficiently tracked to the LN, though some signal was measurable for ZsYellow and DsRed. In summary, we find that detection of antigen uptake and distribution is subject to variabilities related to fluorophore nature. Future experiments need to consider that these processes might be impacted by protein expression, stability, or other unknown factors. Thus, our data sheds light on potential under-appreciated mechanisms regulating antigen transfer and highlights potential uses and necessary caveats to interpretation based on FP use.

The impact of a magnetic field on electrode fouling during electrocoagulation.

Electrocoagulation (EC) in water treatment encounters several challenges, such as electrode fouling and passivation, especially when the effluent has a complex composition, such as produced water in the oil and gas industry. In this study, the effectiveness of applying an external magnetic field during EC with aluminum anodes (Al-EC) or mild steel anodes (Fe-EC) was investigated for the first time for the removal of inorganic contaminants (including silica, calcium, magnesium, and sulfide) from synthetic and field samples of produced waters. For Al-EC, the presence of a magnetic field perpendicular to the electric field was found to enhance the treatment performance and mitigate the fouling formation on the electrode surface. Chronoamperometric investigations indicated that the application of MF in Al-EC enhances the current density and reduces the time to form a fouling layer on the electrode. In contrast, with Fe-EC, the presence of the magnetic field increased the rate of fouling on the electrodes. Potentiodynamic and kinetic investigations indicate that the magnetic field improves mass transfer via Kelvin force and magnetohydrodynamic (MHD) effects with no impact on the type of kinetic model, while the change in the spin states of the accumulated species has a negligible impact on reducing the fouling. The resistivity of the accumulated fouling layer (δRF) was found to reduce by around 23% due to a magnetic field of 0.158 T. Although increasing the strength of the applied MF increases the mass transfer, the effect is not linear. The results indicate that applying a magnetic field in Al-EC can be an effective method to mitigate fouling during water treatment.

Think global but act local: Tuning the dendritic cell response in cancer.

Despite their low abundance in tumours conventional dendritic cells play an outsized role in initiating and perpetuating anti-tumour immunity; however progressively growing tumours suppress dendritic cell function in a range of ways preventing effective anti-tumour T cell responses. While the success of immune checkpoint blockade has focused attention on T-cell directed therapies, activating tumour dendritic cells has been shown to be critical for the efficacy of several immunotherapies and other conventional therapies owing to their ability to activate and restimulate anti-tumour T-cells. As such, the importance of understanding the mechanisms by which dendritic cell function is impaired are being investigated further. Yet, while much attention has been paid to the tumour microenvironment less has been given to the macroenvironment including effects in the bone marrow and the lymph node. It is now clear that dendritic cell function can be impaired in a variety of ways at different anatomical sites and understanding these mechanisms will be critical for developing effective strategies to tune the dendritic cell response in cancer.

A fluorogenic probe for granzyme B enables in-biopsy evaluation and screening of response to anticancer immunotherapies.

Immunotherapy promotes the attack of cancer cells by the immune system; however, it is difficult to detect early responses before changes in tumor size occur. Here, we report the rational design of a fluorogenic peptide able to detect picomolar concentrations of active granzyme B as a biomarker of immune-mediated anticancer action. Through a series of chemical iterations and molecular dynamics simulations, we synthesize a library of FRET peptides and identify probe H5 with an optimal fit into granzyme B. We demonstrate that probe H5 enables the real-time detection of T cell-mediated anticancer activity in mouse tumors and in tumors from lung cancer patients. Furthermore, we show image-based phenotypic screens, which reveal that the AKT kinase inhibitor AZD5363 shows immune-mediated anticancer activity. The reactivity of probe H5 may enable the monitoring of early responses to anticancer treatments using tissue biopsies.

CXCR2 inhibition enables NASH-HCC immunotherapy.

OBJECTIVE: Hepatocellular carcinoma (HCC) is increasingly associated with non-alcoholic steatohepatitis (NASH). HCC immunotherapy offers great promise; however, recent data suggests NASH-HCC may be less sensitive to conventional immune checkpoint inhibition (ICI). We hypothesised that targeting neutrophils using a CXCR2 small molecule inhibitor may sensitise NASH-HCC to ICI therapy. DESIGN: Neutrophil infiltration was characterised in human HCC and mouse models of HCC. Late-stage intervention with anti-PD1 and/or a CXCR2 inhibitor was performed in murine models of NASH-HCC. The tumour immune microenvironment was characterised by imaging mass cytometry, RNA-seq and flow cytometry. RESULTS: Neutrophils expressing CXCR2, a receptor crucial to neutrophil recruitment in acute-injury, are highly represented in human NASH-HCC. In models of NASH-HCC lacking response to ICI, the combination of a CXCR2 antagonist with anti-PD1 suppressed tumour burden and extended survival. Combination therapy increased intratumoural XCR1+ dendritic cell activation and CD8+ T cell numbers which are associated with anti-tumoural immunity, this was confirmed by loss of therapeutic effect on genetic impairment of myeloid cell recruitment, neutralisation of the XCR1-ligand XCL1 or depletion of CD8+ T cells. Therapeutic benefit was accompanied by an unexpected increase in tumour-associated neutrophils (TANs) which switched from a protumour to anti-tumour progenitor-like neutrophil phenotype. Reprogrammed TANs were found in direct contact with CD8+ T cells in clusters that were enriched for the cytotoxic anti-tumoural protease granzyme B. Neutrophil reprogramming was not observed in the circulation indicative of the combination therapy selectively influencing TANs. CONCLUSION: CXCR2-inhibition induces reprogramming of the tumour immune microenvironment that promotes ICI in NASH-HCC.

Investigation of electrode passivation during electrocoagulation treatment with aluminum electrodes for high silica content produced water.

One of the main challenges for the implementation of electrocoagulation (EC) in water treatment are fouling and passivation of the electrodes, especially for applications with high contaminant concentrations. For the first time, we investigated in this study the process of fouling mitigation by polarity reversal during the EC treatment of boiler blowdown water from oil-sands produced water, characterized by high silica concentrations (0.5-4 g L-1). This effluent is typically obtained from an evaporative desalination process in oil production industries. Potentiodynamic characterisation was used to study the impact of passivation on the anode dissolution. Although a charge loading of 4,800 C L-1 was found to remove about 98% of silica from a 1 L batch of 4 g L-1 Si solution, fouling reduced the performance significantly to about 40% in consecutive cycles of direct current EC (DC-EC) treatment. Periodic polarity reversal (PR) was found to reduce the amount of electrode fouling. Decreasing the polarity period from 60 to 10 s led to the formation of a soft powdery fouling layer that was easily removed from the electrodes. In contrast, with DC operation, a hard scale deposit was observed. The presence of organics in the field samples did not significantly affect the Si removal, and organics with high levels of oxygen and sulfate groups were preferentially removed. Detailed electrochemical and economic investigations suggest that the process operating at 85 °C achieves 95% silica removal (from an initial concentration of 481 mg L-1) with an electrical energy requirement of 0.52 kWh m-3, based on a charge loading of 1,200 C L-1, an inter-electrode gap of 1.8 cm and a current density of 16 mA cm-2.