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Oxygen reduction is one of the core steps of non-emissive zero carbon energy conversion. Therefore, enhancement of its sluggish kinetics is extremely important. Very recently researchers focused on oxygen electrocatalysis at porous polymers. Here we applied the non-metalated and pyrolysis free hypercrosslinked polymers with high specific surface area and abundant active sites. Electrode modified with the copolymer prepared from the twisted triphenylbenzene and N containing triphenyl amine exhibits electrocatalytic ORR in alkaline medium. Tafel slope value (0.067 V dec−1) indicates the efficient electrocatalytic activity and fast reaction kinetics. The lack of H2O2 product detected by scanning electrochemical microscopy suggests 4-electron path. The electrocatalytic activity of electrodes modified with hypercrosslinked polymers prepared from single monomers is also seen.

Abstract Developing highly efficient and cost‐effective electrocatalysts for oxygen reduction reaction (ORR) in aqueous media is crucial for energy conversion systems such as fuel cells or Zn‐air batteries. Electrode materials from spent devices such as lithium‐ion batteries (LiBs) are a serious environmental problem. One of the solutions is their reuse for other electrochemical processes. This work demonstrates the application of solid residues of carbon‐based powders left over from the hydrometallurgical recycling process of LIBs’ waste as efficient catalysts for ORR. Microscopic and spectroscopic studies of the residue disclosed their porous structure and various cobalt contents, depending on the recycling procedure. These battery wastes display ORR catalytic activity when deposited at the liquid‐liquid and solid electrode‐electrolyte interfaces. Scanning Electrochemical Microscopy (SECM) tests showed that assembling battery waste at the liquid‐liquid interface boosts the efficiency of H2O2 production by one to two orders of magnitude. The catalytic activity towards 2‐electron ORR strongly depends on waste powder compositions and structures, e.g., porosity, heteroatom presence, level of defects, and graphitization.

N-acylethanolamines (NAEs) are endogenous lipid-signalling molecules involved in inflammation and energy metabolism. The potential pharmacological effect of NAE association in managing inflammation-based metabolic disorders is unexplored. To date, targeting liver-adipose axis can be considered a therapeutic approach for the treatment of obesity and related dysfunctions. Here, we investigated the metabolic effect of OLALIAMID® (OLA), an olive oil-derived NAE mixture, in limiting liver and adipose tissue (AT) dysfunction of high-fat diet (HFD)-fed mice.OLA reduced body weight and fat mass in obese mice, decreasing insulin resistance (IR), as shown by homeostasis model assessment index, and leptin/adiponectin ratio, a marker of adipocyte dysfunction. OLA improved serum lipid and hepatic profile and the immune/inflammatory pattern of metainflammation. In liver of HFD mice, OLA treatment counteracted glucose and lipid dysmetabolism, restoring insulin signalling (phosphorylation of AKT and AMPK), and reducing mRNAs of key markers of fatty acid accumulation. Furthermore, OLA positively affected AT function deeply altered by HFD by reprogramming of genes involved in thermogenesis of interscapular brown AT (iBAT) and subcutaneous white AT (scWAT), and inducing the beigeing of scWAT. Notably, the NAE mixture reduced inflammation in iBAT and promoted M1-to-M2 macrophage shift in scWAT of obese mice. The tissue and systemic anti-inflammatory effects of OLA and the increased expression of glucose transporter 4 in scWAT contributed to the improvement of gluco-lipid toxicity and insulin sensitivity.In conclusion, we demonstrated that this olive oil-derived NAE mixture is a valid nutritional strategy to counteract IR and obesity acting on liver-AT crosstalk, restoring both hepatic and AT function and metabolism.

Biphasic oxygen reduction and hydrogen evolution are studied for almost two decades, because of favourable overpotential decrease as compared to aqueous solution. Until now, polar solvents (ε > 7) were employed as organic phase in these studies. Here, we applied non polar vegetable oils (rapeseed, linen or sunflower) for biphasic H2O2 generation by oxygen reduction. This product was detected at oil|aqueous acid solution interface by scanning electrochemical microscopy, when electron donor – decamethylferrocene, was electrochemically recycled. Ejection of small fraction of decamethylferrocenium cation from oil to aqueous phase was also noticed.

Among the non-communicable neurological diseases, epilepsy is characterized by abnormal brain activity with several peripheral implications. The role of peripheral inflammation in the relationship between seizure development and nonalcoholic fatty liver disease based on sex difference remains still overlooked. Severe early-life infections lead to increased inflammation that can aggravate epilepsy and hepatic damage progression, both related to increased odds of hospitalization for epileptic patients with liver diseases. Here, we induced a post-natal-day 3 (PND3) infection by LPS (1 mg/kg, i.p.) to determine the hepatic damage in a genetic model of young epileptic WAG/Rij rats (PND45). We evaluated intra- and inter-gender differences in systemic and liver inflammation, hepatic lipid dysmetabolism, and oxidative damage related to mitochondrial functional impairment. First, epileptic rats exposed to LPS, regardless of gender, displayed increased serum hepatic enzymes and altered lipid profile. Endotoxin challenge triggered a more severe inflammatory and immune response in male epileptic rats, compared to females in both serum and liver, increasing pro-inflammatory cytokines and hepatic immune cell recruitment. Conversely, LPS-treated female rats showed significant alterations in systemic and hepatic lipid profiles and reduced mitochondrial fatty acid oxidation. The two different sex-dependent mechanisms of LPS-induced liver injury converge in increased ROS production and related mitochondrial oxidative damage in both sexes. Notably, a compensatory increase in antioxidant defense was evidenced only in female rats. Our study with a translational potential demonstrates, for the first time, that early post-natal infections in epileptic rats induced or worsened hepatic disorders in a sex-dependent manner, amplifying inflammation, lipid dysmetabolism, and mitochondrial impairment.

Previous electrochemical studies of redox emulsions have been mainly performed in the context of electro-organic synthesis. More recently, this research has been oriented towards applications of emulsions in flow batteries. Such biphasic systems seem to provide a suitable environment for reactions at the liquid–liquid interface. Taking an emulsion consisting of microdroplets of decamethylferrocene solution in a hydrophobic ionic liquid/toluene mixture in acidic aqueous solution as an example, we have demonstrated that an electrochemical redox reaction involving the hydrophobic redox probe occurs at the glassy carbon electrode|organic liquid film interface. This reaction is followed by ion exchange between liquid phases. This effect is explained by the instability of the emulsion. A portion of the organic liquid stays on the electrode surface after transfer to a purely aqueous electrolyte and remains electroactive.

Obesity is associated with gastrointestinal (GI) tract and central nervous system (CNS) disorders. High-fat diet (HFD) feeding-induced obesity in mice induces dysbiosis, causing a shift toward bacteria-derived metabolites with detrimental effects on metabolism and inflammation: events often contributing to the onset and progression of both GI and CNS disorders. Palmitoylethanolamide (PEA) is an endogenous lipid mediator with beneficial effects in mouse models of GI and CNS disorders. However, the mechanisms underlining its enteroprotective and neuroprotective effects still need to be fully understood. Here, we aimed to study the effects of PEA on intestinal inflammation and microbiota alterations resulting from lipid overnutrition. Ultramicronized PEA (30 mg/kg/die per os) was administered to HFD-fed mice for 7 weeks starting at the 12th week of HFD regimen. At the termination of the study, the effects of PEA on inflammatory factors and cells, gut microbial features and tryptophan (TRP)-kynurenine metabolism were evaluated. PEA regulates the crosstalk between the host immune system and gut microbiota via rebalancing colonic TRP metabolites. PEA treatment reduced intestinal immune cell recruitment, inflammatory response triggered by HFD feeding, and corticotropin-releasing hormone levels. In particular, PEA modulated HFD-altered TRP metabolism in the colon, rebalancing serotonin (5-HT) turnover and reducing kynurenine levels. These effects were associated with a reshaping of gut microbiota composition through increased butyrate-promoting/producing bacteria, such as Bifidobacterium, Oscillospiraceae and Turicibacter sanguinis, with the latter also described as 5-HT sensor. These data indicate that the rebuilding of gut microbiota following PEA supplementation promotes host 5-HT biosynthesis, which is crucial in regulating intestinal function.

The antibiotic-induced intestinal injury (AIJ) is associated with diarrhoea and gastrointestinal discomfort. However, the pathological intestinal mechanisms and related side effects associated with antibiotic use/misuse may be counteracted by probiotics. This study aims to evaluate the effect and the protective mechanisms of a probiotic formulation containing Alkalihalobacillus clausii (formerly Bacillus clausii; BC) spores in an experimental model of AIJ. C57/Bl6J mice were orally challenged with a high dose of ceftriaxone for five days along with BC treatment which lasted up to the 15th day. Our results showed the beneficial effect of the probiotic in preserving colonic integrity and limiting tissue inflammation and immune cell infiltration in AIJ mice. BC increased tight junction expression and regulated the unbalanced production of colonic pro- and anti-inflammatory cytokines, converging toward the full resolution of the intestinal damage. These findings were supported by the histological evaluation of the intestinal mucosa, suggesting a potential restoration of mucus production. Notably, BC treatment increased gene transcription of the secretory products responsible for epithelium repair and mucus synthesis and normalized the expression of antimicrobial peptides involved in immune activation. Reconstruction of complex and diverse gut microbiota in antibiotic-induced dysbiosis was recorded upon BC supplementation. Specifically, the expansion of A. clausii, Prevotella rara and Eubacterium ruminatium drove intestinal microbiota rebalance by primarily impacting Bacteroidota members. Taken together, our data indicate that BC administration alleviates AIJ by multiple converging mechanisms leading to restoring gut integrity and homeostasis and reshaping microbiota composition.

Gut dysbiosis has been involved in the pathogenesis and progression of Parkinson’s disease (PD), but the mechanisms through which gut microbiota (GM) exerts its influences deserve further study. Recently, we proposed a two-hit mouse model of PD in which ceftriaxone (CFX)-induced dysbiosis amplifies the neurodegenerative phenotype generated by striatal 6-hydroxydopamine (6-OHDA) injection in mice. Low GM diversity and the depletion of key gut colonizers and butyrate producers were the main signatures of GM alteration in this model. Here, we used the phylogenetic investigation of communities by reconstruction of unobserved states (PICRUSt2) to unravel candidate pathways of cell-to-cell communication associated with dual-hit mice and potentially involved in PD progression. We focused our analysis on short-chain fatty acids (SCFAs) metabolism and quorum sensing (QS) signaling. Based on linear discriminant analysis, combined with the effect size results, we found increased functions linked to pyruvate utilization and a depletion of acetate and butyrate production in 6-OHDA+CFX mice. The specific arrangement of QS signaling as a possible result of the disrupted GM structure was also observed. With this exploratory study, we suggested a scenario in which SCFAs metabolism and QS signaling might represent the effectors of gut dysbiosis potentially involved in the designation of the functional outcomes that contribute to the exacerbation of the neurodegenerative phenotype in the dual-hit animal model of PD.

The fast and wireless estimation of moisture in sand and other bulk materials usually requires high-tech instrumentation and computation. To overcome the complexity of such systems, we have employed bipolar electrochemistry as a fast, straightforward, and cost-effective method to wirelessly produce an optical signal. An electric field generated across moist sand is used to polarize an immersed light-emitting diode (LED), triggering an electrochemical reaction and causing a current to flow. Therefore, the bipolar activation of the LED by a threshold electric field creates an optically readable moisture sensor. The light emission intensity depends on two factors: the amount of moisture and the salt concentration. As two stimuli control the light emission, the signal can be considered as an AND logic gate, which is expected to open possibilities in wireless and user-friendly moisture sensors.

Developing highly efficient and cost‐effective electrocatalysts for oxygen reduction reaction (ORR) in aqueous media is crucial for energy conversion systems such as fuel cells or Zn‐air batteries. Electrode materials from spent devices such as lithium‐ion batteries (LiBs) are a serious environmental problem. One of the solutions is their reuse for other electrochemical processes. This work demonstrates the application of solid residues of carbon‐based powders left over from the hydrometallurgical recycling process of LIBs' waste as efficient catalysts for ORR. Microscopic and spectroscopic studies of the residue disclosed their porous structure and various cobalt contents, depending on the recycling procedure. These battery wastes display ORR catalytic activity when deposited at the liquid‐liquid and solid electrode‐electrolyte interfaces. Scanning Electrochemical Microscopy (SECM) tests showed that assembling battery waste at the liquid‐liquid interface boosts the efficiency of H2O2 production by one to two orders of magnitude. The catalytic activity towards 2‐electron ORR strongly depends on waste powder compositions and structures, e.g., porosity, heteroatom presence, level of defects, and graphitization. [ABSTRACT FROM AUTHOR]

Among the non-communicable neurological diseases, epilepsy is characterized by abnormal brain activity with several peripheral implications. The role of peripheral inflammation in the relationship between seizure development and nonalcoholic fatty liver disease based on sex difference remains still overlooked. Severe early-life infections lead to increased inflammation that can aggravate epilepsy and hepatic damage progression, both related to increased odds of hospitalization for epileptic patients with liver diseases. Here, we induced a post-natal-day 3 (PND3) infection by LPS (1 mg/kg, i.p.) to determine the hepatic damage in a genetic model of young epileptic WAG/Rij rats (PND45). We evaluated intra- and inter-gender differences in systemic and liver inflammation, hepatic lipid dysmetabolism, and oxidative damage related to mitochondrial functional impairment. First, epileptic rats exposed to LPS, regardless of gender, displayed increased serum hepatic enzymes and altered lipid profile. Endotoxin challenge triggered a more severe inflammatory and immune response in male epileptic rats, compared to females in both serum and liver, increasing pro-inflammatory cytokines and hepatic immune cell recruitment. Conversely, LPS-treated female rats showed significant alterations in systemic and hepatic lipid profiles and reduced mitochondrial fatty acid oxidation. The two different sex-dependent mechanisms of LPS-induced liver injury converge in increased ROS production and related mitochondrial oxidative damage in both sexes. Notably, a compensatory increase in antioxidant defense was evidenced only in female rats. Our study with a translational potential demonstrates, for the first time, that early post-natal infections in epileptic rats induced or worsened hepatic disorders in a sex-dependent manner, amplifying inflammation, lipid dysmetabolism, and mitochondrial impairment. [ABSTRACT FROM AUTHOR]

Lithium-ion battery (LiB) waste powder is a valuable source of various materials, including carbon and metals. Although this material exhibits electrical conductivity, nanostructured morphology, and may contain metal oxides, it has not been used as an electrocatalyst. Here, we demonstrated the application of LiB waste powder as a catalyst for electrochemical H2O2 generation. The powder was both immobilized on a glassy carbon (GC) electrode and assembled at a liquid–liquid interface formed by decamethylferrocene (DMFc) solution in trifluorotoluene and aqueous perchloric acid in the presence of oxygen. The electrochemistry was studied by cyclic voltammetry and also with a rotating disk electrode (RDE), and a 2-electron ORR pathway was confirmed. H2O2 generation at the liquid–liquid interface and oxidation of DMFc were detected by colorimetry, UV–vis spectroscopy and scanning electrochemical microscopy (SECM). The use of LiB waste powder reduces the ORR onset potential by ca. 0.3 V compared to an unmodified GC. When assembled at a liquid–liquid interface the waste powder increases the efficiency of H2O2 generation by ca. 20 times.

Catalase is known for its ability to catalyze disproportionation of hydrogen peroxide into oxygen and water. This work reports the oxygen reduction reaction (ORR) catalyzed by catalase, with a decreased activation energy manifested by a positive shift (+0.2 V) in onset potential. Direct bioelectrocatalysis with bovine liver catalase on a mercury–gold amalgam microelectrode is demonstrated. The background oxygen reduction reaction on the amalgam surface is inhibited by the protein, while the hydrogen evolution reaction (HER) is facilitated. Catalase molecules whose prosthetic groups are not wired to the electrode retain their intrinsic activity towards disproportionation of H2O2 generated at the electrode. The Hg–Au amalgam electrode may also be used to detect dissolved catalase in the absence of its substrate (H2O2) in the solution.

Although the electrochemical behaviour of an aqueous dispersion of nanometer-sized redox active nanoparticles has recently received some attention, there are very few such studies of larger objects. Here, we present a study of the electrochemical behaviour of an aqueous dispersion of redox (2,2′-azino-bis-(3-ethylbenzothiazoline)-6-sulfonate)-tagged multiwalled carbon nanotubes at a rotating disc electrode. The electrochemical signal related to adsorbed redox-tagged nanotubes was recorded by cyclic voltammetry, while the signal related to collisions of their agglomerates or aggregates was detected using chronoamperometric methods. Keywords: Multiwalled carbon nanotubes, Rotating disc electrode, Collisions, ABTS, Voltammetry, Chronoamperometry