RESUMEN

Exposure to traffic-related air pollution and ultrafine particles (<100 nm; UFP) is linked with neurodegeneration. However, the impact of the aromatic content in fuels and the contribution of different fractions of UFP, i.e., solid UFP vs SVOC UFP, on neuronal function is unknown. We therefore studied effects on neuronal activity and viability in rat primary cortical cells exposed for up to 120 h to copper oxide particles (CuO) or UFP (solid and SVOC) emitted from a heavy-duty diesel engine fueled with petroleum diesel (A20; 20 % aromatics) or Hydrotreated Vegetable Oil-type fuel (A0; 0.1 % aromatics), or solid UFP emitted from a non-road Kubota engine fueled with A20. Moreover, effects of UFP and CuO upon simulated inhalation exposure were studied by exposing an lung model (Calu-3 and THP-1 cells) for 48 h and subsequently exposing the cortical cells to the medium collected from the basal compartment of the lung model. Additionally, cell viability, cytotoxicity, barrier function, inflammation, and oxidative and cell stress were studied in the lung model after 48 h exposure to UFP and CuO. Compared to control, direct exposure to CuO and SVOC UFP decreased neuronal activity, which was partly associated with cytotoxicity. Effects on neuronal activity upon direct exposure to solid UFP were limited. A20-derived UFP (solid and SVOC) were more potent in altering neuronal function and viability than A0 counterparts. Effects on neuronal activity from simulated inhalation exposure were minor compared to direct exposures. In the lung model, CuO and A20-derived UFP increased cytokine release compared to control, whereas CuO and SVOC A20 altered gene expression indicative for oxidative stress. Our data indicate that SVOC UFP exhibit higher (neuro)toxic potency for altering neuronal activity in rat primary cortical cells than the solid fraction. Moreover, our data suggest that reducing the aromatic content in fuel decreases the (neuro)toxic potency of emitted UFP.

Asunto(s)

Contaminantes Atmosféricos , Exposición por Inhalación , Material Particulado , Emisiones de Vehículos , Emisiones de Vehículos/toxicidad , Emisiones de Vehículos/análisis , Material Particulado/toxicidad , Ratas , Animales , Contaminantes Atmosféricos/toxicidad , Contaminantes Atmosféricos/análisis , Neuronas/efectos de los fármacos , Tamaño de la Partícula , Cobre/toxicidad , Supervivencia Celular/efectos de los fármacos

RESUMEN

Developmental exposure to carbamates, organophosphates, and pyrethroids has been associated with impaired neurodevelopmental outcomes. Sex-specific differences following chronic insecticide exposure are rather common in vivo. Therefore, we assessed the chronic effects of in vitro exposure to different carbamates (carbaryl, methomyl and aldicarb), organophosphates [chlorpyrifos (CPF), chlorpyrifos-oxon (CPO), and 3,5,6,trichloropyridinol (TCP)], and pyrethroids [permethrin, alpha-cypermethrin and 3-phenoxy benzoic acid (3-PBA)] on neuronal network development in sex-separated rat primary cortical cultures using micro-electrode array (MEA) recordings. Our results indicate that exposure for 1 week to carbaryl inhibited neurodevelopment in male cultures, while a hyperexcitation was observed in female cultures. Methomyl and aldicarb evoked a hyperexcitation after 2 weeks of exposure, which was more pronounced in female cultures. In contrast to acute MEA results, exposure to ≥ 10 µM CPF caused hyperexcitation in both sexes after 10 days. Interestingly, exposure to 10 µM CPO induced a clear hyperexcitation after 10 days of exposure in male but not female cultures. Exposure to 100 µM CPO strongly inhibited neuronal development. Exposure to the type I pyrethroid permethrin resulted in a hyperexcitation at 10 µM and a decrease in neuronal development at 100 µM. In comparison, exposure to ≥ 10 µM of the type II pyrethroid alpha-cypermethrin decreased neuronal development. In female but not in male cultures, exposure to 1 and 10 µM permethrin changed (network) burst patterns, with female cultures having shorter (network) bursts with fewer spikes per (network) burst. Together, these results show that MEA recordings are suitable for measuring sex-specific developmental neurotoxicity in vitro. Additionally, pyrethroid exposure induced effects on neuronal network development at human-relevant concentrations. Finally, chronic exposure has different effects on neuronal functioning compared to acute exposure, highlighting the value of both exposure paradigms.

RESUMEN

Aggression is a fundamental behavior with essential roles in dominance assertion, resource acquisition, and self-defense across the animal kingdom. However, dysregulation of the aggression circuitry can have severe consequences in humans, leading to economic, emotional, and societal burdens. Previous inconsistencies in aggression research have been due to limitations in techniques for studying these neurons at a high spatial resolution, resulting in an incomplete understanding of the neural mechanisms underlying aggression. Recent advancements in optogenetics, pharmacogenetics, single-cell RNA sequencing, and in vivo electrophysiology have provided new insights into this complex circuitry. This review aims to explore the aggression-provoking stimuli and their detection in rodents, particularly through the olfactory systems. Additionally, we will examine the core regions associated with aggression, their interactions, and their connection with the prefrontal cortex. We will also discuss the significance of top-down cognitive control systems in regulating atypical expressions of aggressive behavior. While the focus will primarily be on rodent circuitry, we will briefly touch upon the modulation of aggression in humans through the prefrontal cortex and discuss emerging therapeutic interventions that may benefit individuals with aggression disorders. This comprehensive understanding of the neural substrates of aggression will pave the way for the development of novel therapeutic strategies and clinical interventions. This approach contrasts with the broader perspective on neural mechanisms of aggression across species, aiming for a more focused analysis of specific pathways and their implications for therapeutic interventions.

RESUMEN

Digital PCR (dPCR) is a powerful method for highly sensitive and precise quantification of nucleic acids. However, designing and optimizing new multiplex dPCR assays using target sequence specific probes remains cumbersome, since fluorescent signals must be optimized for every new target panel. As a solution, we established a generic fluorogenic 6-plex reporter set, based on mediator probe technology, that decouples target detection from signal generation. This generic reporter set is compatible with different target panels and thus provides already optimized fluorescence signals from the start of new assay development. Generic reporters showed high population separability in a colorimetric 6-plex mediator probe dPCR, due to their tailored fluorophore and quencher selection. These reporters were further tested using different KRAS, NRAS and BRAF single-nucleotide polymorphisms (SNP), which are frequent point mutation targets in liquid biopsy. We specifically quantified SNP targets in our multiplex approach down to 0.4 copies per microliter (cp/µL) reaction mix, equaling 10 copies per reaction, on a wild-type background of 400 cp/µL for each, equaling 0.1% variant allele frequencies. We also demonstrated the design of an alternative generic reporter set from scratch in order to give detailed step-by-step guidance on how to systematically establish and optimize novel generic reporter sets. Those generic reporter sets can be customized for various digital PCR platforms or target panels with different degrees of multiplexing.

Asunto(s)

Colorimetría , Polimorfismo de Nucleótido Simple , Humanos , Colorimetría/métodos , Reacción en Cadena de la Polimerasa Multiplex/métodos , Proteínas Proto-Oncogénicas B-raf/genética , Proteínas Proto-Oncogénicas p21(ras)/genética , Proteínas de la Membrana/genética , GTP Fosfohidrolasas

RESUMEN

The electrochemical conversion of carbon monoxide (CO) into oxygenated C2+ products at high rates and selectivity offers a promising approach for the two-step conversion of carbon dioxide (CO2). However, a major drawback of the CO electrochemical reduction in alkaline electrolyte is the preference for the acetate pathway over the more valuable ethanol pathway. Recent research has shed light on the significant impact of thermodynamic water activity on the electrochemical CO2 reduction reaction pathways, but less is understood for the electrochemical reduction of CO. In this study, we investigated how the water activity at the electrified interface can be enhanced to adjust the selectivity between acetate and ethanol. We employed an ionomer modifier to lower the local concentration of alkali ions (via Donnan exclusion), successfully enhancing ethanol production while suppressing acetate formation. We observed a remarkable improvement in the Faradaic efficiency of ethanol and alcohol (i.e. ethanol, propanol etc), which reached 42.5% and 55.1%, respectively, at a current density of 700 mA cm-2. The partial current densities of ethanol and alcohol reached 698 and 942 mA cm-2 at 2000 mA cm-2. Furthermore, we achieved a 3.7-fold increase in the ethanol/acetate ratio, providing clear evidence of our successful modulation of product selectivity.

RESUMEN

The significant role of the cathodic binder in modulating mass transport within the catalyst layer (CL) of fuel cells is essential for optimizing cell performance. This investigation focuses on enhancing the membrane electrode assembly (MEA) through the utilization of a short-side-chain perfluoro-sulfonic acid (SSC-PFSA) ionomer as the cathode binder, referred to as SSC-MEA. This study meticulously visualizes the distinctive interpenetrating networks of ionomers and catalysts, and explicitly clarifies the triple-phase interface, unveiling the transport-friendly microstructure and transport mechanisms inherent in SSC-MEA. The SSC-MEA exhibits advantageous microstructural features, including a better-connected ionomer network and well-organized hierarchical porous structure, culminating in superior mass transfer properties. Relative to the MEA bonded by long-side-chain perfluoro-sulfonic acid (LSC-PFSA) ionomer, noted as LSC-MEA, SSC-MEA exhibits a notable peak power density (1.23 W cm-2), efficient O2 transport, and remarkable proton conductivity (65% improvement) at 65 °C and 70% relativity humidity (RH). These findings establish crucial insights into the intricate morphology-transport-performance relationship in the CL, thereby providing strategic guidance for developing highly efficient MEA.

RESUMEN

It is well-established that Pt-based catalysts suffer from the unfavorable linear scaling relationship (LSR) between *OOH and *OH (ΔG(*OOH) = ΔG(*OH) + 3.2 ± 0.2 eV) for the oxygen reduction reaction (ORR), resulting in a great challenge to significantly reduced ORR overpotentials. Herein, we propose a universal and feasible strategy of fluorine-doped carbon supports, which optimize interfacial microenvironment of Pt-based catalysts and thus significantly enhance their reactive kinetics. The introduction of C-F bonds not only weakens the *OH binding energy, but also stabilizes the *OOH intermediate, resulting in a break of LSR. Furthermore, fluorine-doped carbon constructs a local super-hydrophobic interface that facilitates the diffusion of H2O and the mass transfer of O2. Electrochemical tests show that the F-doped carbon-supported Pt catalysts exhibit over 2-fold higher mass activities than those without F modification. More importantly, those catalysts also demonstrate excellent stability in both rotating disk electrode (RDE) and membrane electrode assembly (MEA) tests. This study not only validates the feasibility of tuning the electrocatalytic microenvironment to improve mass transport and to break the scaling relationship, but also provides a universal catalyst design paradigm for other gas-involving electrocatalytic reactions.

RESUMEN

The pathogenic expansion of the intronic GGGGCC hexanucleotide located in the non-coding region of the C9orf72 gene represents the most frequent genetic cause of amyotrophic lateral sclerosis (ALS) and frontotemporal dementia (FTD). This mutation leads to the accumulation of toxic RNA foci and dipeptide repeats (DPRs), as well as reduced levels of the C9orf72 protein. Thus, both gain and loss of function are coexisting pathogenic aspects linked to C9orf72-ALS/FTD. Synaptic alterations have been largely described in C9orf72 models, but it is still not clear which aspect of the pathology mostly contributes to these impairments. To address this question, we investigated the dynamic changes occurring over time at the synapse upon accumulation of poly(GA), the most abundant DPR. Overexpression of this toxic form induced a drastic loss of synaptic proteins in primary neuron cultures, anticipating autophagic defects. Surprisingly, the dramatic impairment characterizing the synaptic proteome was not fully matched by changes in network properties. In fact, high-density multi-electrode array analysis highlighted only minor reductions in the spike number and firing rate of poly(GA) neurons. Our data show that the toxic gain of function linked to C9orf72 affects the synaptic proteome but exerts only minor effects on the network activity.

Asunto(s)

Autofagia , Proteína C9orf72 , Neuronas , Sinapsis , Neuronas/metabolismo , Animales , Sinapsis/metabolismo , Proteína C9orf72/genética , Proteína C9orf72/metabolismo , Células Cultivadas , Péptidos/metabolismo , Humanos , Agregado de Proteínas

RESUMEN

Cockayne Syndrome B (CSB) is a hereditary multiorgan syndrome which-through largely unknown mechanisms-can affect the brain where it clinically presents with microcephaly, intellectual disability and demyelination. Using human induced pluripotent stem cell (hiPSC)-derived neural 3D models generated from CSB patient-derived and isogenic control lines, we here provide explanations for these three major neuropathological phenotypes. In our models, CSB deficiency is associated with (i) impaired cellular migration due to defective autophagy as an explanation for clinical microcephaly; (ii) altered neuronal network functionality and neurotransmitter GABA levels, which is suggestive of a disturbed GABA switch that likely impairs brain circuit formation and ultimately causes intellectual disability; and (iii) impaired oligodendrocyte maturation as a possible cause of the demyelination observed in children with CSB. Of note, the impaired migration and oligodendrocyte maturation could both be partially rescued by pharmacological HDAC inhibition.

Asunto(s)

Síndrome de Cockayne , Células Madre Pluripotentes Inducidas , Oligodendroglía , Humanos , Células Madre Pluripotentes Inducidas/metabolismo , Células Madre Pluripotentes Inducidas/citología , Células Madre Pluripotentes Inducidas/patología , Síndrome de Cockayne/genética , Síndrome de Cockayne/metabolismo , Síndrome de Cockayne/patología , Oligodendroglía/metabolismo , Oligodendroglía/citología , Movimiento Celular , Enzimas Reparadoras del ADN/metabolismo , Enzimas Reparadoras del ADN/genética , Neuronas/metabolismo , Neuronas/patología , Autofagia , Encéfalo/metabolismo , Encéfalo/patología , Proteínas de Unión a Poli-ADP-Ribosa/metabolismo , Proteínas de Unión a Poli-ADP-Ribosa/genética , Ácido gamma-Aminobutírico/metabolismo , ADN Helicasas/metabolismo , ADN Helicasas/genética , Microcefalia/patología , Microcefalia/metabolismo , Microcefalia/genética , Enfermedades Desmielinizantes/patología , Enfermedades Desmielinizantes/metabolismo , Diferenciación Celular

RESUMEN

The synchronization of the electrical and mechanical coupling assures the physiological pump function of the heart, but life-threatening pathologies may jeopardize this equilibrium. Recently, human induced pluripotent stem cell-derived cardiomyocytes (hiPSC-CMs) have emerged as a model for personalized investigation because they can recapitulate human diseased traits, such as compromised electrical capacity or mechanical circuit disruption. This research avails the model of hiPSC-CMs and showcases innovative techniques to study the electrical and mechanical properties as well as their modulation due to inherited cardiomyopathies. In this work, hiPSC-CMs carrying either Brugada syndrome (BRU) or dilated cardiomyopathy (DCM), were organized in a bilayer configuration to first validate the experimental methods and second mimic the physiological environment. High-density CMOS-based microelectrode arrays (HD-MEA) have been employed to study the electrical activity. Furthermore, mechanical function was investigated via quantitative video-based evaluation, upon stimulation with a ß-adrenergic agonist. This study introduces two experimental methods. First, high-throughput mechanical measurements in the hiPSC-CM layers (xy-inspection) are obtained using both a recently developed optical tracker (OPT) and confocal reference-free traction force microscopy (cTFM) aimed to quantify cardiac kinematics. Second, atomic force microscopy (AFM) with FluidFM probes, combined with the xy-inspection methods, supplemented a three-dimensional understanding of cell-cell mechanical coupling (xyz-inspection). This particular combination represents a multi-technique approach to detecting electrical and mechanical latency among the cell layers, examining differences and possible implications following inherited cardiomyopathies. It can not only detect disease characteristics in the proposed in vitro model but also quantitatively assess its response to drugs, thereby demonstrating its feasibility as a scalable tool for clinical and pharmacological studies.

Asunto(s)

Células Madre Pluripotentes Inducidas , Miocitos Cardíacos , Humanos , Miocitos Cardíacos/citología , Miocitos Cardíacos/metabolismo , Células Madre Pluripotentes Inducidas/citología , Células Madre Pluripotentes Inducidas/metabolismo , Microelectrodos , Síndrome de Brugada , Cardiomiopatía Dilatada/patología , Fenómenos Electrofisiológicos , Células Cultivadas

RESUMEN

The electroreduction of nitrate to ammonia via a selective eight-electron transfer nitrate reduction reaction offers a promising, low energy consumption, pollution-free, green NH3 synthesis strategy alternative to the Haber-Bosch method. However, it remains a great challenge to achieve high NH4+ selectivity and complete conversion from NO3--N to NH4+-N. Herein, we report ingredients adjustable Cu2O@CoO yolk-shell nanocubes featured with tunable inner void spaces and diverse activity centers, favoring the rapid cascade conversion of NO3- into NO2- on Cu2O and NO2- into NH4+ on CoO. Cu2O@CoO yolk-shell nanocubes exhibit super NH4+ Faradaic efficiencies (>99%) over a wide potential window (-0.2 V to -0.9 V versus RHE) with a considerable NH4+ yield rate of 15.27 mg h-1 cm-2 and fantastic cycling stability and long-term chronoamperometric durability. Cu2O@CoO yolk-shell nanocubes exhibited glorious NO3--N to NH4+-N conversion efficiency in both dilute (500 ppm) and highly concentrated (0.1 and 1 M) NO3- electrolytes, respectively. The nitrate electrolysis membrane electrode assembly system equipped with Cu2O@CoO yolk-shell nanocubes delivers over 99.8% NH4+ Faradaic efficiency at cell voltages of 1.9-2.3 V.

RESUMEN

Objective.The visual perception provided by retinal prostheses is limited by the overlapping current spread of adjacent electrodes. This reduces the spatial resolution attainable with unipolar stimulation. Conversely, simultaneous multipolar stimulation guided by the measured neural responses-neural activity shaping (NAS)-can attenuate excessive spread of excitation allowing for more precise control over the pattern of neural activation. However, defining effective multipolar stimulus patterns is a challenging task. Previous attempts focused on analytical solutions based on an assumed linear nonlinear model of retinal response; an analytical model inversion (AMI) approach. Here, we propose a model-free solution for NAS, using artificial neural networks (ANNs) that could be trained with data acquired from the implant.Approach.Our method consists of two ANNs trained sequentially. The measurement predictor network (MPN) is trained on data from the implant and is used to predict how the retina responds to multipolar stimulation. The stimulus generator network is trained on a large dataset of natural images and uses the trained MPN to determine efficient multipolar stimulus patterns by learning its inverse model. We validate our methodin silicousing a realistic model of retinal response to multipolar stimulation.Main results.We show that our ANN-based NAS approach produces sharper retinal activations than the conventional unipolar stimulation strategy. As a theoretical bench-mark of optimal NAS results, we implemented AMI stimulation by inverting the model used to simulate the retina. Our ANN strategy produced equivalent results to AMI, while not being restricted to any specific type of retina model and being three orders of magnitude more computationally efficient.Significance.Our novel protocol provides a method for efficient and personalized retinal stimulation, which may improve the visual experience and quality of life of retinal prosthesis users.

Asunto(s)

Aprendizaje Profundo , Prótesis Visuales , Humanos , Retina/fisiología , Redes Neurales de la Computación , Estimulación Luminosa/métodos , Percepción Visual/fisiología

RESUMEN

BACKGROUND: Astrocytes are the most abundant cell type of the central nervous system and are fundamentally involved in homeostasis, neuroprotection, and synaptic plasticity. This regulatory function of astrocytes on their neighboring cells in the healthy brain is subject of current research. In the ischemic brain we assume disease specific differences in astrocytic acting. The renin-angiotensin-aldosterone system regulates arterial blood pressure through endothelial cells and perivascular musculature. Moreover, astrocytes express angiotensin II type 1 and 2 receptors. However, their role in astrocytic function has not yet been fully elucidated. We hypothesized that the angiotensin II receptors impact astrocyte function as revealed in an in vitro system mimicking cerebral ischemia. Astrocytes derived from neonatal wistar rats were exposed to telmisartan (angiotensin II type 1 receptor-blocker) or PD123319 (angiotensin II type 2 receptor-blocker) under normal conditions (control) or deprivation from oxygen and glucose. Conditioned medium (CM) of astrocytes was harvested to elucidate astrocyte-mediated indirect effects on microglia and cortical neurons. RESULT: The blockade of angiotensin II type 1 receptor by telmisartan increased the survival of astrocytes during ischemic conditions in vitro without affecting their proliferation rate or disturbing their expression of S100A10, a marker of activation. The inhibition of the angiotensin II type 2 receptor pathway by PD123319 resulted in both increased expression of S100A10 and proliferation rate. The CM of telmisartan-treated astrocytes reduced the expression of pro-inflammatory mediators with simultaneous increase of anti-inflammatory markers in microglia. Increased neuronal activity was observed after treatment of neurons with CM of telmisartan- as well as PD123319-stimulated astrocytes. CONCLUSION: Data show that angiotensin II receptors have functional relevance for astrocytes that differs in healthy and ischemic conditions and effects surrounding microglia and neuronal activity via secretory signals. Above that, this work emphasizes the strong interference of the different cells in the CNS and that targeting astrocytes might serve as a therapeutic strategy to influence the acting of glia-neuronal network in de- and regenerative context.

Asunto(s)

Bloqueadores del Receptor Tipo 1 de Angiotensina II , Bloqueadores del Receptor Tipo 2 de Angiotensina II , Astrocitos , Accidente Cerebrovascular Isquémico , Microglía , Neuronas , Ratas Wistar , Receptor de Angiotensina Tipo 1 , Receptor de Angiotensina Tipo 2 , Telmisartán , Animales , Ratas , Bloqueadores del Receptor Tipo 1 de Angiotensina II/farmacología , Bloqueadores del Receptor Tipo 2 de Angiotensina II/farmacología , Animales Recién Nacidos , Astrocitos/metabolismo , Astrocitos/efectos de los fármacos , Bencimidazoles/farmacología , Comunicación Celular/fisiología , Comunicación Celular/efectos de los fármacos , Células Cultivadas , Imidazoles/farmacología , Accidente Cerebrovascular Isquémico/metabolismo , Accidente Cerebrovascular Isquémico/patología , Microglía/metabolismo , Microglía/efectos de los fármacos , Neuronas/metabolismo , Neuronas/efectos de los fármacos , Piridinas/farmacología , Receptor de Angiotensina Tipo 1/metabolismo , Receptor de Angiotensina Tipo 2/metabolismo , Telmisartán/farmacología

RESUMEN

We investigated drug-induced acute neuronal electrophysiological changes using Micro-Electrode arrays (MEA) to rat primary neuronal cell cultures. Data based on 6-key MEA parameters were analyzed for plate-to-plate vehicle variability, effects of positive and negative controls, as well as data from over 100 reference drugs, mostly known to have pharmacological phenotypic and clinical outcomes. A Least Absolute Shrinkage and Selection Operator (LASSO) regression, coupled with expert evaluation helped to identify the 6-key parameters from many other MEA parameters to evaluate the drug-induced acute neuronal changes. Calculating the statistical tolerance intervals for negative-positive control effects on those 4-key parameters helped us to develop a new weighted hazard scoring system on drug-induced potential central nervous system (CNS) adverse effects (AEs). The weighted total score, integrating the effects of a drug candidate on the identified six-pivotal parameters, simply determines if the testing compound/concentration induces potential CNS AEs. Hereto, it uses four different categories of hazard scores: non-neuroactive, neuroactive, hazard, or high hazard categories. This new scoring system was successfully applied to differentiate the new compounds with or without CNS AEs, and the results were correlated with the outcome of in vivo studies in mice for one internal program. Furthermore, the Random Forest classification method was used to obtain the probability that the effect of a compound is either inhibitory or excitatory. In conclusion, this new neuronal scoring system on the cell assay is actively applied in the early de-risking of drug development and reduces the use of animals and associated costs.

RESUMEN

In this work, a new concept for the approximate determination of the reaction enthalpy of the reaction between CO2 and monoethanolamine (MEA) in aqueous solution was developed. For this purpose, a CO2 gas stream was flowed into aqueous MEA solutions with different concentrations of 1 wt%, 2.5 wt% and 7.5 wt%. The weight difference ∆T, which is based on the increase in CO2 bound by the MEA over time, was documented using a thermographic camera. The mass difference ∆m, which is also based on the increase in CO2 bound by the MEA over time, was determined using a balance. By determining ∆T and ∆m, an approximate calculation of the reaction enthalpy is possible. The deviation from the values from the data known from the literature was less than 5% in all experiments.

RESUMEN

The presented study is concerned with a new multi-step method to synthesize PtCo/C materials based on composite CoxOy/C that combines the advantages of different liquid-phase synthesis methods. Based on the results of studying the materials at each stage of synthesis with the TG, XRD, TEM, SEI, TXRF, CV and LSV methods, a detailed overview of the sequential changes in catalyst composition and structure at each stage of the synthesis is presented. The PtCo/C catalyst synthesized with the multi-step method is characterized by a uniform distribution of bimetallic nanoparticles of about 3 nm in size over the surface of the support, which result in its high ESA and ORR activity. The activity study for the synthesized PtCo/C catalyst in an MEA showed better current-voltage characteristics and a higher maximum specific power compared with an MEA based on a commercial Pt/C catalyst. Therefore, the results of the presented study demonstrate high prospects for the developed approach to the multi-step synthesis of PtM/C catalysts, which may enhance the characteristics of proton-exchange membrane fuel cells (PEMFCs).

RESUMEN

In view of a catalyst layer (CL) with low-Pt causing higher local transport resistance of O2 (Rlocal), we propose a multi-study methodology that combines CO poisoning, the limiting current density method, and electrochemical impedance spectroscopy to reveal how real CL interfaces dominate Rlocal. Experimental results indicate that the ionomer is not evenly distributed on the catalyst surface, and the uniformity of ionomer distribution does not show a positive correlation with the ionomer content. When the ionomer coverage on the supported catalyst surface is below 20 %, the ECSA is only 10 m2·g-1, and the ionomer coverage on the supported catalyst surface reaches 60 %, the ECSA is close to 40 m2·g-1. The ECSA has a positive correlation with ionomer coverage. Because the ECSA is measured by CO poisoning, it can be inferred that the platinum contacted with ionomer can generate effective active sites. Furthermore, a more uniform distribution of ionomer can create additional proton transport channels and reduce the distance for oxygen transport from the catalyst layer bulk to the active sites. A higher ECSA and a shorter distance for oxygen transport will reduce the Rlocal, leading to better performance.

RESUMEN

This work proposes an innovative approach for the membrane separation of spent and unspent H2S scavengers (SUS) derived from the application of MEA-triazine in offshore oil and gas production. Modified nanofiltration membranes were fabricated by incorporating graphene oxide (GO) and polyvinyl alcohol (PVA) into a thin film composite (TFC) to obtain a thin film nanocomposite (TFN) with enhanced permeability. In addition, various immobilization strategies for GO were investigated. The performance of the membranes and the effect of the GO loading were evaluated in terms of permeability, fouling propensity, and rejection of key components of the SUS, i.e., MEA-triazine (unspent scavenger), dithiazine (spent scavenger), and monoethanolamine, operating on a sample of SUS wastewater obtained from an offshore oil and gas platform. Various characterization techniques, such as contact angle, FTIR, XRD, SEM, TGA, and AFM, were employed to evaluate the structure, composition, and hydrophilicity of the membrane. The results show a remarkable increase in permeability (from 0.22 Lm-2 h-1 bar-1 for the TFC to 5.8 Lm-2 h-1 bar-1 for the TFN membranes), due to the enhanced hydrophilicity from GO incorporation. The strong interfacial interaction between GO and PVA within the TFN membrane results in negligible nanofiller leaching. The incorporation of GO moderately increases the rejection of the unspent scavenger (63%-73%, 62%-79%, 62%-80%, and 68%-76%), while drastically increasing the rejection of the spent scavenger, which is approximately null for the TFC membrane without GO and increases up to 58% in the TFN membrane with GO. Therefore, while the proposed membranes cannot be used for the selective separation of the unspent form the spent scavenger, they can achieve substantial recovery of all the key components contained in the SUS to avoid their discharge into the sea.

Asunto(s)

Grafito , Membranas Artificiales , Triazinas , Grafito/química , Triazinas/química , Sulfuro de Hidrógeno/química , Sulfuro de Hidrógeno/aislamiento & purificación , Permeabilidad , Nanocompuestos/química , Alcohol Polivinílico/química , Filtración/métodos , Aguas Residuales/química , Interacciones Hidrofóbicas e Hidrofílicas

RESUMEN

Background: The prevalence of lung cancer in the Middle East and Africa (MEA) region has steadily increased in recent years and is generally associated with a poor prognosis due to the late detection of most of the cases. We explored the factors leading to delayed diagnoses, as well as the challenges and gaps in the early screening, detection, and referral framework for lung cancer in the MEA. Methods: A steering committee meeting was convened in October 2022, attended by a panel of ten key external experts in the field of oncology from the Kingdom of Saudi Arabia, United Arab Emirates, South Africa, Egypt, Lebanon, Jordan, and Turkey, who critically and extensively analyzed the current unmet needs and challenges in the screening and early diagnosis of lung cancer in the region. Results: As per the experts' opinion, lack of awareness about disease symptoms, misdiagnosis, limited screening initiatives, and late referral to specialists were the primary reasons for delayed diagnoses emphasizing the need for national-level lung cancer screening programs in the MEA region. Screening guidelines recommend low-dose computerized tomography (LDCT) for lung cancer screening in patients with a high risk of malignancy. However, high cost and lack of awareness among the public as well as healthcare providers prevented the judicious use of LDCT in the MEA region. Well-established screening and referral guidelines were available in only a few of the MEA countries and needed to be implemented in others to identify suspected cases early and provide timely intervention thus improving patient outcomes. Conclusions: There is a great need for large-scale screening programs, preferably integrated with tobacco-control programs and awareness programs for physicians and patients, which may facilitate higher adherence to lung cancer screening and improve survival outcomes.

RESUMEN

Bioprinting technology offers unprecedented opportunities to construct in vitro tissue models that recapitulate the 3D morphology and functionality of native tissue. Yet, it remains difficult to obtain adequate functional readouts from such models. In particular, it is challenging to position sensors in desired locations within pre-fabricated 3D bioprinted structures. At the same time, bioprinting tissue directly onto a sensing device is not feasible due to interference with the printer head. As such, a multi-sensing platform inspired by origami that overcomes these challenges by "folding" around a separately fabricated 3D tissue structure is proposed, allowing for the insertion of electrodes into precise locations, which are custom-defined using computer-aided-design software. The multi-sensing origami platform (MSOP) can be connected to a commercial multi-electrode array (MEA) system for data-acquisition and processing. To demonstrate the platform, how integrated 3D MEA electrodes can record neuronal electrical activity in a 3D model of a neurovascular unit is shown. The MSOP also enables a microvascular endothelial network to be cultured separately and integrated with the 3D tissue structure. Accordingly, how impedance-based sensors in the platform can measure endothelial barrier function is shown. It is further demonstrated the device's versatility by using it to measure neuronal activity in brain organoids.

Asunto(s)

Bioimpresión , Impresión Tridimensional , Bioimpresión/métodos , Impresión Tridimensional/instrumentación , Humanos , Ingeniería de Tejidos/métodos , Diseño Asistido por Computadora , Electrodos , Diseño de Equipo/métodos