Measurement of the active width in Sr-doped lanthanum manganate Sofc Cathodes using Nano-ct, impedance spectroscopy and Bayesian calibration

Bayesian model-based analysis (BMA) is a method for producing quantitative models of complex physical systems through the comparison between models and experimental data. A model of a porous LSM cathode (symmetrical cell) was applied to impedance data and its parameters estimated via Bayesian calibration. X-ray computed tomography provided microstructural information for the model. The combination of model calibration and microstructural characterization enabled an estimate of the active thickness for a porous LSM electrode. The active width extended only a few nanometers from the surface, strongly suggesting that future models should explicitly resolve the space-charge region

Characterizing Electrode-Level Oxygen Transport in Polymer Electrolyte Fuel Cells

<p>Polymer electrolyte fuel cells (PEFCs) are a promising technology for environmentally friendly automobiles, among other applications. However, performance losses due to oxygen transport hindrances in the PEFC’s cathode continue to be an issue in widespread commercialization. This dissertation focuses on the transport of oxygen through the thickness of the PEFC cathode, and the effect of the cathode’s microstructure on that transport. In order to react in the cathode, oxygen travels from gas flow channels down through a diffusion medium, through the pores of a catalyst layer, and finally, into and through the ionomer covering the catalyst particles. Transport resistances throughout this path lead to oxygen starvation at some of the catalyst particles. Due to these transport resistances, much of the platinum is underutilized when the fuel cell is operating at appreciable currents. This dissertation aims to characterize the transport resistance in each of these phases. We study (1) oxygen transport throughout the diffusion medium using a commercial electrochemical microsensor at multiple points, (2) oxygen transport through the entire diffusion medium using a thin film oxygen microsensor at one point, (3) transport through the catalyst layer pores using a device that allows oxygen microsensors to contact the side of the catalyst layer at multiple points, (4) the effect of the catalyst layer’s microstructure on oxygen transport using x-ray computed tomography, and (5) transport into and through ionomer-covered catalyst agglomerates using ex-situ experiments. We go on to discuss the application of similar methods to solid oxide fuel cells. Using the methods developed in this work, we determine that the two dominant oxygen transport resistances are the diffusion medium, and a “local” resistance at the interface of the platinum catalyst and the ionomer binder that has previously generated some controversy in the field. The oxygen transport resistance of the diffusion medium in this work (defined as the ratio of the drop in concentration across a component to the flux through it) is 65 s/m, with about 2/3 of that coming from its microporous layer. This value can rise to double or more in the case of liquid water condensation in the diffusion medium’s pores. We find that the oxygen transport resistance in the catalyst layer’s pores is an order of magnitude less than that of the diffusion medium. That value, too, can change depending on liquid water flooding. In previous works, the “local” oxygen transport resistance at the level of the platinum catalyst and ionomer binder was of unclear origin. We have determined that it arises at the Pt|ionomer interface – it does not originate from the ionomer|gas interface, nor is it due to nanoscale confinement effects. In our investigation of the catalyst layer’s morphology, we find that a popular approach to modelling PEFC performance – the agglomerate model – changes significantly when one incorporates a realistic distribution of agglomerate sizes instead of assuming a uniform agglomerate size. This effect, however, is small compared to the oxygen transport resistance of the diffusion medium oxygen resistance and the Pt|ionomer interfacial oxygen resistance.</p

Gas Transport Resistance in Polymer Electrolyte Thin Films on Oxygen Reduction Reaction Catalysts

Significant reductions in expensive platinum catalyst loading for the oxygen reduction reaction are needed for commercially viable fuel cell electric vehicles as well as other important applications. In reducing loading, a resistance at the Pt surface in the presence of thin perfluorosulfonic acid (PFSA) electrolyte film, on the order of 10 nm thick, becomes a significant barrier to adequate performance. However, the resistance mechanism is unresolved and could be due to gas dissolution kinetics, increased diffusion resistance in thin films, or electrolyte anion interactions. A common hypothesis for the origin of the resistance is a highly reduced oxygen permeability in the thin polymer electrolyte films that coat the catalyst relative to bulk permeability that is caused by nanoscale confinement effects. Unfortunately, the prior work has not separated the thin-film gas transport resistance from that associated with PFSA interactions with a polarized catalyst surface. Here, we present the first characterization of the thin-film O₂ transport resistance in the absence of a polarized catalyst, using a nanoporous substrate that geometrically mimics the active catalyst particles. Through a parametric study of varying PFSA film thickness, as thin as 50 nm, we observe no enhanced gas transport resistance in thin films as a result of either interfacial effects or structural changes in the PFSA. Our results suggest that other effects, such as anion poisoning at the Pt catalyst, could be the source of the additional resistance observed at low Pt loading

Meshed Subvolumes for "Advantages of ionic conductors over electronic conductors as infiltrates in solid oxide fuel cell cathodes".

The meshed sub-volume input files (*.inp) and simulation output files (*.csv) are hosted at the linked folders, respectively MeshedFiles and csv_Outputs.   The link to the folders is :  https://drive.google.com/drive/folders/1cnusA0HayBuxmNUzfHsrAjNvAz_pbicG?usp=share_link If no Readme files exist in folders, contact [email protected] for details of each.  If Readme files exist,  they will explain filenaming, contents, and structure. </p

Endothelial transmigration by Trypanosoma cruzi.

Chagas heart disease, the leading cause of heart failure in Latin America, results from infection with the parasite Trypanosoma cruzi. Although T. cruzi disseminates intravascularly, how the parasite contends with the endothelial barrier to escape the bloodstream and infect tissues has not been described. Understanding the interaction between T. cruzi and the vascular endothelium, likely a key step in parasite dissemination, could inform future therapies to interrupt disease pathogenesis. We adapted systems useful in the study of leukocyte transmigration to investigate both the occurrence of parasite transmigration and its determinants in vitro. Here we provide the first evidence that T. cruzi can rapidly migrate across endothelial cells by a mechanism that is distinct from productive infection and does not disrupt monolayer integrity or alter permeability. Our results show that this process is facilitated by a known modulator of cellular infection and vascular permeability, bradykinin, and can be augmented by the chemokine CCL2. These represent novel findings in our understanding of parasite dissemination, and may help identify new therapeutic strategies to limit the dissemination of the parasite

Elucidating determinants for <i>T. cruzi</i> TEM.

<p>ECs and <i>T. cruzi</i> were pre-incubated with the indicated reagents for 30 min prior to infection. Non-specific mouse IgG (ns-mIgG), mouse anti-human PECAM, and mouse anti-human CD99 antibodies were used at 20 µg/mL. Thapsigargin and wortmannin were used at 10 mM and 100 nM, respectively. To disrupt cellular energy production, samples were treated with 10 mM sodium azide and 6 mM deoxyglucose. After adding the parasites to the ECs, samples were then incubated for 3 hours in the continuous presence of the reagents before being washed, fixed and scored for transmigration as described. Data shown are the mean and standard error of the mean for three separate experiments with 2–3 replicates for each condition per experiment. * denotes p<0.05 relative to the control.</p

Comparative TEM among the <i>Kinetoplastidae</i>.

<p>(A) TEM was assayed for <i>T. cruzi</i>, <i>T. brucei</i>, and <i>Leishmania major</i> using our standard TEM method with 1×10⁵ parasites/well. Parasites were prepared as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081187#s2" target="_blank">Methods</a>. Where indicated, samples were treated (both during a 30 minute pre-incubation and during infection/TEM) with HK or HOE 140 at 20 ng/mL and 200 nM, respectively. Data shown represent the total TEM events per high power field to highlight the large differences observed with <i>T. brucei</i> and <i>L. major</i>. Data were collected from three independent experiments with 2–3 replicates per sample per experiment. * denotes significant difference relative to <i>T. cruzi</i> non-treated controls, p <0.05. (B) To confirm that <i>T. brucei</i> TEM was responsive to manipulations of the bradykinin signaling pathway, we treated samples with the indicated reagents (both pre-incubation and during TEM) and assayed TEM using the standard assay<b>.</b> To correct for variations between parasite preparations and aid in visualization, data are shown as the fold change relative to control (no treatment). * denotes p<0.05 relative to the control.</p

CCL2 augments <i>T. cruzi</i> TEM.

<p>(A) To assess the effect of the chemokine CCL2 on TEM, EC monolayers were pre-incubated with CCL2 for 1 hour before the start of the standard TEM assay. Samples were washed briefly before the start of TEM, leaving a gradient of CCL2 in the collagen matrix. Other reagents were also pre-incubated with parasites and EC (in addition to CCL2) for 30 min. at the indicated concentrations before the start of the assay. After adding the parasites to the monolayers, TEM was allowed to proceed for 3 hours. Samples were incubated in the continuous presence of the reagents, except CCL2, which was only present during pre-incubation. Samples were then washed, fixed and scored as described in the <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081187#s2" target="_blank">Methods</a>. Data were collected from three experiments with 2–3 replicates per experiment. To correct for variations between parasite preparations and aid in visualization, data are shown as the fold change relative to control. * denotes p<0.05 relative to the control. (B) Permeability was quantified in samples that were identical to those in panel (A) except that 100 µg/mL FITC-dextran was included in the media during the incubation. After washing and fixation, the amount of FITC-dextran that had crossed the monolayer into the collagen matrix was quantified using fluorescence spectrophotometry. Data represent the average and standard deviation of six independent replicates. *n.s. - None of the indicated samples were statistically significant (p <0.05) relative to each other, and CCL2 treatment (200 nM) under these conditions did not significantly alter monolayer permeability in the presence or absence of <i>T. cruzi</i> (<a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081187#pone-0081187-g006" target="_blank">Figure 6B</a> compared to <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0081187#pone-0081187-g002" target="_blank">Figure 2</a>).</p