The Efficiency of Pd Addition and Sr Substitution on La1−xSrxMnO3 to Remove Ventilation Air Methane in a Catalytic Flow Reversal Reactor

Ventilation air methane (VAM) is the main cause of greenhouse gas emissions in coal mining. Catalytic flow reverse reactor (CFRR) is widely used in VAM to mitigate methane emissions. In this study, palladium (Pd) and La1−xSrxMnO3 were used as catalysts in a CFRR. Different types of catalysts were prepared by loading La0.8Sr0.2MnO3, La0.9Sr0.1MnO3, and 0.1%Pd-La0.9Sr0.1MnO3 on a cordierite honeycomb reactor coated with γ-Al2O3 to compare their performances. In addition, this study compared the performance of the three catalysts in an 800 °C reactor based on different methane inlet concentrations, inlet speeds, and conversion times. The results showed: (1) 0.1% addition of Pd increased methane conversion. (2) La0.8Sr0.2MnO3 had higher efficiency at lower methane inlet concentrations, whereas La0.9Sr0.1MnO3 was more efficient at higher methane concentrations. This study demonstrates that a higher Sr loading is worth implementing only when the methane concentration of VAM is lower than 0.6%. (3) To achieve a higher methane conversion efficiency, the inlet velocity of methane should also be considered.

Impurity leakage and radiative cooling in the first nitrogen and neon seeding study in the slot divertor at DIII-D

A comparative study of nitrogen versus neon has been carried out to analyze the impact of the two radiative species on power dissipation, SOL impurity distribution, divertor and pedestal characteristics. The experimental results show that N remains compressed in the divertor, thereby providing high radiative losses without affecting the pedestal profiles and displacing carbon as dominant radiator. Neon, instead, radiates more upstream than N thus reducing the power flux through the separatrix leading to a reduced ELM frequency and compression in the divertor. A significant amount of neon is measured in the plasma core leading to a steeper density gradient. The different behaviour between the two impurities is confirmed by SOLPS-ITER modelling which for the first time at DIII-D includes multiple impurity species and a treatment of full drifts, currents and neutral-neutral collisions. The impurity transport in the SOL is studied in terms of the parallel momentum balance showing that N is mostly retained in the divertor whereas Ne leaks out consistent with its higher ionization potential and longer mean free path. This is also in agreement with the enrichment factor calculations which indicate lower divertor enrichment for neon. The strong ionization source characterizing the SAS divertor causes a reversal of the main ions and impurity flows. The flow reversal together with plasma drifts and the effect of the thermal force contribute significantly in the shift of the impurity stagnation point affecting impurity leakage. This work provides a demonstration of the impurity leakage mechanism in a closed divertor structure and the consequent impact on pedestal. Since carbon is an intrinsic radiator at DIII-D, in this paper we have also demonstrated the different role of carbon in the N vs Ne seeded cases both in the experiments and in the numerical modeling. Carbon contributes more when neon seeding is injected compared to when nitrogen is used. Finally, the results highlight the importance of accompanying experimental studies with numerical modelling of plasma flows, drifts and ionization profile to determine the details of the SOL impurity transport as the latter may vary with changes in divertor regime and geometry. In the cases presented here, plasma drifts and flow reversal caused by high level of closure in the slot upper divertor at DIII-D play an important role in the underlined mechanism.

Contribution of Vascular Cell Adhesion Molecule to Hemodynamics in Sickle Cell Disease

Vaso-occlusive events (VOEs) and pain crises are common clinical features of sickle cell disease (SCD) that result from sickle-shaped erythrocytes and leukocytes blocking blood flow, particularly in small vessels (Kato 2018). Activated endothelium also plays a role in the pathogenesis of VOEs in SCD. For example, VCAM-1 is expressed on blood vessels after activation by chemical and/or mechanical stimulation, which results in cytokine release. Studies have shown that patients with SCD have higher steady-state serum levels of soluble VCAM-1 compared to controls and that these levels are elevated during VOEs (White 2020). Furthermore, overexpression of these adhesion molecules on the endothelium results in prolonged adherence of white blood cells (WBCs), which has been shown to contribute to the development of VOEs and possibly cerebral vasculopathy. These findings raise the need to explore further the role of aberrant WBC- and/or RBC-endothelial interaction, mediated via VCAM-1, in the pathophysiology of cerebral microvascular hemodynamics and vasculopathy leading to cerebral microinfarcts in SCD. Therefore, we hypothesized that sickle cell mice will show greater cerebral cortical expression of VCAM-1 compared with age-matched controls and that this deposition will be associated with significant evidence of abnormal cerebral microvascular hemodynamic abnormalities. To examine the relationship between abnormalities in cerebral microvascular hemodynamics and VCAM-1 deposition in the cerebral microvasculature, we utilized a humanized sickle cell (with HbSS) and corresponding control (with HbAA). After cranial-window procedures, cortical capillaries, precapillary arterioles, and post-capillary venules were imaged using two-photon microscopy at two time points. In addition, this experiment included pre-and post-transfusion groups as we intend to study the impact of blood transfusion on hemodynamics. Using custom-written but well-validated MATLAB scripts, we analyzed line scans to identify the number and duration of rolling or adherent WBCs and RBCs, the RBC velocity in cerebral microvasculature, and the frequency and magnitude (mL/sec) of cerebral microvascular blood flow reversals. Rolling WBCs were defined as lasting two seconds or more, and adherent RBCs were defined as lasting 0.5 seconds or more. To quantify the expression of VCAM-1, we used immunohistochemistry to stain 50-micron sections of brain tissue for VCAM-1, Lectin to localize the vasculature, and Neun to localize neuronal nuclei. Images were analyzed using Phenochart and ImageJ software to examine the deposition of VCAM-1 throughout the brain tissue. As shown in Figure 1, at the first time point (baseline), we observed a significantly higher maximum RBC velocity (p<0.001) in the sickle cell mice compared to controls (figure 1a). We also found that there was significantly higher expression of VCAM-1 (p<0.001) (figure 1b) as well as significantly more leukocyte rolling (p<0.001) (figure 1c) in the sickle cell mice compared to controls. Additionally, we noted that the sickle cell mice have a significantly higher frequency of blood flow reversals (p<0.01) (figure 1d) as well as higher magnitude of microvascular blood flow reversals (p<0.001) (figure 1e) compared to controls. Interestingly, the sickle cell mice have a slightly lower average or mean capillary blood flow velocity compared to control (figure 1f), but this was not statistically significant (p=0.079). Since the mean capillary velocity is obtained as a smoothened difference between the forward flow and reversals, this decrease was surprising given the significant differences in frequency and magnitude of microvascular blood flow reversal in the sickle cell mice compared to controls (figs 1d and 1e). In conclusion, we see that the high velocity of blood flow might be a mechanical force, among other factors contributing to cerebral microvascular VCAM-1 expression in sickle cell mice. This might be responsible for the increased leukocyte-endothelial interactions and adhesion, ultimately leading to higher frequency and magnitude of cerebral microvascular blood flow reversal. Taken together, this may contribute to the observed slightly lower mean or effective microvascular forward blood flow. These pathophysiological changes might contribute to the reported higher rate of cerebral microinfarct and silent infarct in sickle cell disease. Figure 1 Figure 1. Disclosures Archer: Global Blood Therapeutics: Consultancy, Research Funding; Forma Therapeutics: Research Funding. Hyacinth: Novartis: Consultancy; Acuta Capital: Consultancy.

Abstract 1122‐000192: Transient Blood Flow Reversal in The Vertebral Artery As an Embolic Protection Method During Angioplasty/Stenting

Introduction : Approximately 20% of all acute ischemic strokes occur in the vertebrobasilar (VB) circulation. Similar to carotid stenosis, symptomatic vertebral artery (VA) stenosis is associated with a high risk of stroke recurrence. The use of embolic protection devices for recanalization in the setting of carotid stenosis in order to improve clinical outcomes is well established. Recent randomised trials have failed to demonstrate improvement of clinical outcomes in VB stroke patients treated with stenting. To our knowledge, these studies did not require the use of embolic protection devices or techniques. This may be due to several factors. Firstly, since the caliber of the stenotic segment of VA is not large enough to safely allow the protection device delivery system to pass through, initial angioplasty without protection is needed. Secondly, the most common segment of VA to become stenotic is its origin, and usually after stenting of this segment, the edge of the stent is protruding into the SCA. When the angle of the VA relative to the SCA is acute, passing the filter capture catheter through this protruded stent is very difficult and dangerous. Methods : We are introducing a VA reversal blood flow technique for prevention of emboli through the VB system in the setting of symptomatic extracranial VA stenosis. In this technique, we used a balloon tip guide catheter in order to transiently occlude the proximal segment of the SCA, causing flow arrest. We then evaluated the presence of blood flow reversal in the VA. Theoretically, this induction of blood flow reversal in the VA can be considered protective because it washes the embolic particles into the distal SCA. Results : Of the 11 cases of VA origin symptomatic stenosis, 4 had desirable VA blood flow reversal after balloon occlusion trial. These patients had successful angioplasty‐stenting of the VA origin using balloon mounted stent without major complications such as ischemic stroke in the posterior circulation territory. Conclusions : This study demonstrates the feasibility of proximal SCA balloon occlusion to cause transient flow reversal in the VA during angioplasty +/‐ stenting of the proximal VA. Future studies are required to determine the effectiveness of this approach in the setting of extracranial VA stenosis due to atherosclerosis, especially at its proximal segment.

Abstract 1122‐000218: Flow Reversal After Stent Diversion Causes In‐Stent Thrombosis and Anemia‐Driven Ischemia

Introduction : Large symptomatic ICA aneurysms are rare, but present a life threatening risk of rupture that increases with size, female sex, and age >50 at the time of diagnosis, among other risk factors. Historically, large carotid aneurysms have been treated with intentional carotid sacrifice, requiring recruitment of contralateral, posterior, and ECA‐supplied collaterals to provide flow to the anterior circulation previously supplied by the sacrificed ICA, lest the patient experience an iatrogenic stroke. While still a viable option in some cases, flow diverting stents provide an attractive alternative to vessel sacrifice. By providing a channel for blood to bypass the aneurysm, the stent can effectively exclude the aneurism from active circulation while preserving a path for blood to travel to the anterior cerebral circulation it currently provides. Methods : Here, we present a case of a 1.3 cm symptomatic left cavernous ICA aneurysm treated with such a flow diverting stent. Results : The patient presented to the emergency department with left sided ptosis. CTA head and neck revealed the 1.3 cm left sided cavernous ICA aneurysm. She was treated endovascularly under general anesthesia with continuous intra‐operative monitoring. The procedure was complicated by iatrogenic flow reversal through the Circle of Willis at the time of stent deployment and resultant in situ thrombosis of the stent without alteration in electrical signals recorded at the scalp – thus creating a de facto carotid sacrifice without intra‐operative complication. Follow up doppler study revealed a loss of flow through the left ICA and reversal of flow through the ophthalmic artery on the left side, thus confirming ECA collateral supply to the area. Post‐op course was complicated by extensive bleeding from the scalp electrode sites used for intraoperative monitoring due to hyper‐response to aspirin‐ticagrelor dual‐antiplatelet therapy. This gave rise to a symptomatic anemia that manifested as pressure‐dependent left‐sided circulatory failure on exam – specifically hemiparesis and aphasia. The symptoms ultimately resolved with pressure augmentation, blood transfusion, and supportive care in the Neuro ICU. The patient was successfully transitioned to a general neurology floor with subsequent resolution of the anemia and, correspondingly, the symptoms. Conclusions : The patient was discharged to rehab and at 4‐month follow‐up is again living independently with no residual deficits. This case has significance for pre‐operative anti‐platelet optimization for flow diverting stents, management of post‐operative complications of flow‐diverting stent placement including thrombosis and bleeding, and optimal critical care support for patients with pressure‐dependent ischemia. Specifically, the course of the patient’s symptoms and anemia raise the question of optimal hemoglobin targets in the subset of patients with pressure‐dependent ischemia, and how to best reach those targets.