The voluntary carbon market within the United States has expanded rapidly in recent years and enabled private companies and other organizations to provide revenue streams to carbon dioxide removal (CDR) technologies. For a CDR technology to participate in the voluntary carbon market (VCM), the emissions associated with constructing and operating the technology must be less than the CO2 captured from the atmosphere. Assessing the extent to which this is true for direct air capture with storage (DACS), a relatively energy-intensive CDR technology, strongly depends on the accounting method used to assess the emissions intensity of purchased energy. We simulate the hourly weather-dependent operation of sorbent- and solvent-based DACS in California, Louisiana, Texas, and Wyoming, representing a wide range of local weather and electric and natural gas grid compositions. In all cases, the single most important emissions accounting decision is the method used to estimate the emissions intensity of purchased grid electricity, which varies the calculated net removal by -1049% to +108%. All other factors influencing net removal introduce a variation of at most ±14%. No electricity emissions accounting method is universally conservative across all scenarios, and none is objectively more accurate. High-spatiotemporal-resolution, high-quality, publicly available data sets and models for electricity emissions accounting do not currently exist and are urgently needed to enable standardization of emissions accounting methods to more accurately determine the true emissions impacts of DACS and other energy-intensive facilities.

ABSTRACT Copper catalyst gas diffusion electrodes (GDEs) have demonstrated unique electrochemical selectivity converting CO 2 to C 2 ‐hydrocarbons such as ethylene and ethanol but have been challenged by their hydrophobic chemical stability and internal electrical resistance leading to low energy efficiency. Carbon‐supported GDEs have low electrical resistance but lack sufficient stability at industrially relevant current densities. While polymer‐supported GDEs have improved hydrophobicity, they also display high in‐plane electrical resistance, particularly at industrial scales. In this work, we demonstrate a composite gas diffusion layer that combines hydrophobic porous polymers with an electrically conductive backbone addressing these core gas diffusion electrode (GDE) scaling challenges. We investigate the material properties of standalone porous perfluoropolyether (PFPE) polymers, including porosity and surface morphology, under varying processing conditions and then incorporate these polymers into a porous copper foam. This composite enhances the mechanical rigidity necessary for cell assembly and provides a through‐plane electrical conduction path to reduce electrical resistive losses. This enhanced PFPE composite GDE displays efficient CO 2 reduction, achieving 15% ethylene energy efficiency at 100 cm 2 . These findings contribute to the development of advanced catalyst materials and electrode architectures and promote scalable strategies for electrochemical conversion of CO 2 into high‐value carbon products.

INTRODUCTION:Acute hypoxia can impair cognitive performance, yet the underlying systemic and cerebral physiological mechanisms remain unclear. The objective of this study was to elucidate the systemic and cerebral physiological responses associated with changes in cognitive performance during acute hypoxia. METHODS:There were 11 healthy subjects (5 females) who completed a cognitive test during baseline normoxia (21% fraction of inspired oxygen, FIO2) followed by 2 randomized hypoxia trials: 11.8% FIO2 (moderate hypoxia) and 7.7% FIO2 (severe hypoxia). Subjects were instrumented with an arterial catheter, transcranial doppler ultrasound, and near-infrared spectroscopy to measure systemic (arterial O2 saturation) and cerebral oxygenation (cerebrovascular conductance and cerebral tissue saturation). RESULTS:Moderate hypoxia reduced arterial O2 saturation and cerebral tissue saturation, with no change in cerebrovascular conductance. Severe hypoxia decreased arterial O2 saturation, cerebrovascular conductance, and cerebral tissue saturation. Cognitive performance did not differ from baseline during either hypoxia condition (omission rate, errors/min: baseline 0 ± 1 vs. moderate hypoxia 1 ± 1; baseline 1 ± 1 vs. severe hypoxia 1 ± 1). No associations were observed between physiological changes and cognitive performance during moderate hypoxia. During severe hypoxia, smaller declines in arterial O2 saturation (r = 0.643) and greater declines in cerebrovascular conductance (r = -0.651) were associated with increased omission rates. DISCUSSION:Cognitive performance during acute severe hypoxia correlated with cerebral oxygenation and blood flow. Associations differed between moderate and severe hypoxia, suggesting that both duration and severity of hypoxia influence the relationship between physiological responses and cognitive performance.

Copper catalyst gas diffusion electrodes (GDEs) have demonstrated unique electrochemical selectivity converting CO2 to C2-hydrocarbons such as ethylene and ethanol but have been challenged by their hydrophobic chemical stability and internal electrical resistance leading to low energy efficiency. Carbon-supported GDEs have low electrical resistance but lack sufficient stability at industrially relevant current densities. While polymer-supported GDEs have improved hydrophobicity, they also display high in-plane electrical resistance, particularly at industrial scales. In this work, we demonstrate a composite gas diffusion layer that combines hydrophobic porous polymers with an electrically conductive backbone addressing these core gas diffusion electrode (GDE) scaling challenges. We investigate the material properties of standalone porous perfluoropolyether (PFPE) polymers, including porosity and surface morphology, under varying processing conditions and then incorporate these polymers into a porous copper foam. This composite enhances the mechanical rigidity necessary for cell assembly and provides a through-plane electrical conduction path to reduce electrical resistive losses. This enhanced PFPE composite GDE displays efficient CO2 reduction, achieving 15% ethylene energy efficiency at 100 cm2. These findings contribute to the development of advanced catalyst materials and electrode architectures and promote scalable strategies for electrochemical conversion of CO2 into high-value carbon products.

Energy recovery from gas-phase waste streams is essential for reducing environmental impact, promoting sustainable industrial practices, and increasing profit margins. Compared to thermochemical pathways, biocatalytic conversions offer a compelling alternative due to their mild operating conditions and high specificity. However, conventional systems are hindered by slow gas-to-liquid mass transfer, resulting in high energy consumption and low productivity. Here, we demonstrate a new solid-state bioreactor (SSB) technology through a case study of methane-to-succinate conversion using methanotrophs. SSBs immobilize high densities of methanotrophs within gas-permeable, 3D-printed geometries that operate under gas-phase and static conditions. These reactors exhibit a 1–2 order of magnitude increase in biocatalytic performance compared to traditional liquid-phase reactors. Computational models of the SSB are developed and benchmarked against conventional stirred-tank reactor models to highlight design advantages.

Electrochemical CO2 reduction (eCO2R) is an attractive route for mitigating global CO2 emissions while producing value-added chemicals. Ethylene is one product of eCO2R and is an essential industrial precursor with a global market of $230 billion. The large-scale implementation of C2H4-selective CO2 electrolyzers remains challenging because of low energy efficiencies. In this work, we develop the design principles necessary for incorporating an expanded polytetrafluoroethylene (ePTFE) electrode into a zero-gap electrolyzer while simultaneously developing an integrated electrical front contact that reduces the ohmic resistances inherent to electrically insulating gas diffusion layers. By co-designing the catalyst layer, gas diffusion medium, and operating conditions for a zero-gap ePTFE gas diffusion electrode (GDE), we achieved a full-cell voltage of 2.5 V at 200 mA cm-2 at 25 cm2 geometric area cell with Faradaic efficiencies of 48% for ethylene and 40% for ethanol. This work highlights strategies for developing a scalable, stable, and highly energy-efficient eCO2R for C2 products.

This study tested the hypothesis that neural and vascular α2-adrenergic mechanisms contribute to sympathetic baroreflex regulation of human blood pressure. Muscle sympathetic nerve activity (MSNA; peroneal microneurography) was measured, and sympathetic action potentials (APs) were extracted from the filtered MSNA neurogram (continuous wavelet transform) in eight participants (5 females; 28 ± 7 yr) during a baseline (BSL) condition and a dexmedetomidine infusion (DEX; α2-adrenergic receptor agonist; 10-min loading dose at 0.225 µg/kg; maintenance dose: 0.1-0.5 µg/kg/h). Sympathetic AP baroreflex threshold and sensitivity gains were measured (spontaneous method). We quantified the transduction of integrated MSNA to diastolic blood pressure (DBP; signal averaging) and calculated an index of transduction gain as the slope of the relationship between maximum DBP and the number of cardiac cycles to maximum DBP. DEX reset the baroreflex operating point for medium APs to lower firing probabilities (AP cluster 4; BSL: 20 ± 6 to DEX: 6 ± 5%, P < 0.0004), lower DBP (72 ± 9 to 65 ± 10 mmHg, P < 0.0001), and reduced gain (AP cluster 4: -6.5 ± 2.0 to -2.0 ± 0.7%/mmHg, P < 0.0001). DEX reset the AP baroreflex sensitivity operating point to fewer AP clusters/burst (3.4 ± 0.7 to 2.9 ± 0.8 clusters/burst, P = 0.0156) but did not change gain. DEX reduced DBP transduction (cardiac cycle 6: 4.3 ± 3.2 to 3.3 ± 2.0 mmHg, P = 0.0032), increased the time to peak DBP (6 ± 1 to 11 ± 3 cardiac cycles, P = 0.0054), and reduced the DBP transduction gain (0.81 ± 0.72 to 0.36 ± 0.37 mmHg/cardiac cycle, P = 0.0012). These data suggest that neural and vascular α2-adrenergic mechanisms contribute to integrative sympathetic baroreflex regulation of blood pressure in humans.NEW & NOTEWORTHY Intravenous dexmedetomidine infusion (selective α2-adrenergic receptor agonist) 1) reduced the firing probability and strength of baroreflex control over medium-sized sympathetic action potentials in muscle sympathetic nerve activity (MSNA) and 2) attenuated the transduction of MSNA bursts to changes in blood pressure (BP) by reducing the magnitude of BP responses and increasing the time to peak BP. These data suggest that neural and vascular α2-adrenergic mechanisms contribute to sympathetic baroreflex regulation of human BP.

Electrochemical CO2 reduction (eCO2R) holds promise for decarbonizing industrial sectors by producing valuable commodities, such as ethylene. Incorporating polymer electrolyte ionomers onto Cu-based eCO2R cathodes is crucial for enhancing eCO2R efficiency. These ionomers control mass transport, surface chemistry, and water uptake at the cathode, enabling selectivity tuning toward desired C2 products. Complexities and interdependence of interfacial properties have led to challenges within the field to define design properties of catalyst layer ionomers that can enhance the performance of Cu-based catalysts. Herein, we present a systematic investigation into ionomer properties and their relationship to electrochemical performance and demonstrate a 14.3% energy efficiency for ethylene selectivity at 200 mA cm-2. Through multi-physics modeling, we elucidated that the role of the water content of the ionomer is to mitigate flooding and control the local water concentration at the catalyst surface. Translating knowledge from this study will stimulate the synthesis of ionomers tailored for eCO2R.

Fatiguing inspiratory work has been shown to evoke a sympathetically mediated reflex that has systemic cardiovascular consequences, including increases in heart rate and blood pressure and a decrease in resting limb vascular conductance. Moreover, the response to this reflex appears to be attenuated in females compared with males. It remains to be seen whether this respiratory muscle metaboreflex also exerts an effect on cerebral blood flow. Cerebral blood flow is tightly regulated to maintain homeostasis and critical function. Therefore, it stands to reason that cerebrovascular haemodynamics would not be compromised through this respiratory muscle metaboreflex. We hypothesized that fatiguing inspiratory work would reduce resting limb conductance, but cerebral blood flow would be minimally impaired. Females (34 ± 10 years old, n = 12) and males (31 ± 8 years old, n = 12) performed a 5 min, high-intensity bout of inspiratory pressure threshold loading (IPTL) designed to evoke the respiratory muscle metaboreflex. In response to IPTL, mean arterial pressure increased in both males and females (p < 0.001), and limb vascular conductance decreased to a greater degree in males than in females (p = 0.005). The cerebrovascular conductance index was higher in females (p = 0.007) but not affected by IPTL (p = 0.417). Our findings suggest that cerebral blood flow is spared from the redistribution of blood flow in response to fatiguing inspiratory work and that this protection is true in both males and females.

Introduction: Spontaneous coronary artery dissection (SCAD) is one of the most common causes of myocardial infarction in females under the age of 50 and peripartum females. Furthermore, approximately 10% of patients with a history of SCAD have recurrent SCAD within 5 years. In a subset of patients, SCAD events are preceded by sympathoexcitatory stimuli, such as emotional or physical stress. This implicates the sympathetic nervous system in the pathophysiology of SCAD. Thus, we aimed to investigate this relationship through measuring muscle sympathetic nerve activity (MSNA) and quantifying MSNA transduction into diastolic blood pressure (BP) in females with a history of SCAD compared to healthy female controls. We hypothesized that females with a history of SCAD would have both augmented MSNA and MSNA transduction at rest compared to their healthy counterparts. Methods: Females with a history of SCAD and healthy controls (HC) were recruited for the study. MSNA was continuously recorded using microneurography at the peroneal nerve during 10-minute supine rest. Heart rate (HR, 3-lead electrocardiography) and BP (finger photoplethysmography) were continuously recorded during this period. We plotted binned MSNA burst areas against diastolic BP, using linear regression analysis in MATLAB R2023a to quantify the transduction slope. We compared peak bins of transduction slopes between the two groups. Data are presented as mean±SD. Independent samples t-tests were performed for statistical analyses. Results: Seven females with a history of SCAD (49±11 years; BMI: 28.5±7 kg/m 2 ) and six controls (51±8 years; BMI: 26.2±6.3 kg/m 2 ) participated in the study (both p>0.05). Resting systolic BP (SCAD: 121±8 vs. HC: 122±15 mmHg), diastolic BP (SCAD: 78±9 vs. HC: 75±7 mmHg) and HR (SCAD: 59±13 vs. HC: 67±18 bpm) were not different between groups (all p >0.05). MSNA burst frequency (SCAD: 25±12 vs. HC: 27±7 bursts/minute), burst incidence (SCAD: 42±18 vs. HC: 46±15 bursts/100 heartbeats), and total MSNA (SCAD: 820±286 vs. HC: 1050±119 au/minute) did not differ between groups (all p >0.05). MSNA transduction at rest was not different between females with a history of SCAD and healthy controls (0.02±0.03 vs. 0.05±0.05 mmHg(%·s) -1 , p>0.05). Conclusions: These preliminary data suggest that resting MSNA and transduction do not differ between females with a history of SCAD and healthy controls, contrary to our hypothesis. Further investigation is needed to determine if this observation is preserved with exposure to sympathoexcitatory stimuli. Funding: NIH K23 HL155506, T32 DK07352, K01 HL148144, UL1 TR0022377, and AHA 898649 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

Gigatonne-scale atmospheric carbon dioxide removal (CDR), alongside deep emission cuts, is critical to stabilizing the climate. However, some of the most scalable CDR technologies are also the most land intensive. Here, we examine whether adequate land resources exist in the contiguous United States to meet CDR targets when prioritizing grid emissions reduction, food production, and the protection of sensitive ecosystems. We focus on biomass carbon removal and storage (BiCRS) and direct air capture and storage (DACS) and show that suitable lands exceed the expected needs: 37.6 million hectares of land are available for BiCRS, resulting in 0.26 GtCO2 of CDR/year, and 34 million hectares are suitable for wind-and solar-powered DACS, resulting in 4.8 GtCO2 of CDR/year if facilities are co-located with geologic CO2 storage. We identify biomass and energy supply hotspots to meet CDR targets while ensuring land protection and minimizing land competition.

Menopause is associated with vascular dysfunction. During the menopausal transition, endogenous oestradiol concentrations diminish. Oestradiol is vasoprotective because it has direct and indirect effects on the vasculature. The present study aimed to determine the effect of acute exogenous oestradiol on endothelium-dependent, endothelium independent and β2-adrenergic receptor-induced vasodilatation in females. Forearm blood flow (venous occlusion plethysmography) was measured during brachial intraarterial infusions of ACh (endothelium-dependent agonist), sodium nitroprusside (endothelium independent agonist) and terbutaline (β2-adrenergic receptor agonist) with and without concurrent infusion of 17β-oestradiol. Nine young premenopausal (age: 26 ± 4 years) and nine postmenopausal (PM, age: 58 ± 4 years, 8 ± 1 years post-menopause) females completed the study. Concurrent oestradiol infusion augmented the vasodilatory response to ACh, sodium nitroprusside and terbutaline in young premenopausal (all P < 0.05) but not older postmenopausal (all P > 0.05), females. Local infusion of exogenous 17β-oestradiol augmented endothelial and smooth muscle microvascular vasodilatation in premenopausal but not postmenopausal, females. KEY POINTS: Menopause is associated with vascular dysfunction. Because oestradiol has vasoprotective effects, the menopause-associated drop in oestradiol concentrations is hypothesized to contribute to vascular dysfunction during the menopause transition. The present study shows that local infusion of exogenous oestradiol augmented microvascular vasodilatation in premenopausal but not postmenopausal females.

Background: Spontaneous coronary artery dissection (SCAD) is an acute separation of coronary artery wall layers that blocks blood flow to the heart and leads to acute coronary syndrome. Patients with SCAD are relatively young females (~40-50 years) who have few cardiovascular risk factors. Sympathoexcitatory stress often precedes SCAD events (i.e. intense physical and/or emotional stress), suggesting that patients with SCAD may have augmented hemodynamic responses to sympathoexcitatory stressors. As such, we aimed to evaluate hemodynamic responses to cold stress in females with a history of SCAD and females without a history of SCAD. We hypothesized that females with a history of SCAD would have augmented hemodynamic responses to cold stress relative to females without a history of SCAD. Methods: Females with a history of SCAD were matched to females without a history of SCAD for age and body mass index. Heart rate (electrocardiogram) and beat-to-beat blood pressure (finger photoplethysmography) were recorded and averaged during two minutes of resting baseline and the minute during the cold pressor test that produced the peak hemodynamic response. Delta (Δ) values of the hemodynamic parameters were calculated. Data are reported as mean ± SD. Unpaired t-tests were used to analyze demographics, anthropometrics, resting hemodynamics, and hemodynamic responses between females with a history of SCAD and females without a history of SCAD. Results: Age (50±9 vs 56±8 years) and body mass index (27±6 vs 24±3 kg/m 2 ) did not differ between females with a history of SCAD (n=20) and females without a history of SCAD (n=12, both p>0.05), respectively. Resting heart rate ([HR], 57±10 vs 59±11 bpm), systolic blood pressure ([SBP], 112±14 vs 110±13 mmHg), diastolic blood pressure ([DBP], 72±10 vs 72±9 mmHg), and mean arterial pressure ([MAP], 86±11 vs 85±9 mmHg) were not different between females with a history of SCAD and females without a history of SCAD, respectively (all p>0.05). Hemodynamic responses to cold stress (ΔHR, 6±5 vs 7±5 bpm; ΔSBP, 20±16 vs 18±7 mmHg; ΔDBP, 7±11 vs 11±6 mmHg; ΔMAP, 10±14 vs 13±5 mmHg; all p>0.05) were not different between females with a history of SCAD and females without a history of SCAD, respectively. Conclusion: Hemodynamic responses to cold stress were not different between females with a history of SCAD and females without a history of SCAD, indicating that an augmented pressor response to this stress is likely not a primary predisposing factor to a SCAD. However, it remains important to assess other forms of stress to inform future care and counseling of patients with history of SCAD. Funding: K23HL155506 This abstract was presented at the American Physiology Summit 2025 and is only available in HTML format. There is no downloadable file or PDF version. The Physiology editorial board was not involved in the peer review process.

The present study investigated the impact of central α2-adrenergic mechanisms on sympathetic action potential (AP) discharge, recruitment and latency strategies. We used the microneurographic technique to record muscle sympathetic nerve activity and a continuous wavelet transform to investigate postganglionic sympathetic AP firing during a baseline condition and an infusion of a α2-adrenergic receptor agonist, dexmedetomidine (10 min loading infusion of 0.225 µg kg-1; maintenance infusion of 0.1-0.5 µg kg h-1) in eight healthy individuals (28 ± 7 years, five females). Dexmedetomidine reduced mean pressure (92 ± 7 to 80 ± 8 mmHg, P < 0.001) but did not alter heart rate (61 ± 13 to 60 ± 14 bpm; P = 0.748). Dexmedetomidine reduced sympathetic AP discharge (126 ± 73 to 27 ± 24 AP 100 beats-1, P = 0.003) most strongly for medium-sized APs (normalized cluster 2: 21 ± 10 to 5 ± 5 AP 100 beats-1; P < 0.001). Dexmedetomidine progressively de-recruited sympathetic APs beginning with the largest AP clusters (12 ± 3 to 7 ± 2 clusters, P = 0.002). Despite de-recruiting large AP clusters with shorter latencies, dexmedetomidine reduced AP latency across remaining clusters (1.18 ± 0.12 to 1.13 ± 0.13 s, P = 0.002). A subset of six participants performed a Valsalva manoeuvre (20 s, 40 mmHg) during baseline and the dexmedetomidine infusion. Compared to baseline, AP discharge (Δ 361 ± 292 to Δ 113 ± 155 AP 100 beats-1, P = 0.011) and AP cluster recruitment elicited by the Valsalva manoeuvre were lower during dexmedetomidine (Δ 2 ± 1 to Δ 0 ± 2 AP clusters, P = 0.041). The reduction in sympathetic AP latency elicited by the Valsalva manoeuvre was not affected by dexmedetomidine (Δ -0.09 ± 0.07 to Δ -0.07 ± 0.14 s, P = 0.606). Dexmedetomidine reduced baroreflex gain, most strongly for medium-sized APs (normalized cluster 2: -6.0 ± 5 to -1.6 ± 2 % mmHg-1; P = 0.008). These data suggest that α2-adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans. KEY POINTS: Sympathetic postganglionic neuronal subpopulations innervating the human circulation exhibit complex patterns of discharge, recruitment and latency. However, the central neural mechanisms governing sympathetic postganglionic discharge remain unclear. This microneurographic study investigated the impact of a dexmedetomidine infusion (α2-adrenergic receptor agonist) on muscle sympathetic postganglionic action potential (AP) discharge, recruitment and latency patterns. Dexmedetomidine infusion inhibited the recruitment of large and fast conducting sympathetic APs and attenuated the discharge of medium sized sympathetic APs that fired during resting conditions and the Valsalva manoeuvre. Dexmedetomidine infusion elicited shorter sympathetic AP latencies during resting conditions but did not affect the reductions in latency that occurred during the Valsalva manoeuvre. These data suggest that α2-adrenergic mechanisms within the central nervous system modulate sympathetic postganglionic neuronal discharge, recruitment and latency strategies in humans.

Numerous cutting-edge scientific technologies originate at the laboratory scale, but transitioning them to practical industry applications is a formidable challenge. Traditional pilot projects at intermediate scales are costly and time-consuming. An alternative, the E-pilot, relies on high-fidelity numerical simulations, but even these simulations can be computationally prohibitive at larger scales. To overcome these limitations, we propose a scalable, physics-constrained reduced order model (ROM) method. ROM identifies critical physics modes from small-scale unit components, projecting governing equations onto these modes to create a reduced model that retains essential physics details. We also employ Discontinuous Galerkin Domain Decomposition (DG-DD) to apply ROM to unit components and interfaces, enabling the construction of large-scale global systems without data at such large scales. This method is demonstrated on the Poisson and Stokes flow equations, showing that it can solve equations about $15 - 40$ times faster with only $\sim$ $1\%$ relative error. Furthermore, ROM takes one order of magnitude less memory than the full order model, enabling larger scale predictions at a given memory limitation.

Carbon dioxide removal (CDR) technologies are essential to address climate change and serve to compensate for legacy and hard-to-abate greenhouse gas emissions. Although near-term emissions reductions should be the priority, development and deployment of CDR must proceed now to ensure that relevant technologies are ready at scale in the future. Despite a rapid growth in CDR purchases, no single standardized methodology for evaluating project-level net CO2 removal exists. Life cycle assessment (LCA) frequently produces net-negative emissions footprints, but only a small subset of those systems achieves a net flux of CO2 out of the atmosphere. In contrast to LCA, CDR accounting uses expansive system boundaries and excludes avoidance credits to distinguish between systems that achieve net removal from those that only contribute to emissions mitigation. This primer discusses a framework and set of metrics for CDR accounting.

Invited for this issue's Front Cover are researchers from the Carbon Initiative at Lawrence Livermore National Laboratory and the SUNCAT Center at Stanford University. The front cover shows a cross-section of the cathode of a membrane electrode assembly for CO2 electrolysis looking down the feed channel. CO2 molecules flow down the channel and diffuse up through the gas diffusion layer to the silver catalyst, where CO2 reacts to form CO, while also competing against hydrogen reduction from water. Some of the CO2 molecules react to form bicarbonate and carbonate ions, which can diffuse across the membrane, where they react at the anode to form CO2 again. The top of the image shows CO2 that has crossed over through the membrane into the anolyte. Cover design by Brendan Thompson. Read the full text of the Research Article at 10.1002/celc.202300566.