Maximizing the Mitigation Potential of Curtailed Wind: A Comparison Between Carbon Capture and Utilization, and Direct Air Capture Processes for the UK

Carbon capture and storage (CCS) with fossil fuel or biomass plants (BECCS) is considered a critical technology to meet mitigation targets set by the Paris Agreement1. However, several drawbacks including high upfront investment costs, significant energy penalty and long-term permanent storage challenges have limited the uptake of CCS on the required scale. Carbon capture and utilisation (CCU) provides an alternative route to recycle CO2 into chemical feedstock and/or synthetic transport fuels (e.g. methanol, DME) that can displace fossil-derived fuels. As the carbon is only transformed, CCU must be integrated with capture/storage to actually offset subsequent emissions from the vehicles consuming them. The mitigation of decentralised emissions poses significant challenges and necessitates the use of carbon dioxide removal technologies (CDR), one of which is direct capture of CO2 from the atmosphere (DAC). The last decade has seen increasing penetration of wind power in the UK electricity system to meet mitigation targets. Because of this, periods of surplus wind generation and low demand or limited/full storage capacity arise. Constraint payments then have to be made to wind farms to curtail generation. This work investigates two possible options to achieve mitigation with this curtailed electricity. In Process A, curtailed electricity is used to produce electrolytic hydrogen and operate methanol synthesis plants. It is then integrated with a direct air capture (DAC) plant to recapture and recycle emissions from the vehicles. Process B assumes curtailed electricity is used to run a DAC plant directly in order to capture decentralised carbon emissions and provide CO2 feedstock for CCU processes. The UK was used as a case study and the methanol synthesis process described by Rihko-Struckmann et al.2 was used as the reference. A range of energy requirements for DAC are cited in literature; the lower and upper bounds of 6.7 GJ/tCO2 and 12.6 GJ/tCO23, respectively, were used. This work has taken a base case curtailment level of 2.5% of the UK total electricity demand, which is equivalent to 390 GWh/y4. Both processes have been compared on the basis of mitigation potential, defined by the proportion of CO2 emissions from gasoline vehicles that are avoided, and mitigation costs per tonne of CO2 captured. Process A resulted in avoiding 0.12% of gasoline emissions (~0.05 MtCO2/y). Surplus energy (~64% of the curtailed electricity) was required to run the DAC plant and an associated air separation unit. The mitigation of potential of Process B was 0.10% or 0.18%, depending on energy requirement used. Therefore, the process that maximises mitigation potential depends on the DAC process considered; using the lower-bound energy requirement, surplus electricity for DAC only is preferable. Neither process is economically viable. CCU costs ($905/tCO2) were found to be double the DAC-only costs ($449/tCO2), mainly due to high H2 costs. It will remain financially-unattractive unless the methanol production becomes profitable. This is unlikely as it requires methanol price to almost double, a carbon price of $313/t to be in effect, or H2 price to reduce to a third of today’s price to$1800/t. References 1. IPCC. Climate Change 2014: Mitigation of Climate Change. Working Group III Contribution to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change (2014). doi:10.1017/CBO9781107415416 2. Rihko-Struckmann, L. K., Peschel, A., Hanke-Rauschenbach, R. & Sundmacher, K. Assessment of methanol synthesis utilizing exhaust CO2 for chemical storage of electrical energy. Ind. Eng. Chem. Res. 49, 11073–11078 (2010). 3. Socolow, R. et al. Direct Air Capture of CO 2 with Chemicals Panel on Public Affairs. Am. Phys. Soc. - Panel Public Aff. 100 (2011). 4. Messiou, A. Centre for Environmental Policy Investigating the role of power storage in accommodating the future wind. (2012)

Power-to-transport: Using curtailed wind to run CCU processes

The Paris Agreement signaled global commitment to limit average global temperature rise to 2˚C and to make efforts to achieve 1.5˚C increase (UNFCCC, 2015). The IPCC AR5 cites carbon capture and storage (CCS) as a necessary technology to achieve this (IPCC, 2014). However, several drawbacks including high upfront investment costs, significant energy penalty and long-term permanent storage challenges have limited the uptake of CCS on the required scale (Styring, et al., 2011). Carbon capture and utilisation (CCU) provides an alternative route to recycle CO2 into chemical feedstock and/or synthetic transport fuels (e.g. methanol, DME) that can displace fossil-derived fuels. As the carbon is only transformed, CCU must be integrated with capture/storage to actually offset subsequent emissions from the vehicles consuming them. The mitigation of decentralised emissions poses significant challenges and necessitates the use of carbon dioxide removal technologies (CDR), one of which is direct capture of CO2 from the atmosphere (DAC). This work investigates two possible options for CCU integrated with DAC: Option A is the storage of curtailed wind as methanol which can be used in road vehicles to displace gasoline emissions (power-to-transport), and Option B is the use curtailed wind directly to run a DAC plant in order to capture decentralised carbon emissions and provide CO2 feedstock for CCU processes. A high-level analysis has been carried out to determine the gasoline substitution and emissions offset potential of both options, the overall conversion efficiency of the power-to-transport process, and the economics of each option. The UK was used as a case study and the methanol synthesis process described by (Rihko-Struckmann, et al., 2010) was used as the reference. Work by (Messiou, 2012) investigated the curtailment levels for the UK electricity system with increased wind generation; the ‘medium integration’ scenario assumed the UK had 5 times the current wind generation capacity. A corresponding curtailment level of 2.5% (of total electricity dispatched) was determined, this has been used as the base case in our analysis. The gasoline substitution potential of methanol produced via option A was ~0.12% (equivalent to ~0.05 MtCO2/y) with the overall power-to-transport efficiency being ~11%. Surplus energy (~64% of the curtailed electricity) was required to run the DAC plant and an associated air separation unit. The methanol production plant was found to be economically infeasible unless current methanol price increased by a factor of 1.8 to $988/t, the cost of hydrogen fell by a factor of 2.3 to$1811/t or a carbon price of $313/t was in effect. For option B, the emissions offset potential of the DAC process was ~0.18% for the same curtailment, capturing ~0.07 MtCO2/y. Therefore, the utilisation of curtailed electricity for direct capture of CO2 from the atmosphere results in greater avoided emissions than if it was stored as methanol. References IPCC, 2014. Climate Change 2014: Mitigation of Climate Change. Working Group III Contribution to the Fifth Assessment Report of the Intergovernmental Panel on Climate Change, s.l.: Cambridge University Press. Messiou, A., 2012. Investigating the role of power storage in accommodating the future wind integration into UK’s power system. London: Imperial College London. Rihko-Struckmann, L. K., Peschel, A., Hanke-Rauschenbach, R. & Sundmacher, K., 2010. Assessment of Methanol Synthesis Utilizing Exhaust CO2 for Chemical Storage of Electrical Energy. Industrial and Engineering Chemistry Research, Issue 49, pp. 11073-11078. Styring, P., Jansen, D., de Coninck, H. & Reith, H., 2011. Carbon Capture and Utilisation in the green economy: Using CO2 to manufacture fuel, chemicals and materials, s.l.: The Centre for Low Carbon Futures

PLZF-expressing CD4 T cells show the characteristics of terminally differentiated effector memory CD4 T cells in humans

In humans, promyelocytic leukaemia zinc finger (PLZF)+CD161+CD4 T cells develop in the fetal thymus [1] but these cells were not detectable in thymi obtained from children (11 days to 5.5 years) (Fig. 1A). However, we found PLZF+CD4 T cells within CD45RA+RO+CD4 T cells from tonsils and spleens but rarely in blood (Fig. 1B, left panel and 1C; Supporting Information Fig. 1A and B). PLZF expression was also confirmed by mRNA analysis in these cells from tonsils (Fig. 1B, right panel). CD8 T cells had a very low frequency of CD45RA+RO+ cells compared to CD4 T cells and these cells did not express PLZF (Fig. 1B). We also validated that CD45RA+RO+CD4 T cells are not mucosalassociated invariant T cells [2] (data not shown). PLZF-expressing NKT cells were excluded from all our analyses by CD1d- Tetramer staining (Supporting Information Fig. 2

PLZFâ expressing CD4 TÂ cells show the characteristics of terminally differentiated effector memory CD4 TÂ cells in humans

Peer Reviewedhttps://deepblue.lib.umich.edu/bitstream/2027.42/144627/1/eji4225_am.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/144627/2/eji4225.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/144627/3/eji4225-sup-0001-PRC.pdfhttps://deepblue.lib.umich.edu/bitstream/2027.42/144627/4/eji4225-sup-0002-SuppMat.pd

Deficiency of UCHL1 results in insufficient decidualization accompanied by impaired dNK modulation and eventually miscarriage

Abstract Background Miscarriage is a frustrating complication of pregnancy that is common among women of reproductive age. Insufficient decidualization which not only impairs embryo implantation but disturbs fetomaternal immune-tolerance, has been widely regarded as a major cause of miscarriage; however, the underlying mechanisms resulting in decidual impairment are largely unknown. Methods With informed consent, decidual tissue from patients with spontaneous abortion or normal pregnant women was collected to detect the expression profile of UCHL1. Human endometrial stromal cells (HESCs) were used to explore the roles of UCHL1 in decidualization and dNK modulation, as well as the mechanisms involved. C57/BL6 female mice (7–10 weeks old) were used to construct pregnancy model or artificially induced decidualization model to evaluate the effect of UCHL1 on mice decidualization and pregnancy outcome. Results The Ubiquitin C-terminal hydrolase L1 (UCHL1), as a deubiquitinating enzyme, was significantly downregulated in decidua from patients with miscarriage, along with impaired decidualization and decreased dNKs. Blockage of UCHL1 led to insufficient decidualization and resultant decreased expression of cytokines CXCL12, IL-15, TGF-β which were critical for generation of decidual NK cells (dNKs), whereas UCHL1 overexpression enhanced decidualization accompanied by increase in dNKs. Mechanistically, the promotion of UCHL1 on decidualization was dependent on its deubiquitinating activity, and intervention of UCHL1 inhibited the activation of JAK2/STAT3 signaling pathway, resulting in aberrant decidualization and decreased production of cytokines associated with dNKs modulation. Furthermore, we found that inhibition of UCHL1 also disrupted the decidualization in mice and eventually caused adverse pregnancy outcome. Conclusions UCHL1 plays significant roles in decidualization and dNKs modulation during pregnancy in both humans and mice. Its deficiency indicates a poor pregnancy outcome due to defective decidualization, making UCHL1 a potential target for the diagnosis and treatment of miscarriage. Graphical Abstrac

Prostaglandin E2 induction during mouse adenovirus type 1 respiratory infection regulates inflammatory mediator generation but does not affect viral pathogenesis.

Respiratory viruses cause substantial disease and are a significant healthcare burden. Virus-induced inflammation can be detrimental to the host, causing symptoms during acute infection and leading to damage that contributes to long-term residual lung disease. Prostaglandin E2 (PGE2) is a lipid mediator that is increased in response to many viral infections, and inhibition of PGE2 production during respiratory viral infection often leads to a decreased inflammatory response. We tested the hypothesis that PGE2 promotes inflammatory responses to mouse adenovirus type 1 (MAV-1) respiratory infection. Acute MAV-1 infection increased COX-2 expression and PGE2 production in wild type mice. Deficiency of the E prostanoid 2 receptor had no apparent effect on MAV-1 pathogenesis. Virus-induced induction of PGE2, IFN-γ, CXCL1, and CCL5 was reduced in mice deficient in microsomal PGE synthase-1 (mPGES-1(-/-) mice). However, there were no differences between mPGES-1(+/+) and mPGES-1(-/-) mice in viral replication, recruitment of leukocytes to airways or lung inflammation. Infection of both mPGES‑1(+/+) and mPGES-1(-/-) mice led to protection against reinfection. Thus, while PGE2 promotes the expression of a variety of cytokines in response to acute MAV-1 infection, PGE2 synthesis does not appear to be essential for generating pulmonary immunity