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Surface modification of electrodes with glycans was investigated as a strategy for modulating the development of electrocatalytic biofilms for microbial fuel cell applications. Covalent attachment of phenyl-mannoside and phenyl-lactoside adlayers on graphite rod electrodes was achieved via electrochemically assisted grafting of aryldiazonium cations from solution. To test the effects of the specific bio-functionalities, modified and unmodified graphite rods were used as anodes in two-chamber microbial fuel cell devices. Devices were set up with wastewater as inoculum and acetate as nutrient and their performance, in terms of output potential (open circuit and 1 kΩ load) and peak power output, was monitored over two months. The presence of glycans was found to lead to significant differences in startup times and peak power outputs. Lactosides were found to inhibit the development of biofilms when compared to bare graphite. Mannosides were found, instead, to promote exoelectrogenic biofilm adhesion and anode colonization, a finding that is supported by quartz crystal microbalance experiments in inoculum media. These differences were observed despite both adlayers possessing thickness in the nm range and similar hydrophilic character. This suggests that specific glycan-mediated bioaffinity interactions can be leveraged to direct the development of biotic electrocatalysts in bioelectrochemical systems and microbial fuel cell devices.

As SARS-CoV-2 infections continue to cause hospital admissions around the world, there is a continued need to accurately assess those at highest risk of death to guide resource use and clinical management. The ISARIC 4C mortality score provides mortality risk prediction at admission to hospital based on demographic and physiological parameters. Here we evaluate dynamic use of the 4C score at different points following admission. Score components were extracted for 6,373 patients admitted to Barts Health NHS Trust hospitals between 1 st August 2020 and 19 th July 2021 and total score calculated every 48 hours for 28 days. Area under the receiver operating characteristic (AUC) statistics were used to evaluate discrimination of the score at admission and subsequent inpatient days. Patients who were still in hospital at day 6 were more likely to die if they had a higher score at day 6 than others also still in hospital who had the same score at admission. Discrimination of dynamic scoring in those still in hospital was superior with the area under the curve 0.71 (95% CI 0.69–0.74) at admission and 0.82 (0.80–0.85) by day 8. Clinically useful changes in the dynamic parts of the score are unlikely to be associated with subject-level measurements. Dynamic use of the ISARIC 4C score is likely to provide accurate and timely information on mortality risk during a patient’s hospital admission.

The [Burnley] winger, Ted McMinn, seemed to be highlighted for special treatment in the opening 10 minutes. He limped off with a calf injury in the second half after a series of over-zealous tackles. The home manager, Jimmy Mullen, was so irate at Keith Hill's body check on McMinn that he left his seat to remonstrate with Mr [Keith Cooper], after he brandished only a yellow card. Plymouth Argyle (4-4-2): [Alan Nicholls]; Patterson, Burrows, Comyn, Hill; Barlow, Castle, McCall, Dalton; Landon (Burnett, 59), [Dwight Marshall] (Nugent, 83). Substitute not used: Newland (gk).

It is well documented that firms respond to regulations in their home jurisdictions. We present hypotheses that firms also respond to regulations in jurisdictions where they do not operate. We examine renewable-power provision in the U.S. electric utility sector between 2001 and 2006, and find that firms adopt more renewable-power generation when their peers (i.e., firms in the same regulatory jurisdiction) face greater renewable-power standards in other jurisdictions. The underlying mechanism is that forward-looking firms assess when extrajurisdictional regulations foreshadow regulatory changes where they operate. Our analyses support this mechanism versus plausible alternatives. We demonstrate firms acting strategically to respond to extrajurisdictional regulations and show that the central conduit motivating this response is the extrajurisdictional footprint of firms operating in the same jurisdiction as a focal firm.

Estimates of the anthropogenic effective radiative forcing (ERF) trend have increased by 50% since 2000 (from +0.4 W m−2 decade−1 in 2000–09 to +0.6 W m−2 decade−1 in 2010–19), the majority of which is driven by changes in the aerosol ERF trend, as a result of aerosol emissions reductions. Here we study the extent to which observations of the climate system agree with these ERF assumptions. We use a large ERF ensemble from the IPCC’s Sixth Assessment Report (AR6) to attribute the anthropogenic contributions to global mean surface temperature (GMST), top-of-atmosphere radiative flux, and we use aerosol optical depth observations. The GMST trend has increased from +0.18°C decade−1 in 2000–09 to +0.35°C decade−1 in 2010–19, coinciding with the anthropogenic warming trend rising from +0.19°C decade−1 in 2000–09 to +0.24°C decade−1 in 2010–19. This, as well as observed trends in top-of-atmosphere radiative fluxes and aerosol optical depths, supports the claim of an aerosol-induced temporary acceleration in the rate of warming. However, all three observation datasets additionally suggest that smaller aerosol ERF trend changes are compatible with observations since 2000, since radiative flux and GMST trends are significantly influenced by internal variability over this period. A zero-trend-change aerosol ERF scenario results in a much smaller anthropogenic warming acceleration since 2000 but is poorly represented in AR6’s ERF ensemble. Short-term ERF trends are difficult to verify using observations, so caution is required in predictions or policy judgments that depend on them, such as estimates of current anthropogenic warming trend, and the time remaining to, or the outstanding carbon budget consistent with, 1.5°C warming. Further systematic research focused on quantifying trends and early identification of acceleration or deceleration is required.

The global quantum internet will require long-lived, telecommunications-band photon–matter interfaces manufactured at scale 1 . Preliminary quantum networks based on photon–matter interfaces that meet a subset of these demands are encouraging efforts to identify new high-performance alternatives 2 . Silicon is an ideal host for commercial-scale solid-state quantum technologies. It is already an advanced platform within the global integrated photonics and microelectronics industries, as well as host to record-setting long-lived spin qubits 3 . Despite the overwhelming potential of the silicon quantum platform, the optical detection of individually addressable photon–spin interfaces in silicon has remained elusive. In this work, we integrate individually addressable ‘T centre’ photon–spin qubits in silicon photonic structures and characterize their spin-dependent telecommunications-band optical transitions. These results unlock immediate opportunities to construct silicon-integrated, telecommunications-band quantum information networks. Individually addressable ‘T centre’ photon-spin qubits are integrated in silicon photonic structures and their spin-dependent telecommunications-band optical transitions characterized, creating opportunities to construct silicon-integrated, telecommunications-band quantum information networks.

Rheumatoid arthritis is a prototypical autoimmune disease that causes joint inflammation and destruction 1 . There is currently no cure for rheumatoid arthritis, and the effectiveness of treatments varies across patients, suggesting an undefined pathogenic diversity 1 , 2 . Here, to deconstruct the cell states and pathways that characterize this pathogenic heterogeneity, we profiled the full spectrum of cells in inflamed synovium from patients with rheumatoid arthritis. We used multi-modal single-cell RNA-sequencing and surface protein data coupled with histology of synovial tissue from 79 donors to build single-cell atlas of rheumatoid arthritis synovial tissue that includes more than 314,000 cells. We stratified tissues into six groups, referred to as cell-type abundance phenotypes (CTAPs), each characterized by selectively enriched cell states. These CTAPs demonstrate the diversity of synovial inflammation in rheumatoid arthritis, ranging from samples enriched for T and B cells to those largely lacking lymphocytes. Disease-relevant cell states, cytokines, risk genes, histology and serology metrics are associated with particular CTAPs. CTAPs are dynamic and can predict treatment response, highlighting the clinical utility of classifying rheumatoid arthritis synovial phenotypes. This comprehensive atlas and molecular, tissue-based stratification of rheumatoid arthritis synovial tissue reveal new insights into rheumatoid arthritis pathology and heterogeneity that could inform novel targeted treatments. Single-cell transcriptomic and proteomic data from synovial tissue from individuals with rheumatoid arthritis classify patients into groups based on abundance of cell states that can provide insights into pathology and predict individual treatment responses.

Improvements in pediatric cancer survival are attributed to cooperative clinical trials. Under-representation of specific demographic groups has been described in adult and pediatric cancer trials and poses a threat to the generalizability of results. An evaluation of data provided by the Children's Oncology Group (COG) of upfront trial enrollment for US patients 0 to 29 years old between 2004 and 2015 was performed. US cancer cases were estimated using incidence data and US population estimates from the Surveillance, Epidemiology, and End Results Program and compared to observed COG cases. Percent enrollment and standardized ratios of enrollment were calculated across demographic, disease, and socioeconomic groups. The COG website was utilized to quantify available trials and assess age eligibility. 19.9% of estimated US cancer patients age 0 to 19 years enrolled on COG trials. Younger patients were more represented across diseases and races/ethnicities. Patients with hematologic malignancies were more represented compared to solid and central nervous system (CNS) tumors. COG trial enrollment rates are declining when compared to previously published data, potentially from challenges in pediatric drug development, difficulty designing feasible trials for highly curable diagnoses, and issues ensuring trial availability for the heterogeneous group of solid and CNS tumors. Though racial/ethnic groups and county-level socioeconomic factors were proportionally represented, under representation of the adolescent/young adult (AYA) population and younger patients with solid and CNS tumors remains a concern. Targeted efforts should focus on these subgroups and further research should evaluate AYA enrollment rates across all available trials.

Mammalian orthoreovirus (reovirus) nonstructural protein μNS nucleates viral factories (VFs), which are sites of viral genome replication, protein synthesis, and particle assembly. Reovirus mRNAs are not polyadenylated, yet these transcripts are efficiently translated. To identify host factors associated with translation in VFs, we conducted a proteomics screen and identified ataxin-2-like (ATXN2L) as a μNS-interacting protein. CRISPR-mediated gene knockout (KO) of ATXN2L impairs reovirus replication. The ATXN2L RNA-binding domains are required for reovirus replication and association with the 3′ terminus of nonpolyadenylated reovirus mRNAs. Synthesis of viral proteins is diminished in ATXN2L-KO cells following reovirus infection. Translation of a reovirus reporter construct is diminished following transfection of ATXN2L-KO cells with nonpolyadenylated mRNA but not with polyadenylated mRNA. These data identify ATXN2L as an essential mediator of translation of nonpolyadenylated reovirus mRNA. Reovirus mRNAs lack polyadenylated tails yet are efficiently translated. Here, the authors identify host protein ataxin-2-like (ATXN2L) as a mediator of reovirus nonpolyadenylated mRNA translation.