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Rapid growth in the market for electric vehicles is imperative, to meet global targets for reducing greenhouse gas emissions, to improve air quality in urban centres and to meet the needs of consumers, with whom electric vehicles are increasingly popular. However, growing numbers of electric vehicles present a serious waste-management challenge for recyclers at end-of-life. Nevertheless, spent batteries may also present an opportunity as manufacturers require access to strategic elements and critical materials for key components in electric-vehicle manufacture: recycled lithium-ion batteries from electric vehicles could provide a valuable secondary source of materials. Here we outline and evaluate the current range of approaches to electric-vehicle lithium-ion battery recycling and re-use, and highlight areas for future progress. Processes for dismantling and recycling lithium-ion battery packs from scrap electric vehicles are outlined.

The newly emerged severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) highlights the urgent need for assays that detect protective levels of neutralizing antibodies. We studied the relationship among anti-spike ectodomain (anti-ECD), anti-receptor-binding domain (anti-RBD) IgG titers, and SARS-CoV-2 virus neutralization (VN) titers generated by 2 in vitro assays using convalescent plasma samples from 68 patients with COVID-19. We report a strong positive correlation between both plasma anti-RBD and anti-ECD IgG titers and in vitro VN titers. The probability of a VN titer of ≥160, the FDA-recommended level for convalescent plasma used for COVID-19 treatment, was ≥80% when anti-RBD or anti-ECD titers were ≥1:1350. Of all donors, 37% lacked VN titers of ≥160. Dyspnea, hospitalization, and disease severity were significantly associated with higher VN titer. Frequent donation of convalescent plasma did not significantly decrease VN or IgG titers. Analysis of 2814 asymptomatic adults found 73 individuals with anti-ECD IgG titers of ≥1:50 and strong positive correlation with anti-RBD and VN titers. Fourteen of these individuals had VN titers of ≥1:160, and all of them had anti-RBD titers of ≥1:1350. We conclude that anti-RBD or anti-ECD IgG titers can serve as a surrogate for VN titers to identify suitable plasma donors. Plasma anti-RBD or anti-ECD titers of ≥1:1350 may provide critical information about protection against COVID-19 disease.

Abstract Rationale Ineffective repair of a damaged alveolar epithelium has been postulated to cause pulmonary fibrosis. In support of this theory, epithelial cell abnormalities, including hyperplasia, apoptosis, and persistent denudation of the alveolar basement membrane, are found in the lungs of humans with idiopathic pulmonary fibrosis and in animal models of fibrotic lung disease. Furthermore, mutations in genes that affect regenerative capacity or that cause injury/apoptosis of type II alveolar epithelial cells have been identified in familial forms of pulmonary fibrosis. Although these findings are compelling, there are no studies that demonstrate a direct role for the alveolar epithelium or, more specifically, type II cells in the scarring process. Objectives To determine if a targeted injury to type II cells would result in pulmonary fibrosis. Methods A transgenic mouse was generated to express the human diphtheria toxin receptor on type II alveolar epithelial cells. Diphtheria toxin was administered to these animals to specifically target the type II epithelium for injury. Lung fibrosis was assessed by histology and hydroxyproline measurement. Measurements and Main Results Transgenic mice treated with diphtheria toxin developed an approximately twofold increase in their lung hydroxyproline content on Days 21 and 28 after diphtheria toxin treatment. The fibrosis developed in conjunction with type II cell injury. Histological evaluation revealed diffuse collagen deposition with patchy areas of more confluent scarring and associated alveolar contraction. Conclusions The development of lung fibrosis in the setting of type II cell injury in our model provides evidence for a causal link between the epithelial defects seen in idiopathic pulmonary fibrosis and the corresponding areas of scarring.

There is concern about second and subsequent waves of COVID-19 caused by the SARS-CoV-2 coronavirus occurring in communities globally that had an initial disease wave. Metropolitan Houston, TX, with a population of 7 million, is experiencing a massive second disease wave that began in late May 2020. To understand SARS-CoV-2 molecular population genomic architecture and evolution and the relationship between virus genotypes and patient features, we sequenced the genomes of 5,085 SARS-CoV-2 strains from these two waves. Our report provides the first molecular characterization of SARS-CoV-2 strains causing two distinct COVID-19 disease waves. We sequenced the genomes of 5,085 severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) strains causing two coronavirus disease 2019 (COVID-19) disease waves in metropolitan Houston, TX, an ethnically diverse region with 7 million residents. The genomes were from viruses recovered in the earliest recognized phase of the pandemic in Houston and from viruses recovered in an ongoing massive second wave of infections. The virus was originally introduced into Houston many times independently. Virtually all strains in the second wave have a Gly614 amino acid replacement in the spike protein, a polymorphism that has been linked to increased transmission and infectivity. Patients infected with the Gly614 variant strains had significantly higher virus loads in the nasopharynx on initial diagnosis. We found little evidence of a significant relationship between virus genotype and altered virulence, stressing the linkage between disease severity, underlying medical conditions, and host genetics. Some regions of the spike protein—the primary target of global vaccine efforts—are replete with amino acid replacements, perhaps indicating the action of selection. We exploited the genomic data to generate defined single amino acid replacements in the receptor binding domain of spike protein that, importantly, produced decreased recognition by the neutralizing monoclonal antibody CR3022. Our report represents the first analysis of the molecular architecture of SARS-CoV-2 in two infection waves in a major metropolitan region. The findings will help us to understand the origin, composition, and trajectory of future infection waves and the potential effect of the host immune response and therapeutic maneuvers on SARS-CoV-2 evolution. IMPORTANCE There is concern about second and subsequent waves of COVID-19 caused by the SARS-CoV-2 coronavirus occurring in communities globally that had an initial disease wave. Metropolitan Houston, TX, with a population of 7 million, is experiencing a massive second disease wave that began in late May 2020. To understand SARS-CoV-2 molecular population genomic architecture and evolution and the relationship between virus genotypes and patient features, we sequenced the genomes of 5,085 SARS-CoV-2 strains from these two waves. Our report provides the first molecular characterization of SARS-CoV-2 strains causing two distinct COVID-19 disease waves.

The purpose of this pilot study was to evaluate whether physician assistant (PA) programs in the Midwest integrate both disabilities and emergency preparedness education into 1 curriculum. A convenience sample was utilized to survey program directors and deans of PA programs. Emails were obtained from the Physician Assistant Education Association. A 26, closed-ended question Qualtrics survey was based on an original study by Tanenhaus et al. Out of 43 accredited physician assistant programs surveyed, 9 programs replied (21%), and 1 program did not complete the survey. Six of the 10 programs (66%) responded that their program provided lectures specific to emergency preparedness. All 9 programs responded they do not offer a graduate-level track or concentration in emergency/disaster preparedness, and they do not offer a dual degree or a multidisciplinary program that highlights emergency/disaster preparedness. This study was conducted to bring awareness to physician assistant students' education regarding disabilities and emergency preparedness. As public health crises continue to arise, such as coronavirus disease (COVID-19), it is critical to have appropriately trained health care professionals. The study revealed that most programs lack a graduate-level track or concentrations, dual degrees, or extracurricular opportunities related to disabilities and emergency and disaster preparedness.

Airways of the peripheral lung are prone to closure at low lung volumes. Deficiency or dysfunction of pulmonary surfactant during various lung diseases compounds this event by destabilizing the liquid lining of small airways and giving rise to occluding liquid plugs in airways. Propagation of liquid plugs in airways during inflation of the lung exerts large mechanical forces on airway cells. We describe a microfluidic model of small airways of the lung that mimics airway architecture, recreates physiologic levels of pulmonary pressures, and allows studying cellular response to repeated liquid plug propagation events. Substantial cellular injury happens due to the propagation of liquid plugs devoid of surfactant. We show that addition of a physiologic concentration of a clinical surfactant, Survanta, to propagating liquid plugs protects the epithelium and significantly reduces cell death. Although the protective role of surfactants has been demonstrated in models of a propagating air finger in liquid-filled airways, this is the first time to study the protective role of surfactants in liquid plugs where fluid mechanical stresses are expected to be higher than in air fingers. Our parallel computational simulations revealed a significant decrease in mechanical forces in the presence of surfactant, confirming the experimental observations. The results support the practice of providing exogenous surfactant to patients in certain clinical settings as a protective mechanism against pathologic flows. More importantly, this platform provides a useful model to investigate various surface tension-mediated lung diseases at the cellular level.

Measuring flame lengths and areas from turbulent flame flares developing from lithium-ion battery failures is complex due to the varying directions of the flares, the thin flame zone, the spatially and temporally rapid changes of the thermal runaway event, as well as the hazardous nature of the event. This paper reports a novel methodology for measuring heat release rate from flame flares resulting from thermal runaway of electric vehicle lithium-ion modules comprising eight 56.3Ah lithium nickel manganese cobalt (NMC) pouch cells using digital cameras and a newly developed numerical code to process the distortion of the flame size based on distance, direction, and shape. The model is tested with a set of experiments using lithium-ion battery packs and validated with a reference set of measurements using calibration boxes, a method commonly used in the reconstruction of flame areas. The experiments showed that the effect of calibration is large, and thus digital imaging without the appropriate calibration can give very large errors in measurement of flames. The combined imaging and processing method proposed in this work allows the determination of heat release rates from lithium-ion battery packs, one of the most challenging variables to quantify during the failure of a battery pack outside the laboratory. In the example experiment that this method was applied to, almost double the heat released was accounted for, meaning 50% of the total heat released would not have been accounted for without this image processing method.

Fibrosis of the lung constitutes a major clinical challenge and novel therapies are required to alleviate the associated morbidity and mortality. Investigating the antifibrotic efficacy of drugs that are already in clinical practice offers an efficient strategy to identify new therapies. The phosphodiesterase 4 (PDE4) inhibitors, approved for the treatment of chronic obstructive pulmonary disease, harbor therapeutic potential for pulmonary fibrosis by augmenting the activity of endogenous antifibrotic mediators that signal through cyclic AMP. In this study, we tested the efficacy of several PDE4 inhibitors including a novel compound (Compound 1) in a murine model of lung fibrosis that results from a targeted type II alveolar epithelial cell injury. We also compared the antifibrotic activity of PDE4 inhibition to the two therapies that are FDA‐approved for idiopathic pulmonary fibrosis (pirfenidone and nintedanib). We found that both preventative (day 0–21) and therapeutic (day 11–21) dosing regimens of the PDE4 inhibitors significantly ameliorated the weight loss and lung collagen accumulation that are the sequelae of targeted epithelial cell damage. In a therapeutic protocol, the reduction in lung fibrosis with PDE4 inhibitor administration was equivalent to pirfenidone and nintedanib. Treatment with this class of drugs also resulted in a decrease in plasma surfactant protein D concentration, a reduction in the plasma levels of several chemokines implicated in lung fibrosis, and an in vitro inhibition of fibroblast profibrotic gene expression. These results motivate further investigation of PDE4 inhibition as a treatment for patients with fibrotic lung disease. We demonstrate that prophylactic and therapeutic inhibition of phosphodiesterase 4 with several different antagonists reduces lung fibrosis induced by a targeted injury to the type II alveolar epithelium. In conjunction with the reduction in lung collagen content, phosphodiesterase inhibition also reduced serum surfactant protein C levels and the expression of profibrotic genes by lung fibroblasts.

Background The importance of self-management strategies that optimise physical health and mental health in the management of rheumatoid arthritis (RA) is recognised, but access to multidisciplinary teams to support this can be challenging. Furthermore, evidence for the impact of multidisciplinary interventions, especially in early RA, is lacking. Methods The Resilience and Healthy Lifestyle for Rheumatoid Arthritis (RA-HEAL) Trial is a pragmatic RCT that aims to compare the effects of a structured multidisciplinary lifestyle intervention with self-directed activities in best-practice usual care. The 20-week multi-modal intervention incorporates structured resilience training conducted by a clinical health psychologist (CHP), followed by an exercise physiologist (EP)-led exercise programme, dietary education conducted by a dietitian nutritionist (DN), a smoking cessation programme (where applicable) and psychologist-led behaviour-change support. The comparison group will receive written information on a healthy lifestyle in accordance with standard best practice care. The primary outcome is health-related quality of life (QoL) at 6 months. Discussion RA-HEAL tests whether a tailored intervention including formal resilience training with a clinical psychologist followed by Mediterranean diet, exercise, smoking cessation and behaviour change support has a greater effect on health-related QoL at 6 months than written advice given in current best-practice settings. QoL is a composite endpoint that is highly valued by patients with RA. RA-HEAL is unique in that it targets RA within 12 months of onset. RA-HEAL’s linkage with the Australian Autoimmune Arthritis Biobank Cooperative (A3BC) supports 6 monthly follow-up data and biosampling to 24 months post-intervention and linkage to health data collections, creating a valuable resource for future research and the potential to determine medium and long-term effects of behaviour change. In its secondary outcomes, RA-HEAL will analyse the longevity of effects of intervention or best-practice usual care for up to 2 years and cost utility. The outcomes should provide evidence to underpin a scalable approach to support people with newly diagnosed RA. Trial registration ACTRN12625000050459, ANZCTR. Registered on 20 January 2025.