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In recent decades, glaciers in the Amundsen Sea Embayment in West Antarctica have made the largest contribution to mass loss from the entire Antarctic Ice Sheet. Glacier retreat and acceleration have led to concerns about the stability of the region and the effects of future climate change. Coastal thinning and near-synchronous increases in ice flux across neighbouring glaciers suggest that ocean-driven melting is one of the main drivers of mass imbalance. However, the response of individual glaciers to changes in ocean conditions varies according to their local geometry. One of the largest and fastest-flowing of these glaciers, Pine Island Glacier (PIG), underwent a retreat from a subglacial ridge in the 1940s following a period of unusually warm conditions. Despite subsequent cooler periods, the glacier failed to recover back to the ridge and continued retreating to its present-day position. Here, we use the ice-flow model Úa to investigate the sensitivity of this retreat to changes in basal melting. We show that a short period of increased basal melt was sufficient to force the glacier from its stable position on the ridge and undergo an irreversible retreat to the next topographic high. Once high melting begins upstream of the ridge, only near-zero melt rates can stop the retreat, indicating a possible hysteresis in the system. Our results suggest that unstable and irreversible responses to warm anomalies are possible and can lead to substantial changes in ice flux over relatively short periods of only a few decades. [ABSTRACT FROM AUTHOR]

Numerical modeling of ice sheet dynamics is a critical tool for projecting future sea level rise. Among all the processes responsible for the loss of mass of the ice sheets, enhanced ice discharge triggered by the retreat of marine-terminating glaciers is one of the key drivers. Numerical models of ice sheet flow are therefore required to include ice front migration in order to reproduce today's mass loss and to be able to predict their future. However, the discontinuous nature of calving poses a significant numerical challenge for accurately capturing the motion of the ice front. In this study, we explore different stabilization techniques combined with varying reinitialization strategies to enhance the numerical stability and accuracy of solving the level-set function, which tracks the position of the ice front. Through rigorous testing on an idealized domain with a semicircular and a straight-line ice front, including scenarios with diverse front velocities, we assess the performance of these techniques. The findings contribute to advancing our ability to model ice sheet dynamics, specifically calving processes, and provide valuable insights into the most effective strategies for simulating and tracking the motion of the ice front. [ABSTRACT FROM AUTHOR]

The Greenland Ice Sheet contributed 10.6 mm to global sea level rise between 1992 and 2018, and it is projected to be the largest glacial contributor to sea level rise by 2100. Here we assess the relative importance of two major sources of uncertainty in 21st century ice loss projections: (1) the choice of sliding law and (2) the surface mass balance (SMB) forecast. Specifically, we used the ice flow model Úa to conduct an ensemble of runs for 48 combinations of sliding law and SMB forecast for three major Greenland outlet glaciers (Kangerlussuaq (KG), Humboldt (HU) and Petermann (PG) glaciers) with differing characteristics and evaluated how the sensitivity to these factors varied between the study glaciers. Overall, our results show that SMB forecasts were responsible for 4.45 mm of the variability in sea level rise by 2100 compared with 0.33 mm sea level equivalent (SLE) due to sliding law. HU had the largest absolute contribution to sea level rise and the largest range (2.16–7.96 mm SLE), followed by PG (0.84–5.42 mm SLE), and these glaciers showed similar patterns of ice loss across the SMB forecasts and sliding laws. KG had the lowest range and absolute values (- 0.60 to 3.45 mm SLE) of sea level rise, and the magnitude of mass loss by SMB forecast differed markedly between HU and PG. Our results highlight SMB forecasts as a key focus for improving estimates of Greenland's contribution to 21st century sea level rise. [ABSTRACT FROM AUTHOR]

Over the past decade, a wealth of research has been devoted to the detection of crevasses in glaciers and ice sheets via remote sensing and machine learning techniques. It is often argued that remotely sensed damage maps can function as early warning signals for shifts in ice shelf conditions from intact to damaged states and can serve as an important tool for ice sheet modellers to improve future sea level rise predictions. Here, we provide evidence for the Filchner–Ronne and Pine Island ice shelves that remotely sensed damage maps are only weakly related to the ice rate factor field A derived by an ice flow model when inverting for surface velocities. This technique is a common procedure in ice flow models, as it guarantees that any inferred changes in A relate to changes in ice flow measured through observations. The weak relationship found is improved when investigating heavily damaged shear margins, as observed on the Pine Island Ice Shelf; however, even in this setting, this association remains modest. Our findings suggest that many features identified as damage through remote sensing methods are not of direct relevance to present-day ice shelf flow. While damage can clearly play an important role in ice shelf processes and thus be relevant for ice sheet behaviour and sea level rise projections, our results imply that mapping ice damage directly from satellite observations may not directly help improve the representation of these processes in ice flow models. [ABSTRACT FROM AUTHOR]

The rate at which the Antarctic Ice Sheet loses mass is to a large degree controlled by ice-ocean interactions underneath small ice shelves, with the most sensitive regions concentrated in even smaller areas near grounding lines and local pinning points. Sufficient horizontal resolution is key to resolving critical ice-ocean processes in these regions, but difficult to afford in large-scale models used to predict the coupled response of the entire Antarctic Ice Sheet and the global ocean to climate change. In this study we describe the implementation of a framework that couples the ice sheet flow model Úa with the Finite Element Sea Ice Ocean Model (FESOM-1.4) in a configuration using depth-dependent vertical coordinates. The novelty of this approach is the use of horizontally unstructured grids in both model components, allowing us to resolve critical processes directly, while keeping computational demands within the range of feasibility. We use the Marine Ice Sheet–Ocean Model Intercomparison Project framework to verify that ice retreat and readvance is reliably simulated, and inaccuracies in mass, heat and salt conservation are small compared to the forcing signal. Further, we demonstrate the capabilities of our approach for a global ocean/Antarctic Ice Sheet domain. In a 39-year hindcast simulation (1979–2018) we resolve retreat behaviour of Pine Island Glacier, a known challenge for coarser resolution models. We conclude that Úa-FESOM is well suited to improve predictions of the Antarctic Ice Sheet evolution over centennial time scales. [ABSTRACT FROM AUTHOR]

The collapse of ice shelves could expose tall ice cliffs at ice sheet margins. The marine ice cliff instability (MICI) is a hypothesis that predicts that, if these cliffs are tall enough, ice may fail structurally leading to self-sustained retreat. To date, projections that include MICI have been performed with a single model based on a simple parameterization. Here, we implement a physically motivated parameterization in three ice sheet models and simulate the response of the Amundsen Sea Embayment after a hypothetical collapse of floating ice. All models show that Thwaites Glacier would not retreat further in the 21st century. In another set of simulations, we force the grounding line to retreat into Thwaites' deeper basin to expose a taller cliff. In these simulations, rapid thinning and velocity increase reduce the calving rate, stabilizing the cliff. These experiments show that Thwaites may be less vulnerable to MICI than previously thought, and model projections that include this process should be re-evaluated. [ABSTRACT FROM AUTHOR]

Background: Exacerbations of COPD (ECOPD) have a major impact on patients and healthcare systems across the world. Precise estimates of the global burden of ECOPD on mortality and hospital readmission are needed to inform policy makers and aid preventive strategies to mitigate this burden. The aims of the present study were to explore global in-hospital mortality, post-discharge mortality and hospital readmission rates after ECOPD-related hospitalisation using an individual patient data meta-analysis (IPDMA) design., Methods: A systematic review was performed identifying studies that reported in-hospital mortality, post-discharge mortality and hospital readmission rates following ECOPD-related hospitalisation. Data analyses were conducted using a one-stage random-effects meta-analysis model. This study was conducted and reported in accordance with the PRISMA-IPD statement., Results: Data of 65 945 individual patients with COPD were analysed. The pooled in-hospital mortality rate was 6.2%, pooled 30-, 90- and 365-day post-discharge mortality rates were 1.8%, 5.5% and 10.9%, respectively, and pooled 30-, 90- and 365-day hospital readmission rates were 7.1%, 12.6% and 32.1%, respectively, with noticeable variability between studies and countries. Strongest predictors of mortality and hospital readmission included noninvasive mechanical ventilation and a history of two or more ECOPD-related hospitalisations <12 months prior to the index event., Conclusions: This IPDMA stresses the poor outcomes and high heterogeneity of ECOPD-related hospitalisation across the world. Whilst global standardisation of the management and follow-up of ECOPD-related hospitalisation should be at the heart of future implementation research, policy makers should focus on reimbursing evidence-based therapies that decrease (recurrent) ECOPD., Competing Interests: Conflict of interest: K. Waeijen-Smit, M. Crutsen, S. Keene, T.J. Ringbæk, F. Fabbian, C-t. Lun, B. Ergan, C. Estebam, J.M. Quintana Lopez, C.L. Chang, R.J. Hancox, E. Shafuddin, H. Ellis, C. Janson, G. Gudmundsson, D. Epstein, A. Lacoma, C. Osadnik, I. Alia, F. Spannella, Z. Karakurt, H. Mehravaran, C. Utens, M.D. de Kruif, F.W.S. Ko, S.P. Trethewey, K. Vermeersch, S. Zilberman-Itskovich, C. Echevarria, R.T.M. Sprooten, P. Faverio, H.J. Prins and S. Houben-Wilke have no grants or personal fees to report. Conflict of interest: M. Miravitlles has received speaker fees from AstraZeneca, Boehringer Ingelheim, Chiesi, Cipla, Menarini, Kamada, Takeda, Zambon, CSL Behring, Specialty Therapeutics, Janssen, Grifols and Novartis, consulting fees from AstraZeneca, Atriva Therapeutics, Boehringer Ingelheim, Chiesi, GlaxoSmithKline, CSL Behring, Inhibrx, Ferrer, Menarini, Mereo Biopharma, Spin Therapeutics, ONO Pharma, Palobiofarma SL, Takeda, Novartis, Novo Nordisk, Sanofi and Grifols and research grants from Grifols. Conflict of interest: E. Crisafulli has received honoraria for lecturing, scientific advisory boards and participation in clinical studies for AstraZeneca, Boehringer Ingelheim, Chiesi, GSK, Menarini, Novartis, Qbgroup and Sanofi. Conflict of interest: A. Torres reports speaker/consulting honoraria from Pfizer, MSD, Janssen and Biomerieux. Conflict of interest: C. Mueller has received research support from the Swiss National Science Foundation, the Swiss Heart Foundation, the University of Basel, the University Hospital Basel, the KTI, Abbott, Beckman Coulter, BRAHMS, Idorsia, LSI-Medience, Ortho Diagnostics, Novartis, Roche, Siemens, SpinChip and Singulex, as well as speaker/consulting honoraria from Amgen, AstraZeneca, Bayer, BMS, Boehringer Ingelheim, Daiichi Sankyo, Idorsia, Novartis, Osler, Roche, SpinChip and Sanofi, all outside the submitted work. Conflict of interest: P. Schuetz has received grants from Nestle, Abbot, bioMerieux and Thermofisher outside the submitted work. Conflict of interest: E. Mekov has received grants and personal fees from Chiesi, and speaker or consulting fees from AstraZeneca and Chiesi. Conflict of interest: T.H. Harries is supported by a National Institute for Health and Care Research Academic Clinical Lectureship. Conflict of interest: J.L. López-Campos has received honoraria during the last 3 years for lecturing, scientific advice, participation in clinical studies or writing for publications for (alphabetical order): AstraZeneca, Bial, Boehringer, Chiesi, CSL Behring, Faes, Ferrer, Gebro, Grifols, GSK, Megalabs, Menarini and Novartis. Conflict of interest: C.S. Ulrik has received personal fees and grants from AstraZeneca, Chiesi, Boehringer Ingelheim, GSK, Novartis, Sanofi, Menarini, TEVA, ALK-Abello, Takeda, Orion Pharma, TFF Pharmaceuticals and Covis Pharma outside the submitted work. Conflict of interest: J. Dominguez has received honoraria for lectures from Oxford Immunotec (UK) and received payments for license transference from GenID (Germany), and grants from La Fundació La Marató TV3, Instituto de Salud Carlos III (CP03/00112), Catalan Pulmonology Society (SOCAP), Catalan Pulmonology Foundation (FUCAP) and Spanish Society of Pulmonology and Thoracic Surgery (SEPAR). Conflict of interest: A.M. Turner reports research grants outside the submitted work from AstraZeneca, Resmed, Phillips, Chiesi, Grifols, CSL Behring and NIHR, and honoraria from GSK and Boehringer Ingelheim. Conflict of interest: D. Bumbacea has received grants and personal fees in the last 3 years from AstraZeneca, Eli Lilly, Novartis, Sanofi and Synairgen outside of the submitted work. Conflict of interest: PBM has received grants and personal fees from Philips, ResMed, Breas, Chiesi, Fischer & Paykel and, Sanofi outside the submitted work. Conflict of interest: J. Steer has received grants and honoraria, outside the submitted work, from Chiesi, Menarini Group, AstraZeneca and Pfizer. Conflict of interest: S.C. Bourke has received research grants from GSK (BEC COPD IRAS 285200), and additional support from Radiometer for an NIHR-funded study (NIVOW IRAS 313485), Philips, ResMed, and Pfizer Open Air, took part in clinical advisory boards with Philips and AstraZeneca, and has received honoraria from Boehringer Ingelheim, Chiesi, GSK, and AstraZeneca. Conflict of interest: N. Lane reports research grants from Bright Northumbria and The ResMed Foundation; and nonfinancial support from Chiesi and BREAS outside the submitted work. Conflict of interest: J. de Batlle acknowledges receiving financial support from Instituto de Salud Carlos III (Miguel Servet 2019: CP19/00108), co-funded by the European Social Fund, “Investing in your future”. Conflict of interest: R. Russell has received personal fees, outside of the submitted work, from AstraZeneca, Chiesi, Covis, GlaxoSmithKline and Boehringer Ingelheim. Conflict of interest: J.L. Cross has received grants from National Institute of Health Research. Conflict of interest: M.A. Spruit has received grants from the Netherlands Lung Foundation, Stichting Asthma Bestrijding, AstraZeneca, Boehringer Ingeheim, TEVA and CHIESI outside the submitted work. Conflict of interest: S.O. Simons has received grants and personal fees from AstraZeneca, Boehringer Ingelheim, GlaxoSmithKline and Chiesi outside the submitted work. Conflict of interest: F.M.E. Franssen has received grants and personal fees from AstraZeneca, Chiesi, Boehringer Ingelheim, Glaxosmithkline, Novartis and MSD outside the submitted work. Conflict of interest: All authors declare no conflicts of interest in relation to the present study., (Copyright ©The authors 2024.)

Background: Surgical lung biopsy (SLB) is required for diagnosis in patients with suspected interstitial lung disease (ILD) if other less invasive diagnostic methods are non-conclusive. We evaluated the outcome of SLB by using centralized databases in a whole-nation patient-cohort., Methods: A population-based retrospective study on 68 consecutive patients (mean age 58 years, 58.8% males) that underwent SLB in Iceland between the years 2008 and 2020. Patient information was obtained from patient charts and peri- and postoperative complications were registered together with 30- and 90-day mortality. Computed tomography (CT) scans, histological biopsies and spirometry results were reviewed, and overall survival (Kaplan-Meier) estimated. Mean follow-up was 61.3 months (range, 3-155 months)., Results: Out of 68 SLB-patients 41 (60.3%) had preoperatively undergone non-conclusive transbronchial biopsies (TBB) obtained with bronchoscopy. Spirometry showed forced vital capacity (FVC) 3.0 L and forced expiratory volume in 1 second (FEV1) 2.3 L, or 73.0% and 71.6% of predicted value, respectively. Video-assisted thoracoscopic surgery (VATS) technique was used in all cases and provided a histologic and disease specific diagnosis in 92.6% of cases; most often being nonspecific interstitial pneumonia (NSIP) (29.4%) and usual interstitial pneumonia (UIP) (23.5%). One patient (1.5%) sustained a major postoperative complication (excessive bleeding) and seven patients (10.3%) minor complications. Median chest tube time and length of stay was 1 and 2 days, respectively. No patients died <90 days postoperatively. Overall survival at 1 and 5 years was 95.6% and 73.5%, respectively, and 5-year survival for NSIP and UIP was 85% and 43.7%, respectively. Long-term mortality for UIP was four times higher when compared with NSIP and other diagnosis., Conclusions: Lung biopsy with VATS-technique provided a definitive histological and disease specific diagnosis in majority of cases. The procedure is safe, reflected in low complication-rates and short hospital stay, and can therefore be used to diagnose and tailor treatment of ILD patients., Competing Interests: Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://jtd.amegroups.com/article/view/10.21037/jtd-23-1107/coif). G.G. reports funding from the Landspitali Scientific Fund (No. A2020-019) and the University of Iceland Research Fund. The other authors have no conflicts of interest to declare., (2024 Journal of Thoracic Disease. All rights reserved.)

Background: A decline in forced expiratory volume (FEV1) is a hallmark of respiratory diseases that are an important cause of morbidity among the elderly. While some data exist on biomarkers that are related to FEV1, we sought to do a systematic analysis of causal relations of biomarkers with FEV1., Methods: Data from the population-based AGES-Reykjavik study were used. Serum proteomic measurements were done using 4782 DNA aptamers (SOMAmers). Data from 1479 participants with spirometric data were used to assess the association of SOMAmer measurements with FEV1 using linear regression. Bi-directional two-sample Mendelian randomisation (MR) analyses were done to assess causal relations of observationally associated SOMAmers with FEV1, using genotype and SOMAmer data from 5368 AGES-Reykjavik participants and genetic associations with FEV1 from a publicly available GWAS (n = 400,102)., Results: In observational analyses, 530 SOMAmers were associated with FEV1 after multiple testing adjustment (FDR < 0.05). The most significant were Retinoic Acid Receptor Responder 2 (RARRES2), R-Spondin 4 (RSPO4) and Alkaline Phosphatase, Placental Like 2 (ALPPL2). Of the 257 SOMAmers with genetic instruments available, eight were associated with FEV1 in MR analyses. Three were directionally consistent with the observational estimate, Thrombospondin 2 (THBS2), Endoplasmic Reticulum Oxidoreductase 1 Beta (ERO1B) and Apolipoprotein M (APOM). THBS2 was further supported by a colocalization analysis. Analyses in the reverse direction, testing whether changes in SOMAmer levels were caused by changes in FEV1, were performed but no significant associations were found after multiple testing adjustments., Conclusions: In summary, this large scale proteogenomic analyses of FEV1 reveals circulating protein markers of FEV1, as well as several proteins with potential causality to lung function., (© 2024. The Author(s).)