Beyond 2020: How General Education Archaeology Curricula Should Adapt to the COVID-19 Pandemic

Archaeology often justifies its existence by invoking the trope that we must learn about the past in order to create a better future. The COVID-19 pandemic is itself an event that will enter the historical record. Thus, the universality of this public health crisis is a unique opportunity to assess the relevance of university-level archaeology curricula to our present historical moment. We studied an upper division general education course on the archaeology of complex societies at a public liberal arts college in California. The instrument of data collection was a questionnaire administered at the end of the Fall 2020, Spring 2021, and Spring 2022 semesters. Students read an article about archaeological approaches to pandemics, then reflected on how it connected to course content and to their own experiences during the COVID-19 pandemic. Content analysis of student responses suggests that course themes of complex societies, the environment, archaeological evidence, the future, and social hierarchy resonated most with students on both intellectual and personal levels. We also identified emergent concerns with diseases (COVID-19 and others) and cultural responses to them, employment status, and psychological effects, suggesting that these themes are increasingly relevant to archaeology students during and beyond the COVID-19 pandemic

Consistently Using a Transportation Department for Patient Discharge to Sustain Nursing Staffing Levels

IMPROVING PATIENT FLOW BY UTILIZING A HOSPITAL TRANSPORTATION DEPARTMENT FOR DISCHARGES Using a transportation department for transporting patients for discharge is the industry standard. At a large urban hospital, inconsistent use of this department has resulted in frontline caregivers (RNs) having to pick up this function, resulting in potentially unsafe staffing levels on the floor. The goal of this quality improvement project was to improve the percent of discharges with the transport department from ≤10% to 70% by the end is fiscal year 2018 in an academic tertiary medical center. Baseline metrics demonstrated the current state and a root cause of analysis were initiated. As a result of this analysis, it was established that staff did not understand the best practice for transporting patients for discharge. A number of KPIs were developed for the utilization of the department for patient discharge. Post Kaizen pilot implementation, teletracking metrics demonstrated improvements in utilization. Next step is to rollout to all units and monthly reinforcement with continuous educational/data support from transport, access/flow and operational excellence

Patient Transport in the Time of COVID-19: Using Health Care Failure Mode and Effect Analysis with Simulation to Test and Modify a Protocol

Introduction: In March 2020, in response to the COVID-19 pandemic, an interprofessional, interdisciplinary team at Maine Medical Center used Healthcare Failure Mode and Effect Analysis (HFMEA) and in situ simulation to rapidly identify and mitigate latent safety threats (LST) in patient transport protocols. Methods: Following HFMEA steps, stakeholders representing a variety of disciplines assembled to address transport of patients with COVID-19. A process map was created to describe the process. With hazard analysis using table-top simulation followed by in situ simulation, we identified, categorized, and scored LSTs. Mitigation strategies were identified during structured debriefing. Results: Fourteen LSTs were identified in the categories of infection prevention (4), care coordination (2), equipment (2), facilities (2), teams (2), clinical skills (1), and diagnosis and treatment (1). Of these, 10 had “critical” hazard scores. Mitigation solutions were tested with in situ simulation. Results were shared with leadership and led to changes in hospital-wide protocols. Discussion: The COVID-19 pandemic presented an urgent need to create or adapt protocols to keep patients and staff safe. Our team combined simulation with HFMEA methodology to improve the safety of protocols for transporting patients with COVID-19. Simulation enabled recreation of real-world experience that exposed LSTs more thoroughly than mental walkthroughs alone. Use of HFMEA methodology supported quantifying identified LSTs and proposing mitigation strategies, while in situ simulation facilitated testing many proposed strategies. Conclusions: HFMEA used with in situ simulation provides an effective method to efficiently and thoroughly probe a process for failure modes, providing practical mitigation strategies

Target genes, variants, tissues and transcriptional pathways influencing human serum urate levels.

Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poorly understood mechanisms. We performed a trans-ancestry genome-wide association study of serum urate in 457,690 individuals, identifying 183 loci (147 previously unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals. Serum urate showed significant genetic correlations with many cardiometabolic traits, with genetic causality analyses supporting a substantial role for pleiotropy. Enrichment analysis, fine-mapping of urate-associated loci and colocalization with gene expression in 47 tissues implicated the kidney and liver as the main target organs and prioritized potentially causal genes and variants, including the transcriptional master regulators in the liver and kidney, HNF1A and HNF4A. Experimental validation showed that HNF4A transactivated the promoter of ABCG2, encoding a major urate transporter, in kidney cells, and that HNF4A p.Thr139Ile is a functional variant. Transcriptional coregulation within and across organs may be a general mechanism underlying the observed pleiotropy between urate and cardiometabolic traits.The Genotype-Tissue Expression (GTEx) Project was supported by the Common Fund of the Office of the Director of the National Institutes of Health, and by NCI, NHGRI, NHLBI, NIDA, NIMH, and NINDS. Variant annotation was supported by software resources provided via the Caché Campus program of the InterSystems GmbH to Alexander Teumer

Consistency of satellite climate data records for Earth system monitoring

Climate Data Records (CDRs) of Essential Climate Variables (ECVs) as defined by the Global Climate Observing System (GCOS) derived from satellite instruments help to characterize the main components of the Earth system, to identify the state and evolution of its processes, and to constrain the budgets of key cycles of water, carbon and energy. The Climate Change Initiative (CCI) of the European Space Agency (ESA) coordinates the derivation of CDRs for 21 GCOS ECVs. The combined use of multiple ECVs for Earth system science applications requires consistency between and across their respective CDRs. As a comprehensive definition for multi-ECV consistency is missing so far, this study proposes defining consistency on three levels: (1) consistency in format and metadata to facilitate their synergetic use (technical level); (2) consistency in assumptions and auxiliary datasets to minimize incompatibilities among datasets (retrieval level); and (3) consistency between combined or multiple CDRs within their estimated uncertainties or physical constraints (scientific level). Analysing consistency between CDRs of multiple quantities is a challenging task and requires coordination between different observational communities, which is facilitated by the CCI program. The inter-dependencies of the satellite-based CDRs derived within the CCI program are analysed to identify where consistency considerations are most important. The study also summarizes measures taken in CCI to ensure consistency on the technical level, and develops a concept for assessing consistency on the retrieval and scientific levels in the light of underlying physical knowledge. Finally, this study presents the current status of consistency between the CCI CDRs and future efforts needed to further improve it

The PREDICTS database: a global database of how local terrestrial biodiversity responds to human impacts

Biodiversity continues to decline in the face of increasing anthropogenic pressures such as habitat destruction, exploitation, pollution and introduction of alien species. Existing global databases of species’ threat status or population time series are dominated by charismatic species. The collation of datasets with broad taxonomic and biogeographic extents, and that support computation of a range of biodiversity indicators, is necessary to enable better understanding of historical declines and to project – and avert – future declines. We describe and assess a new database of more than 1.6 million samples from 78 countries representing over 28,000 species, collated from existing spatial comparisons of local-scale biodiversity exposed to different intensities and types of anthropogenic pressures, from terrestrial sites around the world. The database contains measurements taken in 208 (of 814) ecoregions, 13 (of 14) biomes, 25 (of 35) biodiversity hotspots and 16 (of 17) megadiverse countries. The database contains more than 1% of the total number of all species described, and more than 1% of the described species within many taxonomic groups – including flowering plants, gymnosperms, birds, mammals, reptiles, amphibians, beetles, lepidopterans and hymenopterans. The dataset, which is still being added to, is therefore already considerably larger and more representative than those used by previous quantitative models of biodiversity trends and responses. The database is being assembled as part of the PREDICTS project (Projecting Responses of Ecological Diversity In Changing Terrestrial Systems – www.predicts.org.uk). We make site-level summary data available alongside this article. The full database will be publicly available in 2015

Effect of angiotensin-converting enzyme inhibitor and angiotensin receptor blocker initiation on organ support-free days in patients hospitalized with COVID-19

IMPORTANCE Overactivation of the renin-angiotensin system (RAS) may contribute to poor clinical outcomes in patients with COVID-19. Objective To determine whether angiotensin-converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB) initiation improves outcomes in patients hospitalized for COVID-19. DESIGN, SETTING, AND PARTICIPANTS In an ongoing, adaptive platform randomized clinical trial, 721 critically ill and 58 non–critically ill hospitalized adults were randomized to receive an RAS inhibitor or control between March 16, 2021, and February 25, 2022, at 69 sites in 7 countries (final follow-up on June 1, 2022). INTERVENTIONS Patients were randomized to receive open-label initiation of an ACE inhibitor (n = 257), ARB (n = 248), ARB in combination with DMX-200 (a chemokine receptor-2 inhibitor; n = 10), or no RAS inhibitor (control; n = 264) for up to 10 days. MAIN OUTCOMES AND MEASURES The primary outcome was organ support–free days, a composite of hospital survival and days alive without cardiovascular or respiratory organ support through 21 days. The primary analysis was a bayesian cumulative logistic model. Odds ratios (ORs) greater than 1 represent improved outcomes. RESULTS On February 25, 2022, enrollment was discontinued due to safety concerns. Among 679 critically ill patients with available primary outcome data, the median age was 56 years and 239 participants (35.2%) were women. Median (IQR) organ support–free days among critically ill patients was 10 (–1 to 16) in the ACE inhibitor group (n = 231), 8 (–1 to 17) in the ARB group (n = 217), and 12 (0 to 17) in the control group (n = 231) (median adjusted odds ratios of 0.77 [95% bayesian credible interval, 0.58-1.06] for improvement for ACE inhibitor and 0.76 [95% credible interval, 0.56-1.05] for ARB compared with control). The posterior probabilities that ACE inhibitors and ARBs worsened organ support–free days compared with control were 94.9% and 95.4%, respectively. Hospital survival occurred in 166 of 231 critically ill participants (71.9%) in the ACE inhibitor group, 152 of 217 (70.0%) in the ARB group, and 182 of 231 (78.8%) in the control group (posterior probabilities that ACE inhibitor and ARB worsened hospital survival compared with control were 95.3% and 98.1%, respectively). CONCLUSIONS AND RELEVANCE In this trial, among critically ill adults with COVID-19, initiation of an ACE inhibitor or ARB did not improve, and likely worsened, clinical outcomes. TRIAL REGISTRATION ClinicalTrials.gov Identifier: NCT0273570

A Metabolomic Study To Identify New Globotriaosyl­ceramide-Related Biomarkers in the Plasma of Fabry Disease Patients

Fabry disease is an X-linked lysosomal storage disorder caused by a deficiency of the enzyme α-galactosidase A, which results in the progressive accumulation of glycosphingolipids. In addition to the two biomarkers, globotriaosyl­ceramide (Gb₃) and globotriaosyl­sphingosine (lyso-Gb₃), which are routinely used for detection and high-risk screening of Fabry disease patients, novel urinary Gb₃-related isoforms/analogues as well as newly defined lyso-Gb₃ analogues in plasma and urine from Fabry patients have recently been described by our group. The aim of this study was to extend our recent analyses to identify and evaluate new potential Gb₃-related biomarkers in the plasma of untreated male Fabry disease patients using a mass spectrometry metabolomic approach. A multivariate statistical analysis revealed five Gb₃-related novel biomarkers in the plasma of male Fabry patients. Three of these new biomarkers correspond to Gb₃, which has an extra double bond on the sphingosine with C16:0, C18:0, and C22:1 fatty acid chains. The fourth biomarker corresponds to a mixture of two structural isomers, the first with a d16:1 sphingosine and a C16:0 fatty acid and the second with a d18:1 sphingosine and a C14:0 fatty acid. To our knowledge, it is the first time that a Gb₃ analogue with a d16:1 sphingosine moiety has been reported. In addition, this Gb₃ analogue was also present in its methylated form. These biomarkers are part of a metabolic profile that may provide insight into the pathophysiology of Fabry disease