ADEPT:Exploring the Design, Pedagogy, and Analysis of a Mixed Reality Application for Piano Training

(Abstract to follow

‘Superpolicies’ and ‘policy-omnishambles’

No abstract available

How have changes in death by cause and age group contributed to the recent stalling of life expectancy gains in Scotland? Comparative decomposition analysis of mortality data, 2000–2002 to 2015–2017

Objective: Annual gains in life expectancy in Scotland were slower in recent years than in the previous two decades. This analysis investigates how deaths in different age groups and from different causes have contributed to annual average change in life expectancy across two time periods: 2000–2002 to 2012–2014 and 2012–2014 to 2015–2017. Setting Scotland. Methods: Life expectancy at birth was calculated from death and population counts, disaggregated by 5 year age group and by underlying cause of death. Arriaga’s method of life expectancy decomposition was applied to produce estimates of the contribution of different age groups and underlying causes to changes in life expectancy at birth for the two periods. Results: Annualised gains in life expectancy between 2012–2014 and 2015–2017 were markedly smaller than in the earlier period. Almost all age groups saw worsening mortality trends, which deteriorated for most cause of death groups between 2012–2014 and 2015–2017. In particular, the previously observed substantial life expectancy gains due to reductions in mortality from circulatory causes, which most benefited those aged 55–84 years, more than halved. Mortality rates for those aged 30–54 years and 90+ years worsened, due in large part to increases in drug-related deaths, and dementia and Alzheimer’s disease, respectively. Conclusion: Future research should seek to explain the changes in mortality trends for all age groups and causes. More investigation is required to establish to what extent shortcomings in the social security system and public services may be contributing to the adverse trends and preventing mitigation of the impact of other contributing factors, such as influenza outbreaks

Is austerity responsible for the recent change in mortality trends across high-income nations? A protocol for an observational study

Introduction: Mortality rates in many high-income countries have changed from their long-term trends since around 2011. This paper sets out a protocol for testing the extent to which economic austerity can explain the variance in recent mortality trends across high-income countries. Methods and analysis: This is an ecological natural experiment study, which will use regression adjustment to account for differences in exposure, outcomes and confounding. All high-income countries with available data will be included in the sample. The timing of any changes in the trends for four measures of austerity (the Alesina-Ardagna Fiscal Index, real per capita government expenditure, public social spending and the cyclically adjusted primary balance) will be identified and the cumulative difference in exposure to these measures thereafter will be calculated. These will be regressed against the difference in the mean annual change in life expectancy, mortality rates and lifespan variation compared with the previous trends, with an initial lag of 2 years after the identified change point in the exposure measure. The role of underemployment and individual incomes as outcomes in their own right and as mediating any relationship between austerity and mortality will also be considered. Sensitivity analyses varying the lag period to 0 and 5 years, and adjusting for recession, will be undertaken. Ethics and dissemination: All of the data used for this study are publicly available, aggregated datasets with no individuals identifiable. There is, therefore, no requirement for ethical committee approval for the study. The study will be lodged within the National Health Service research governance system. All results of the study will be published following sharing with partner agencies. No new datasets will be created as part of this work for deposition or curation

Beth Levine in memoriam

Beth Levine was born on 7 April 1960 in Newark, New Jersey. She went to college at Brown University where she received an A.B. Magna Cum Laude, and she attended medical school at Cornell University Medical College, receiving her MD in 1986. She completed her internship and residency in Internal Medicine at Mount Sinai Hospital in New York, and her fellowship in Infectious Diseases at The Johns Hopkins Hospital. Most recently, Beth was a Professor of Internal Medicine and Microbiology, Director of the Center for Autophagy Research, and holder of the Charles Sprague Distinguished Chair in Biomedical Science at the University of Texas Southwestern Medical Center in Dallas. Beth died on 15 June 2020 from cancer. Beth is survived by her husband, Milton Packer, and their two children, Rachel (26 years old) and Ben (25 years old). Dr. Levine was as an international leader in the field of autophagy research. Her laboratory identified the mammalian autophagy gene BECN1/beclin 1; identified conserved mechanisms underlying the regulation of autophagy (e.g. BCL2-BECN1 complex formation, insulin-like signaling, EGFR, ERBB2/HER2 and AKT1-mediated BECN1 phosphosphorylation); and provided the first evidence that autophagy genes are important in antiviral host defense, tumor suppression, lifespan extension, apoptotic corpse clearance, metazoan development, Na,K-ATPase-regulated cell death, and the beneficial metabolic effects of exercise. She developed a potent autophagy-inducing cell permeable peptide, Tat-beclin 1, which has potential therapeutic applications in a range of diseases. She was a founding Associate Editor of the journal Autophagy and an editorial board member of Cell and Cell Host & Microbe. She has received numerous awards/honors in recognition of her scientific achievement, including: The American Cancer Society Junior Faculty Research Award (1994); election into the American Society of Clinical Investigation (2000); the Ellison Medical Foundation Senior Scholars Award in Global Infectious Diseases (2004); elected member, American Association of Physicians (2005); appointment as a Howard Hughes Medical Institute Investigator (2008); Edith and Peter O’Donnell Award in Medicine (2008); elected fellow, American Association for the Advancement of Science (2012); election into the National Academy of Sciences (2013); election into the Academy of Medicine, Engineering and Science of Texas (2013); the ASCI Stanley J. Korsmeyer Award (2014); Phyllis T. Bodel Women in Medicine Award, Yale University School of Medicine (2018); recipient, Barcroft Medal, Queen’s University Belfast (2018).Fil: An, Zhenyi. No especifíca;Fil: Ballabi, Andrea. No especifíca;Fil: Bennett, Lynda. No especifíca;Fil: Boya, Patricia. No especifíca;Fil: Cecconi, Francesco. No especifíca;Fil: Chiang, Wei Chung. No especifíca;Fil: Codogno, Patrice. No especifíca;Fil: Colombo, Maria Isabel. No especifíca;Fil: Cuervo, Ana Maria. No especifíca;Fil: Debnath, Jayanta. No especifíca;Fil: Deretic, Vojo. No especifíca;Fil: Dikic, Ivan. No especifíca;Fil: Dionne, Keith. No especifíca;Fil: Dong, Xiaonan. No especifíca;Fil: Elazar, Zvulun. No especifíca;Fil: Galluzzi, Lorenzo. No especifíca;Fil: Gentile, Frank. No especifíca;Fil: Griffin, Diane E.. No especifíca;Fil: Hansen, Malene. No especifíca;Fil: Hardwick, J. Marie. No especifíca;Fil: He, Congcong. No especifíca;Fil: Huang, Shu Yi. No especifíca;Fil: Hurley, James. No especifíca;Fil: Jackson, William T.. No especifíca;Fil: Jozefiak, Cindy. No especifíca;Fil: Kitsis, Richard N.. No especifíca;Fil: Klionsky, Daniel J.. No especifíca;Fil: Kroemer, Guido. No especifíca;Fil: Meijer, Alfred J.. No especifíca;Fil: Meléndez, Alicia. No especifíca;Fil: Melino, Gerry. No especifíca;Fil: Mizushima, Noboru. No especifíca;Fil: Murphy, Leon O.. No especifíca;Fil: Nixon, Ralph. No especifíca;Fil: Orvedahl, Anthony. No especifíca;Fil: Pattingre, Sophie. No especifíca;Fil: Piacentini, Mauro. No especifíca;Fil: Reggiori, Fulvio. No especifíca;Fil: Ross, Theodora. No especifíca;Fil: Rubinsztein, David C.. No especifíca;Fil: Ryan, Kevin. No especifíca;Fil: Sadoshima, Junichi. No especifíca;Fil: Schreiber, Stuart L.. No especifíca;Fil: Scott, Frederick. No especifíca;Fil: Sebti, Salwa. No especifíca;Fil: Shiloh, Michael. No especifíca;Fil: Shoji, Sanae. No especifíca;Fil: Simonsen, Anne. No especifíca;Fil: Smith, Haley. No especifíca;Fil: Sumpter, Kathryn M.. No especifíca;Fil: Thompson, Craig B.. No especifíca;Fil: Thorburn, Andrew. No especifíca;Fil: Thumm, Michael. No especifíca;Fil: Tooze, Sharon. No especifíca;Fil: Vaccaro, Maria Ines. Consejo Nacional de Investigaciones Científicas y Técnicas. Oficina de Coordinación Administrativa Houssay. Instituto de Bioquímica y Medicina Molecular. Universidad de Buenos Aires. Facultad Medicina. Instituto de Bioquímica y Medicina Molecular; ArgentinaFil: Virgin, Herbert W.. No especifíca;Fil: Wang, Fei. No especifíca;Fil: White, Eileen. No especifíca;Fil: Xavier, Ramnik J.. No especifíca;Fil: Yoshimori, Tamotsu. No especifíca;Fil: Yuan, Junying. No especifíca;Fil: Yue, Zhenyu. No especifíca;Fil: Zhong, Qing. No especifíca

Sex-stratified Genome-wide Association Studies Including 270,000 Individuals Show Sexual Dimorphism in Genetic Loci for Anthropometric Traits

Peer reviewe

Multiorgan MRI findings after hospitalisation with COVID-19 in the UK (C-MORE): a prospective, multicentre, observational cohort study

Introduction: The multiorgan impact of moderate to severe coronavirus infections in the post-acute phase is still poorly understood. We aimed to evaluate the excess burden of multiorgan abnormalities after hospitalisation with COVID-19, evaluate their determinants, and explore associations with patient-related outcome measures. Methods: In a prospective, UK-wide, multicentre MRI follow-up study (C-MORE), adults (aged ≥18 years) discharged from hospital following COVID-19 who were included in Tier 2 of the Post-hospitalisation COVID-19 study (PHOSP-COVID) and contemporary controls with no evidence of previous COVID-19 (SARS-CoV-2 nucleocapsid antibody negative) underwent multiorgan MRI (lungs, heart, brain, liver, and kidneys) with quantitative and qualitative assessment of images and clinical adjudication when relevant. Individuals with end-stage renal failure or contraindications to MRI were excluded. Participants also underwent detailed recording of symptoms, and physiological and biochemical tests. The primary outcome was the excess burden of multiorgan abnormalities (two or more organs) relative to controls, with further adjustments for potential confounders. The C-MORE study is ongoing and is registered with ClinicalTrials.gov, NCT04510025. Findings: Of 2710 participants in Tier 2 of PHOSP-COVID, 531 were recruited across 13 UK-wide C-MORE sites. After exclusions, 259 C-MORE patients (mean age 57 years [SD 12]; 158 [61%] male and 101 [39%] female) who were discharged from hospital with PCR-confirmed or clinically diagnosed COVID-19 between March 1, 2020, and Nov 1, 2021, and 52 non-COVID-19 controls from the community (mean age 49 years [SD 14]; 30 [58%] male and 22 [42%] female) were included in the analysis. Patients were assessed at a median of 5·0 months (IQR 4·2–6·3) after hospital discharge. Compared with non-COVID-19 controls, patients were older, living with more obesity, and had more comorbidities. Multiorgan abnormalities on MRI were more frequent in patients than in controls (157 [61%] of 259 vs 14 [27%] of 52; p<0·0001) and independently associated with COVID-19 status (odds ratio [OR] 2·9 [95% CI 1·5–5·8]; padjusted=0·0023) after adjusting for relevant confounders. Compared with controls, patients were more likely to have MRI evidence of lung abnormalities (p=0·0001; parenchymal abnormalities), brain abnormalities (p<0·0001; more white matter hyperintensities and regional brain volume reduction), and kidney abnormalities (p=0·014; lower medullary T1 and loss of corticomedullary differentiation), whereas cardiac and liver MRI abnormalities were similar between patients and controls. Patients with multiorgan abnormalities were older (difference in mean age 7 years [95% CI 4–10]; mean age of 59·8 years [SD 11·7] with multiorgan abnormalities vs mean age of 52·8 years [11·9] without multiorgan abnormalities; p<0·0001), more likely to have three or more comorbidities (OR 2·47 [1·32–4·82]; padjusted=0·0059), and more likely to have a more severe acute infection (acute CRP >5mg/L, OR 3·55 [1·23–11·88]; padjusted=0·025) than those without multiorgan abnormalities. Presence of lung MRI abnormalities was associated with a two-fold higher risk of chest tightness, and multiorgan MRI abnormalities were associated with severe and very severe persistent physical and mental health impairment (PHOSP-COVID symptom clusters) after hospitalisation. Interpretation: After hospitalisation for COVID-19, people are at risk of multiorgan abnormalities in the medium term. Our findings emphasise the need for proactive multidisciplinary care pathways, with the potential for imaging to guide surveillance frequency and therapeutic stratification

The exceptional manager: making the difference

How do businesses go beyond prescriptive policies and make the shift from the 'low road' of cost to the 'high road' of innovation and value? This ground-breaking book gives a clear analysis of the context and the challenges, and offers managers and consultants a range of ideas that could take their companies well beyond 'business as usual'