Improving driver behaviour by design : a cognitive work analysis methodology

Within the European Community both the environmental and safety costs of road transport are unacceptably high. ‘Foot-LITE’ is a UK project which aims to encourage drivers to adopt ‘greener’ and safer driving practices, with real-time and retrospective feedback being given both in-vehicle and off-line. This paper describes the early concept development of Foot-LITE, for which a Cognitive Work Analysis (CWA) was conducted. In this paper, we present the results of the first phase of CWA – the Work Domain Analysis, as well as some concept interface designs based on the WDA to illustrate its application. In summary, the CWA establishes a common framework for the project, and will ultimately contribute to the design of the in-vehicle interface

Detection, attribution, and sensitivity of trends toward earlier streamflow in the Sierra Nevada

Observed changes in the timing of snowmelt dominated streamflow in the western United States are often linked to anthropogenic or other external causes. We assess whether observed streamflow timing changes can be statistically attributed to external forcing, or whether they still lie within the bounds of natural (internal) variability for four large Sierra Nevada (CA) basins, at inflow points to major reservoirs. Streamflow timing is measured by “center timing” (CT), the day when half the annual flow has passed a given point. We use a physically based hydrology model driven by meteorological input from a global climate model to quantify the natural variability in CT trends. Estimated 50-year trends in CT due to natural climate variability often exceed estimated actual CT trends from 1950 to 1999. Thus, although observed trends in CT to date may be statistically significant, they cannot yet be statistically attributed to external influences on climate. We estimate that projected CT changes at the four major reservoir inflows will, with 90% confidence, exceed those from natural variability within 1–4 decades or 4–8 decades, depending on rates of future greenhouse gas emissions. To identify areas most likely to exhibit CT changes in response to rising temperatures, we calculate changes in CT under temperature increases from 1 to 5°. We find that areas with average winter temperatures between −2°C and −4°C are most likely to respond with significant CT shifts. Correspondingly, elevations from 2000 to 2800 m are most sensitive to temperature increases, with CT changes exceeding 45 days (earlier) relative to 1961–1990

Football’s InfluencE on Lifelong health and Dementia risk (FIELD): protocol for a retrospective cohort study of former professional footballers

Introduction: In the past decade, evidence has emerged suggesting a potential link between contact sport participation and increased risk of late neurodegenerative disease, in particular chronic traumatic encephalopathy. While there remains a lack of clear evidence to test the hypothesis that contact sport participation is linked to an increased incidence of dementia, there is growing public concern regarding the risk. There is, therefore, a pressing need for research to gain greater understanding of the potential risks involved in contact sports participation, and to contextualise these within holistic health benefits of sport. Methods and analysis: Football’s InfluencE on Lifelong health and Dementia risk is designed as a retrospective cohort study, with the aim to analyse data from former professional footballers (FPF) in order to assess the incidence of neurodegenerative disease in this population. Comprehensive electronic medical and death records will be analysed and compared with those of a demographically matched population control cohort. As well as neurodegenerative disease incidence, all-cause, and disease-specific mortality, will be analysed in order to assess lifelong health. Cox proportional hazards models will be run to compare the data collected from FPFs to matched population controls. Ethics and dissemination: Approvals for study have been obtained from the University of Glasgow College of Medical, Veterinary and Life Sciences Research Ethics Committee (Project Number 200160147) and from National Health Service Scotland’s Public Benefits and Privacy Panel (Application 1718-0120)

Neurodegenerative disease mortality among former professional soccer players

Background: Neurodegenerative disorders have been reported in elite athletes who participated in contact sports. The incidence of neurodegenerative disease among former professional soccer players has not been well characterized. Methods: We conducted a retrospective cohort study to compare mortality from neurodegenerative disease among 7676 former professional soccer players (identified from databases of Scottish players) with that among 23,028 controls from the general population who were matched to the players on the basis of sex, age, and degree of social deprivation. Causes of death were determined from death certificates. Data on medications dispensed for the treatment of dementia in the two cohorts were also compared. Prescription information was obtained from the national Prescribing Information System. Results: Over a median of 18 years, 1180 former soccer players (15.4%) and 3807 controls (16.5%) died. All-cause mortality was lower among former players than among controls up to the age of 70 years and was higher thereafter. Mortality from ischemic heart disease was lower among former players than among controls (hazard ratio, 0.80; 95% confidence interval [CI], 0.66 to 0.97; P=0.02), as was mortality from lung cancer (hazard ratio, 0.53; 95% CI, 0.40 to 0.70; P<0.001). Mortality with neurodegenerative disease listed as the primary cause was 1.7% among former soccer players and 0.5% among controls (subhazard ratio [the hazard ratio adjusted for competing risks of death from ischemic heart disease and death from any cancer], 3.45; 95% CI, 2.11 to 5.62; P<0.001). Among former players, mortality with neurodegenerative disease listed as the primary or a contributory cause on the death certificate varied according to disease subtype and was highest among those with Alzheimer’s disease (hazard ratio [former players vs. controls], 5.07; 95% CI, 2.92 to 8.82; P<0.001) and lowest among those with Parkinson’s disease (hazard ratio, 2.15; 95% CI, 1.17 to 3.96; P=0.01). Dementia-related medications were prescribed more frequently to former players than to controls (odds ratio, 4.90; 95% CI, 3.81 to 6.31; P<0.001). Mortality with neurodegenerative disease listed as the primary or a contributory cause did not differ significantly between goalkeepers and outfield players (hazard ratio, 0.73; 95% CI, 0.43 to 1.24; P=0.24), but dementia-related medications were prescribed less frequently to goalkeepers (odds ratio, 0.41; 95% CI, 0.19 to 0.89; P=0.02). Conclusions: In this retrospective epidemiologic analysis, mortality from neurodegenerative disease was higher and mortality from other common diseases lower among former Scottish professional soccer players than among matched controls. Dementia-related medications were prescribed more frequently to former players than to controls. These observations need to be confirmed in prospective matched-cohort studies. (Funded by the Football Association and Professional Footballers’ Association.

Carbon turnover in the water-soluble protein of the adult human lens.

PurposeHuman eye lenses contain cells that persist from embryonic development. These unique, highly specialized fiber cells located at the core (nucleus) of the lens undergo pseudo-apoptosis to become devoid of cell nuclei and most organelles. Ostensibly lacking in protein transcriptional capabilities, it is currently believed that these nuclear fiber cells owe their extreme longevity to the perseverance of highly stable and densely packed crystallin proteins. Maintaining the structural and functional integrity of lenticular proteins is necessary to sustain cellular transparency and proper vision, yet the means by which the lens actually copes with a lifetime of oxidative stress, seemingly without any capacity for protein turnover and repair, is not completely understood. Although many years of research have been predicated upon the assumption that there is no protein turnover or renewal in nuclear fiber cells, we investigated whether or not different protein fractions possess protein of different ages by using the (14)C bomb pulse.MethodsAdult human lenses were concentrically dissected by gently removing the cell layers in water or shaving to the nucleus with a curved micrometer-controlled blade. The cells were lysed, and the proteins were separated into water-soluble and water-insoluble fractions. The small molecules were removed using 3 kDa spin filters. The (14)C/C was measured in paired protein fractions by accelerator mass spectrometry, and an average age for the material within the sample was assigned using the (14)C bomb pulse.ResultsThe water-insoluble fractions possessed (14)C/C ratios consistent with the age of the cells. In all cases, the water-soluble fractions contained carbon that was younger than the paired water-insoluble fraction.ConclusionsAs the first direct evidence of carbon turnover in protein from adult human nuclear fiber cells, this discovery supports the emerging view of the lens nucleus as a dynamic system capable of maintaining homeostasis in part due to intricate protein transport mechanisms and possibly protein repair. This finding implies that the lens plays an active role in the aversion of age-related nuclear (ARN) cataract

Cognitive work analysis for safe and efficient driving

Both the environmental and safety costs of road transport are considered to be unacceptably high. The ‘Foot-LITE’ project aims to encourage drivers to adopt greener and safer driving practices, with real-time feedback being given in-vehicle (during driving) and retrospective feedback off-line (pre- and post-driving). This article focuses on the early concept development of the Foot-LITE system, for which a Cognitive Work Analysis methodology was adopted. Presented are results from a Work Domain Analysis (WDA) conducted to scope the relevant driving domain and to identify the constraints on the system. Besides establishing a common framework and language for the project, the process will ultimately contribute to the design of the in-vehicle interface. This article also suggests an extension to the WDA framework to include novel methods for assessing the priority of lower level nodes and contributions of these nodes to the high-level objectives of the system

Control and Non-Payload Communications (CNPC) Prototype Radio - Generation 2 Security Architecture Lab Test Report

NASA Glenn Research Center, in cooperation with Rockwell Collins, is working to develop a prototype Control and Non-Payload Communications (CNPC) radio platform as part of NASA Integrated Systems Research Program's (ISRP) Unmanned Aircraft Systems (UAS) Integration in the National Airspace System (NAS) project. A primary focus of the project is to work with the FAA and industry standards bodies to build and demonstrate a safe, secure, and efficient CNPC architecture that can be used by industry to evaluate the feasibility of deploying a system using these technologies in an operational capacity. GRC has been working in conjunction with these groups to assess threats, identify security requirements, and to develop a system of standards-based security controls that can be applied to the current GRC prototype CNPC architecture as a demonstration platform. The security controls were integrated into a lab test bed mock-up of the Mobile IPv6 architecture currently being used for NASA flight testing, and a series of network tests were conducted to evaluate the security overhead of the controls compared to the baseline CNPC link without any security. The aim of testing was to evaluate the performance impact of the additional security control overhead when added to the Mobile IPv6 architecture in various modes of operation. The statistics collected included packet captures at points along the path to gauge packet size as the sample data traversed the CNPC network, round trip latency, jitter, and throughput. The effort involved a series of tests of the baseline link, a link with Robust Header Compression (ROHC) and without security controls, a link with security controls and without ROHC, and finally a link with both ROHC and security controls enabled. The effort demonstrated that ROHC is both desirable and necessary to offset the additional expected overhead of applying security controls to the CNPC link

Refining the risk of HTLV-1-associated myelopathy in people living with HTLV-1: identification of a HAM-like phenotype in a proportion of asymptomatic carriers

Up to 3.8% of human T-lymphotropic virus type-1 (HTLV-1)-infected asymptomatic carriers (AC) eventually develop HTLV-1-associated myelopathy (HAM). HAM occurs in patients with high (> 1%) HTLV proviral load (PVL). However, this cut-off includes more than 50% of ACs and therefore the risk needs to be refined. As HAM is additionally characterised by an inflammatory response to HTLV-1, markers of T cell activation (TCA), β2-microglobulin (β2M) and neuronal damage were accessed for the identification of ACs at high risk of HAM. Retrospective analysis of cross-sectional and longitudinal routine clinical data examining differences in TCA (CD4/CD25, CD4/HLA-DR, CD8/CD25 & CD8/HLA-DR), β2M and neurofilament light (NfL) in plasma in ACs with high or low PVL and patients with HAM. Comparison between 74 low PVL ACs, 84 high PVL ACs and 58 patients with HAM revealed a significant, stepwise, increase in TCA and β2M. Construction of receiver operating characteristic (ROC) curves for each of these blood tests generated a profile that correctly identifies 88% of patients with HAM along with 6% of ACs. The 10 ACs with this 'HAM-like' profile had increased levels of NfL in plasma and two developed myelopathy during follow-up, compared to none of the 148 without this viral-immune-phenotype. A viral-immuno-phenotype resembling that seen in patients with HAM identifies asymptomatic carriers who are at increased risk of developing HAM and have markers of subclinical neuronal damage

The first NINDS/NIBIB consensus meeting to define neuropathological criteria for the diagnosis of chronic traumatic encephalopathy.

Chronic traumatic encephalopathy (CTE) is a neurodegeneration characterized by the abnormal accumulation of hyperphosphorylated tau protein within the brain. Like many other neurodegenerative conditions, at present, CTE can only be definitively diagnosed by post-mortem examination of brain tissue. As the first part of a series of consensus panels funded by the NINDS/NIBIB to define the neuropathological criteria for CTE, preliminary neuropathological criteria were used by 7 neuropathologists to blindly evaluate 25 cases of various tauopathies, including CTE, Alzheimer's disease, progressive supranuclear palsy, argyrophilic grain disease, corticobasal degeneration, primary age-related tauopathy, and parkinsonism dementia complex of Guam. The results demonstrated that there was good agreement among the neuropathologists who reviewed the cases (Cohen's kappa, 0.67) and even better agreement between reviewers and the diagnosis of CTE (Cohen's kappa, 0.78). Based on these results, the panel defined the pathognomonic lesion of CTE as an accumulation of abnormal hyperphosphorylated tau (p-tau) in neurons and astroglia distributed around small blood vessels at the depths of cortical sulci and in an irregular pattern. The group also defined supportive but non-specific p-tau-immunoreactive features of CTE as: pretangles and NFTs affecting superficial layers (layers II-III) of cerebral cortex; pretangles, NFTs or extracellular tangles in CA2 and pretangles and proximal dendritic swellings in CA4 of the hippocampus; neuronal and astrocytic aggregates in subcortical nuclei; thorn-shaped astrocytes at the glial limitans of the subpial and periventricular regions; and large grain-like and dot-like structures. Supportive non-p-tau pathologies include TDP-43 immunoreactive neuronal cytoplasmic inclusions and dot-like structures in the hippocampus, anteromedial temporal cortex and amygdala. The panel also recommended a minimum blocking and staining scheme for pathological evaluation and made recommendations for future study. This study provides the first step towards the development of validated neuropathological criteria for CTE and will pave the way towards future clinical and mechanistic studies

Association of field position and career length with risk of neurodegenerative disease in male former professional soccer players

Importance: Neurodegenerative disease mortality is higher among former professional soccer players than general population controls. However, the factors contributing to increased neurodegenerative disease mortality in this population remain uncertain. Objective: To investigate the association of field position, professional career length, and playing era with risk of neurodegenerative disease among male former professional soccer players. Design, Setting, and Participants: This cohort study used population-based health record linkage in Scotland to evaluate risk among 7676 male former professional soccer players born between January 1, 1900, and January 1, 1977, and 23 028 general population control individuals matched by year of birth, sex, and area socioeconomic status providing 1 812 722 person-years of follow-up. Scottish Morbidity Record and death certification data were available from January 1, 1981, to December 31, 2016, and prescribing data were available from January 1, 2009, to December 31, 2016. Database interrogation was performed on December 10, 2018, and data were analyzed between April 2020 and May 2021. Exposures: Participation in men’s soccer at a professional level. Main Outcomes and Measures: Outcomes were obtained by individual-level record linkage to national electronic records of mental health and general hospital inpatient and day-case admissions as well as prescribing information and death certification. Risk of neurodegenerative disease was evaluated between former professional soccer players and matched general population control individuals. Results: In this cohort study of 30 704 male individuals, 386 of 7676 former soccer players (5.0%) and 366 of 23 028 matched population control individuals (1.6%) were identified with a neurodegenerative disease diagnosis (hazard ratio [HR], 3.66; 95% CI, 2.88-4.65; P < .001). Compared with the risk among general population control individuals, risk of neurodegenerative disease was highest for defenders (HR, 4.98; 95% CI, 3.18-7.79; P < .001) and lowest for goalkeepers (HR, 1.83; 95% CI, 0.93-3.60; P = .08). Regarding career length, risk was highest among former soccer players with professional career lengths longer than 15 years (HR, 5.20; 95% CI, 3.17-8.51; P < .001). Regarding playing era, risk remained similar for all players born between 1910 and 1969. Conclusions and Relevance: The differences in risk of neurodegenerative disease observed in this cohort study imply increased risk with exposure to factors more often associated with nongoalkeeper positions, with no evidence this association has changed over the era studied. While investigations to confirm specific factors contributing to increased risk of neurodegenerative disease among professional soccer players are required, strategies directed toward reducing head impact exposure may be advisable in the meantime