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The majority of variation in six traits critical to the growth, survival and reproduction of plant species is thought to be organised along just two dimensions, corresponding to strategies of plant size and resource acquisition. However, it is unknown whether global plant trait relationships extend to climatic extremes, and if these interspecific relationships are confounded by trait variation within species. We test whether trait relationships extend to the cold extremes of life on Earth using the largest database of tundra plant traits yet compiled. We show that tundra plants demonstrate remarkably similar resource economic traits, but not size traits, compared to global distributions, and exhibit the same two dimensions of trait variation. Three quarters of trait variation occurs among species, mirroring global estimates of interspecific trait variation. Plant trait relationships are thus generalizable to the edge of global trait-space, informing prediction of plant community change in a warming world.

BACKGROUND: It is well known that health status of paramedics may be altered by their job demands. However, it is unknown whether health conditions have a negative impact on occupational performance. The goal of this study was to explore whether a paramedic’s health status affects performance during a patient-care simulation. More precisely, this paper aims to identify which health conditions (i.e., cardiovascular diseases (CVD), musculoskeletal disorders (MSD), post-traumatic stress disorders (PTSD), generalized anxiety disorders (GAD)) could be associated with negative performance. METHODS: Nineteen paramedics aged 38.2 ± 8.6 years old with 15.0 ± 8.7 years of paramedic experience participated in this study. Participants completed two assessments: i) health conditions measurements and ii) patient-care simulation. Heart rate variability (HRV), an indicator of vagal activity was collected during the patient-care simulation. The simulation was used in order to challenge experienced paramedics in a realistic setting. Based on the provincial standard of New Brunswick, an experienced paramedic instructor graded (passed or failed) the patient-care simulation using the provincial standard charts, videos and data from manikin. RESULTS: The current study suggests that only paramedics with self-reported elevated symptoms of PTSD were less likely to successfully complete the simulated patient-care scenario. An inhibition of the vagal activity was noted during the patient-care simulation among individuals identified with PTSD. No link was observed between physical health conditions (CVD, MSD) and simulated patient-care performance. Overall, paramedics who passed the patient-care simulation presented higher vagal activity during the patient assessment. CONCLUSIONS: This research suggests that the presence of self-reported elevated symptoms of PTSD negatively impacts paramedics’ performance during a stressful work task simulation. Therefore, to help paramedics maintain optimal performance, it may be important to ensure that paramedics have access to appropriate resources to monitor and improve their psychosocial health. Future studies should investigate more complex work tasks with larger sample sizes and more complex simulations.

Background: Frontotemporal dementia is a heterogenous neurodegenerative disorder, with about a third of cases being genetic. Most of this genetic component is accounted for by mutations in GRN, MAPT, and C9orf72. In this study, we aimed to complement previous phenotypic studies by doing an international study of age at symptom onset, age at death, and disease duration in individuals with mutations in GRN, MAPT, and C9orf72. Methods: In this international, retrospective cohort study, we collected data on age at symptom onset, age at death, and disease duration for patients with pathogenic mutations in the GRN and MAPT genes and pathological expansions in the C9orf72 gene through the Frontotemporal Dementia Prevention Initiative and from published papers. We used mixed effects models to explore differences in age at onset, age at death, and disease duration between genetic groups and individual mutations. We also assessed correlations between the age at onset and at death of each individual and the age at onset and at death of their parents and the mean age at onset and at death of their family members. Lastly, we used mixed effects models to investigate the extent to which variability in age at onset and at death could be accounted for by family membership and the specific mutation carried. Findings: Data were available from 3403 individuals from 1492 families: 1433 with C9orf72 expansions (755 families), 1179 with GRN mutations (483 families, 130 different mutations), and 791 with MAPT mutations (254 families, 67 different mutations). Mean age at symptom onset and at death was 49·5 years (SD 10·0; onset) and 58·5 years (11·3; death) in the MAPT group, 58·2 years (9·8; onset) and 65·3 years (10·9; death) in the C9orf72 group, and 61·3 years (8·8; onset) and 68·8 years (9·7; death) in the GRN group. Mean disease duration was 6·4 years (SD 4·9) in the C9orf72 group, 7·1 years (3·9) in the GRN group, and 9·3 years (6·4) in the MAPT group. Individual age at onset and at death was significantly correlated with both parental age at onset and at death and with mean family age at onset and at death in all three groups, with a stronger correlation observed in the MAPT group (r=0·45 between individual and parental age at onset, r=0·63 between individual and mean family age at onset, r=0·58 between individual and parental age at death, and r=0·69 between individual and mean family age at death) than in either the C9orf72 group (r=0·32 individual and parental age at onset, r=0·36 individual and mean family age at onset, r=0·38 individual and parental age at death, and r=0·40 individual and mean family age at death) or the GRN group (r=0·22 individual and parental age at onset, r=0·18 individual and mean family age at onset, r=0·22 individual and parental age at death, and r=0·32 individual and mean family age at death). Modelling showed that the variability in age at onset and at death in the MAPT group was explained partly by the specific mutation (48%, 95% CI 35–62, for age at onset; 61%, 47–73, for age at death), and even more by family membership (66%, 56–75, for age at onset; 74%, 65–82, for age at death). In the GRN group, only 2% (0–10) of the variability of age at onset and 9% (3–21) of that of age of death was explained by the specific mutation, whereas 14% (9–22) of the variability of age at onset and 20% (12–30) of that of age at death was explained by family membership. In the C9orf72 group, family membership explained 17% (11–26) of the variability of age at onset and 19% (12–29) of that of age at death. Interpretation: Our study showed that age at symptom onset and at death of people with genetic frontotemporal dementia is influenced by genetic group and, particularly for MAPT mutations, by the specific mutation carried and by family membership. Although estimation of age at onset will be an important factor in future pre-symptomatic therapeutic trials for all three genetic groups, our study suggests that data from other members of the family will be particularly helpful only for individuals with MAPT mutations. Further work in identifying both genetic and environmental factors that modify phenotype in all groups will be important to improve such estimates. Funding: UK Medical Research Council, National Institute for Health Research, and Alzheimer's Society. © 2020 Elsevier Ltd

Summary Objective Studies examining associations between movement behaviours (i.e. physical activity, sedentary behaviour and sleep duration) and obesity focus on average values of these movement behaviours, despite important within‐country and between‐country variability. A better understanding of movement behaviour inequalities is important for developing public health policies and behaviour‐change interventions. The objective of this ecologic analysis at the country level was to determine if inequality in movement behaviours is a better correlate of obesity than average movement behaviour volume in children from all inhabited continents of the world. Methods This multinational, cross‐sectional study included 6,128 children 9–11 years of age. Moderate‐to‐vigorous physical activity (MVPA), total sedentary time (SED) and sleep period time were monitored over 7 consecutive days using waist‐worn accelerometry. Screen time was self‐reported. Inequality in movement behaviours was determined using Gini coefficients (ranging from 0 [complete equality] to 1 [complete inequality]). Results The largest inequality in movement behaviours was observed for screen time (Gini of 0.32; medium inequality), followed by MVPA (Gini of 0.21; low inequality), SED (Gini of 0.07; low inequality) and sleep period time (Gini of 0.05; low inequality). Average MVPA (h d−1) was a better correlate of obesity than MVPA inequality (r = −0.77 vs. r = 0.00, p = 0.03). Average SED (h d−1) was also a better correlate of obesity than SED inequality (r = 0.52 vs. r = −0.32, p = 0.05). Differences in associations for screen time and sleep period time were not statistically significant. MVPA in girls was found to be disproportionally lower in countries with more MVPA inequality. Conclusions Findings from this study show that average MVPA and SED should continue to be used in population health studies of children as they are better correlates of obesity than inequality in these behaviours. Moreover, the findings suggest that MVPA inequality could be greatly reduced through increases in girls' MVPA alone.

For patients with incurable neurodegenerative disorders\ud such as Huntington’s (HD) and Parkinson’s disease,\ud cell transplantation has been explored as a potential\ud treatment option. Here, we present the first clinicopathological study of a patient with HD in receipt of\ud cell-suspension striatal allografts who took part in the\ud NEST-UK multicenter clinical transplantation trial. Using\ud various immunohistochemical techniques, we found a\ud discrepancy in the survival of grafted projection neurons\ud with respect to grafted interneurons as well as\ud major ongoing inflammatory and immune responses to\ud the grafted tissue with evidence of mutant huntingtin\ud aggregates within the transplant area. Our results indicate\ud that grafts can survive more than a decade posttransplantation,\ud but show compromised survival with\ud inflammation and mutant protein being observed\ud within the transplant site.