Ranges of critical temperature and water potential values for the germination of species worldwide: Contribution to a seed trait database

Germination is the first essential stage in crop and food production, as well as for the establishment of trees and regeneration of wild species. Temperature and water potential are the primary environmental factors that control germination in all species, and affect both the rate and final percentage germination. A comprehensive description of intra- and inter-variations between groups of species (perennials and annuals, trees, grasses, crops and wild species) helps understand where these species are currently able to grow on earth and will be in the future. By collecting germination trait data on 243 species from the literature and unpublished data, we provide a wide spectrum of species’ seed germination traits, in the form of a set of parameter values describing germination responses to variations in temperature and water potential. Major differences in germination traits were seen to depend on the climatic conditions where the species grow or originated, with species able to germinate on ice and others unable to germinate below 18 °C. By contrast, within the different plant groups, similar ranges of threshold values were found, linked to the species geo-climatic origin. Crops however germinate faster, their range of threshold temperatures and water potential values is wider, and some crops have higher optimum and maximum temperatures as well as lower water potential threshold values. This is likely the result of human selection for rapid germination and for species able to grow in the wide range of environmental conditions where agriculture was developed. Our analyses revealed correlation between traits: negative correlations appeared between germination speed and temperature thresholds, and between temperature and water potential thresholds. The collected data also form a valuable database, enabling plant establishment to be better taken into account in modeling and simulation studies of vegetation boundaries (wild or cultivated) under changing land-use and climate

Association of physical health multimorbidity with mortality in people with schizophrenia spectrum disorders: Using a novel semantic search system that captures physical diseases in electronic patient records

OBJECTIVE Single physical comorbidities have been associated with the premature mortality in people with schizophrenia-spectrum disorders (SSD). We investigated the association of physical multimorbidity (≥two physical health conditions) with mortality in people with SSD. METHODS A retrospective cohort study between 2013 and 2017. All people with a diagnosis of SSD (ICD-10: F20–F29), who had contact with secondary mental healthcare within South London during 2011–2012 were included. A novel semantic search system captured conditions from electronic mental health records, and all-cause mortality were retrieved. Hazard ratios (HRs) and population attributable fractions (PAFs) were calculated for associations between physical multimorbidity and all-cause mortality. RESULTS Among the 9775 people with SSD (mean (SD) age, 45.9 (15.4); males, 59.3%), 6262 (64%) had physical multimorbidity, and 880 (9%) died during the 5-year follow-up. The top three physical multimorbidity combinations with highest mortality were cardiovascular-respiratory (HR: 2.23; 95% CI, 1.49–3.32), respiratory-skin (HR: 2.06; 95% CI, 1.31–3.24), and respiratory-digestive (HR: 1.88; 95% CI, 1.14–3.11), when adjusted for age, gender, and all other physical disease systems. Combinations of physical diseases with highest PAFs were cardiovascular-respiratory (PAF: 35.7%), neurologic-respiratory (PAF: 32.7%), as well as respiratory-skin (PAF: 29.8%). CONCLUSIONS Approximately 2/3 of patients with SSD had physical multimorbidity and the risk of mortality in these patients was further increased compared to those with none or single physical conditions. These findings suggest that in order to reduce the physical health burden and subsequent mortality in people with SSD, proactive coordinated prevention and management efforts are required and should extend beyond the current focus on single physical comorbidities

Effects of sleep deprivation on neural functioning: an integrative review

Sleep deprivation has a broad variety of effects on human performance and neural functioning that manifest themselves at different levels of description. On a macroscopic level, sleep deprivation mainly affects executive functions, especially in novel tasks. Macroscopic and mesoscopic effects of sleep deprivation on brain activity include reduced cortical responsiveness to incoming stimuli, reflecting reduced attention. On a microscopic level, sleep deprivation is associated with increased levels of adenosine, a neuromodulator that has a general inhibitory effect on neural activity. The inhibition of cholinergic nuclei appears particularly relevant, as the associated decrease in cortical acetylcholine seems to cause effects of sleep deprivation on macroscopic brain activity. In general, however, the relationships between the neural effects of sleep deprivation across observation scales are poorly understood and uncovering these relationships should be a primary target in future research

Whole-genome sequencing reveals host factors underlying critical COVID-19

Critical COVID-19 is caused by immune-mediated inflammatory lung injury. Host genetic variation influences the development of illness requiring critical care1 or hospitalization2,3,4 after infection with SARS-CoV-2. The GenOMICC (Genetics of Mortality in Critical Care) study enables the comparison of genomes from individuals who are critically ill with those of population controls to find underlying disease mechanisms. Here we use whole-genome sequencing in 7,491 critically ill individuals compared with 48,400 controls to discover and replicate 23 independent variants that significantly predispose to critical COVID-19. We identify 16 new independent associations, including variants within genes that are involved in interferon signalling (IL10RB and PLSCR1), leucocyte differentiation (BCL11A) and blood-type antigen secretor status (FUT2). Using transcriptome-wide association and colocalization to infer the effect of gene expression on disease severity, we find evidence that implicates multiple genes—including reduced expression of a membrane flippase (ATP11A), and increased expression of a mucin (MUC1)—in critical disease. Mendelian randomization provides evidence in support of causal roles for myeloid cell adhesion molecules (SELE, ICAM5 and CD209) and the coagulation factor F8, all of which are potentially druggable targets. Our results are broadly consistent with a multi-component model of COVID-19 pathophysiology, in which at least two distinct mechanisms can predispose to life-threatening disease: failure to control viral replication; or an enhanced tendency towards pulmonary inflammation and intravascular coagulation. We show that comparison between cases of critical illness and population controls is highly efficient for the detection of therapeutically relevant mechanisms of disease

Analysis of oilseeds, fats and fatty foods/Edit.: J.B. Rossell

xii, 558 hal: ill., tab; 21 cm

Analysis of oilseeds, fats and fatty foods/Edit.: J.B. Rossell

xii, 558 hal: ill., tab; 21 cm