TRY plant trait database – enhanced coverage and open access

Plant traits—the morphological, anatomical, physiological, biochemical and phenological characteristics of plants—determine how plants respond to environmental factors, affect other trophic levels, and influence ecosystem properties and their benefits and detriments to people. Plant trait data thus represent the basis for a vast area of research spanning from evolutionary biology, community and functional ecology, to biodiversity conservation, ecosystem and landscape management, restoration, biogeography and earth system modelling. Since its foundation in 2007, the TRY database of plant traits has grown continuously. It now provides unprecedented data coverage under an open access data policy and is the main plant trait database used by the research community worldwide. Increasingly, the TRY database also supports new frontiers of trait‐based plant research, including the identification of data gaps and the subsequent mobilization or measurement of new data. To support this development, in this article we evaluate the extent of the trait data compiled in TRY and analyse emerging patterns of data coverage and representativeness. Best species coverage is achieved for categorical traits—almost complete coverage for ‘plant growth form’. However, most traits relevant for ecology and vegetation modelling are characterized by continuous intraspecific variation and trait–environmental relationships. These traits have to be measured on individual plants in their respective environment. Despite unprecedented data coverage, we observe a humbling lack of completeness and representativeness of these continuous traits in many aspects. We, therefore, conclude that reducing data gaps and biases in the TRY database remains a key challenge and requires a coordinated approach to data mobilization and trait measurements. This can only be achieved in collaboration with other initiatives

Ten-minute umbilical cord occlusion markedly reduces cerebral blood flow and heat production in fetal sheep.

Contains fulltext : 87158.pdf (publisher's version ) (Closed access)OBJECTIVE: The study was undertaken to determine to what extent a 10-minute total umbilical cord occlusion affects autoregulation of cerebral blood flow and cerebral heat production in the fetus. STUDY DESIGN: In seven chronically catheterized late-gestation fetal sheep (127-131 days' gestation), we studied fetal blood gas, hemodynamic, and thermal responses to 10-minute total umbilical cord occlusion. RESULTS: Ten-minute umbilical cord occlusion resulted in marked hypoxia/ischemia, with oxygen content decreasing from 6.5 +/- 0.4 to 0.6 +/- 0.1 vol% and lactate concentration increasing from 1.8 +/- 0.2 to 10.7 +/- 0.7 mmol/L. During this period, the fetuses showed reductions in heart rate from 163.5 +/- 3.4 to 97.1 +/- 5.4 beats/min, mean arterial pressure from 39.4 +/- 2.1 to 21.2 +/- 2.5 mm Hg, cerebral blood flow from 101.3% +/- 8.9% to 49.7% +/- 10.3%, and cerebral heat production from 95.0% +/- 6.3% to 29.6% +/- 4.8%. During cord occlusion, cerebral blood flow was pressure passive from the fourth minute onward. The reduction in cerebral heat production preceded the reduction in perfusion pressure and cerebral blood flow. Recovery of cerebral blood flow and heat production to control values was incomplete for more than 60 minutes after restoration of umbilical flow. CONCLUSION: Ten-minute total umbilical cord occlusion results in major reductions in cerebral blood flow and heat production. Autoregulation of cerebral blood flow was lost within 4 minutes of occlusion, probably as a result of hypoxia, combined with hypotension. The fact that the reduction in cerebral heat production preceded and exceeded the reduction in blood flow may suggest active down-regulation of cerebral metabolism, the mechanism of which is unclear at present

An Endogenously activated antiviral state restricts SARS-CoV-2 infection in differentiated primary airway epithelial cells

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of the coronavirus disease-19 (COVID-19) pandemic, was identified in late 2019 and caused >5 million deaths by February 2022. To date, targeted antiviral interventions against COVID-19 are limited. The spectrum of SARS-CoV-2 infection ranges from asymptomatic to fatal disease. However, the reasons for varying outcomes to SARS-CoV-2 infection are yet to be elucidated. Here we show that an endogenously activated interferon lambda (IFNλ1) pathway leads to resistance against SARS-CoV-2 infection. Using a well-differentiated primary nasal epithelial cell (WD-PNEC) culture model derived from multiple adult donors, we discovered that susceptibility to SARS-CoV-2 infection, but not respiratory syncytial virus (RSV) infection, varied. One of four donors was resistant to SARS-CoV-2 infection. High baseline IFNλ1 expression levels and associated interferon stimulated genes correlated with resistance to SARS-CoV-2 infection. Inhibition of the JAK/STAT pathway in WD-PNECs with high endogenous IFNλ1 secretion resulted in higher SARS-CoV-2 titres. Conversely, prophylactic IFNλ treatment of WD-PNECs susceptible to infection resulted in reduced viral titres. An endogenously activated IFNλ response, possibly due to genetic differences, may be one explanation for the differences in susceptibility to SARS-CoV-2 infection in humans. Importantly, our work supports the continued exploration of IFNλ as a potential pharmaceutical against SARS-CoV-2 infection