The rise, fall and resurrection of chemical‐induced resistance agents

Since the discovery that the plant immune system could be augmented for improved deployment against biotic stressors through the exogenous application of chemicals that lead to induced resistance (IR), many such IR‐eliciting agents have been identified. Initially it was hoped that these chemical IR agents would be a benign alternative to traditional chemical biocides. However, owing to low efficacy and/or a realization that their benefits sometimes come at the cost of growth and yield penalties, chemical IR agents fell out of favour and were seldom used as crop protection products. Despite the lack of interest in agricultural use, researchers have continued to explore the efficacy and mechanisms of chemical IR. Moreover, as we move away from the approach of ‘zero tolerance’ toward plant pests and pathogens toward integrated pest management, chemical IR agents could have a place in the plant protection product list. In this review, we chart the rise and fall of chemical IR agents, and then explore a variety of strategies used to improve their efficacy and remediate their negative adverse effects

Total prompt γ

The total prompt γ-ray energy distributions for the neutron-induced fission of 235U, 239,241Pu at incident neutron energy of 0.025 eV ‒ 100 keV, and the spontaneous fission of 252Cf were measured using the Detector for Advanced Neutron Capture Experiments (DANCE) array in coincidence with the detection of fission fragments by a parallel-plate avalanche counter. DANCE is a highly segmented, highly efficient 4π γ-ray calorimeter. Corrections were made to the measured distribution by unfolding the two-dimension spectrum of total γ-ray energy vs multiplicity using a simulated DANCE response matrix. The mean values of the total prompt γ-ray energy, determined from the unfolded distributions, are ~ 20% higher than those derived from measurements using single γ-ray detector for all the fissile nuclei studied. This raises serious concern on the validity of the mean total prompt γ-ray energy obtained from the product of mean values for both prompt γ-ray energy and multiplicity

Explosive volcanic activity on Venus: The roles of volatile contribution, degassing, and external environment

We investigate the conditions that will promote explosive volcanic activity on Venus. Conduit processes were simulated using a steady-state, isothermal, homogeneous flow model in tandem with a degassing model. The response of exit pressure, exit velocity, and degree of volatile exsolution was explored over a range of volatile concentrations (H2O and CO2), magma temperatures, vent altitudes, and conduit geometries relevant to the Venusian environment. We find that the addition of CO2 to an H2O-driven eruption increases the final pressure, velocity, and volume fraction gas. Increasing vent elevation leads to a greater degree of magma fragmentation, due to the decrease in the final pressure at the vent, resulting in a greater likelihood of explosive activity. Increasing the magmatic temperature generates higher final pressures, greater velocities, and lower final volume fraction gas values with a correspondingly lower chance of explosive volcanism. Cross-sectionally smaller, and/or deeper, conduits were more conducive to explosive activity. Model runs show that for an explosive eruption to occur at Scathach Fluctus, at Venus’ mean planetary radius (MPR), 4.5% H2O or 3% H2O with 3% CO2 (from a 25 m radius conduit) would be required to initiate fragmentation; at Ma’at Mons (~9 km above MPR) only ~2% H2O is required. A buoyant plume model was used to investigate plume behaviour. It was found that it was not possible to achieve a buoyant column from a 25 m radius conduit at Scathach Fluctus, but a buoyant column reaching up to ~20 km above the vent could be generated at Ma’at Mons with an H2O concentration of 4.7% (at 1300 K) or a mixed volatile concentration of 3% H2O with 3% CO2 (at 1200 K). We also estimate the flux of volcanic gases to the lower atmosphere of Venus, should explosive volcanism occur. Model results suggest explosive activity at Scathach Fluctus would result in an H2O flux of ~107 kg s-1. Were Scathach Fluctus emplaced in a single event, our model suggests that it may have been emplaced in a period of ~15 days, supplying 1-2 x 104 Mt H2O to the atmosphere locally. An eruption of this scale might increase local atmospheric H2O abundance by several ppm over an area large enough to be detectable by near-infrared nightside sounding using the 1.18 µm spectral window such as that carried out by the Venus Express/VIRTIS spectrometer. Further interrogation of the VIRTIS dataset is recommended to search for ongoing volcanism on Venus

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