COVID-19 Personal Reflection_Corona Chronicles

COVID-19 experiences of members of an Orono Public Library writing circle compiled by Barbara Wicks as the Corona Chronicles , starting in March 2020. Subsequent issues are included as supplemental content

Coordination changes in liquid tin under shock compression determined using in situ femtosecond x-ray diffraction

Little is known regarding the liquid structure of materials compressed to extreme conditions, and even less is known about liquid structures undergoing rapid compression on nanosecond timescales. Here, we report on liquid structure factor and radial distribution function measurements of tin shock compressed to 84(19) GPa. High-quality, femtosecond x-ray diffraction measurements at the Linac Coherent Light Source were used to extract the liquid diffuse scattering signal. From the radial distribution function, we find that the structural evolution of the liquid with increasing pressure mimics the evolution of the solid phase. With increasing pressure, we find that the liquid structure evolves from a complex structure, with a low coordination number, to a simple liquid structure with a coordination number of 12. We provide a pathway for future experiments to study liquids at elevated pressures using high-energy lasers to shock compress materials beyond the reach of static diamond anvil cell techniques

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 hospitalization2–4 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

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

Synthesis, molecular structure and palladium(II) and platinum(II) complex chemistry of 3-(ferrocen-1-yl)-1-(pyridin-2-yl)pyrazole

Treatment of the potassium salt of 3(5)-(ferrocen-1-yl)pyrazole L1 with 2-bromopyridine in diglyme (2,5,8-trioxononane) at 130 °C for 3 d, followed by an aqueous quench, yielded the compound 3-(ferrocen-1-yl)-1-(pyridin-2-yl)pyrazole L2 in 37% recrystallised yield. A single-crystal structure determination of L2 confirmed the proposed 1,3-disubstitution pattern at the pyrazole ring, the substituted cyclopentadienyl and two heterocyclic rings being approximately coplanar. Treatment of L2 with a stoichiometric amount of [{MCl(C3H5)}x](M = Pd, x= 2; M = Pt, x= 4) and NH4PF6 gave [M(η3-C3H5)(L2)]PF6(M = Pd 1 or Pt 2) while a similar reaction with [PdCl2(NCPh)2] afforded [PdCl2(L2)]3. Treatment of 3 with 1 molar equivalent of K2C2O4, Na2(cat) or Na(acac)–NH4PF6 yielded [Pd(L)L2][L = C2O42–4 or catecholate (cat)5] and [Pd(acac)(L2)]PF66(acac = acetylacetonate) as analytically pure solids. The 1H NMR behaviour of 4–6 is complex and suggestive of extensive ligand dissociation in solution; molecular models imply that this may reflect steric interactions between the pendant ferrocenyl moiety and metal-bound anionic chelate O-donors. The UV/VIS and electrochemical data show that the ferrocenyl group becomes significantly electron-poorer upon co-ordination of L2, reflecting an inductive interaction with the co-ordinated M2+(M = Pd or Pt) electrophiles

Fine-scale nutrient and carbonate system dynamics around cold-water coral reefs in the northeast Atlantic

Ocean acidification has been suggested as a serious threat to the future existence of cold-water corals (CWC). However, there are few fine-scale temporal and spatial datasets of carbonate and nutrients conditions available for these reefs, which can provide a baseline definition of extant conditions. Here we provide observational data from four different sites in the northeast Atlantic that are known habitats for CWC. These habitats differ by depth and by the nature of the coral habitat. At depths where CWC are known to occur across these sites the dissolved inorganic carbon ranged from 2088 to 2186 μmol kg−1, alkalinity ranged from 2299 to 2346 μmol kg−1, and aragonite Ω ranged from 1.35 to 2.44. At two sites fine-scale hydrodynamics caused increased variability in the carbonate and nutrient conditions over daily time-scales. The observed high level of variability must be taken into account when assessing CWC sensitivities to future environmental change

Differential response to abiotic stress controls species distributions at biogeographic transition zones

Understanding range limits is critical to predicting species responses to climate change. Subtropical environments, where many species overlap at their range margins, are cooler, more light-limited and variable than tropical environments. It is thus likely that species respond variably to these multi-stressor regimes and that factors other than mean climatic conditions drive biodiversity patterns. Here, we tested these hypotheses for scleractinian corals at their high-latitude range limits in eastern Australia and investigated the role of mean climatic conditions and of parameters linked to abiotic stress in explaining the distribution and abundance of different groups of species. We found that environmental drivers varied among taxa and were predominantly linked to abiotic stress. The distribution and abundance of tropical species and gradients in species richness (alpha diversity) and turnover (beta diversity) were best explained by light limitation, whereas minimum temperatures and temperature fluctuations best explained gradients in subtropical species, species nestedness and functional diversity. Variation in community structure (considering species composition and abundance) was most closely linked to the combined thermal and light regime. Our study demonstrates the role of abiotic stress in controlling the distribution of species towards their high-latitude range limits and suggests that, at biogeographic transition zones, robust predictions of the impacts of climate change require approaches that account for various aspects of physiological stress and for species abundances and characteristics. These findings support the hypothesis that abiotic stress controls high-latitude range limits and caution that projections solely based on mean temperature could underestimate species’ vulnerabilities to climate change