44 research outputs found

    Sporopollenin chemistry and its durability in the geological record: an integration of extant and fossil chemical data across the seed plants.

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    Sporopollenin is a highly resistant biopolymer that forms the outer wall of pollen and spores (sporomorphs). Recent research into sporopollenin chemistry has opened up a range of new avenues for palynological research, including chemotaxonomic classification of morphologically cryptic taxa. However, there have been limited attempts to directly integrate extant and fossil sporopollenin chemical data. Of particular importance is the impact of sample processing to isolate sporopollenin from fresh sporomorphs, and the extent of chemical changes that occur once sporomorphs enter the geological record. Here, we explore these issues using Fourier transform infrared (FTIR) microspectroscopy data from extant and fossil grass, Nitraria (a steppe plant), and conifer pollen. We show a 98% classification success rate at subfamily level with extant grass pollen, demonstrating a strong taxonomic signature in isolated sporopollenin. However, we also reveal substantial chemical differences between extant and fossil sporopollenin, which can be tied to both early diagenetic changes acting on the sporomorphs and chemical derivates of sample processing. Our results demonstrate that directly integrating extant and late Quaternary chemical data should be tractable as long as comparable sample processing routines are maintained. Consistent differences between extant and deeper time sporomorphs, however, suggests that classifying fossil specimens using extant training sets will be challenging. Further work is therefore required to understand and simulate the effects of diagenetic processes on sporopollenin chemistry

    Accretion, Outflows, and Winds of Magnetized Stars

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    Many types of stars have strong magnetic fields that can dynamically influence the flow of circumstellar matter. In stars with accretion disks, the stellar magnetic field can truncate the inner disk and determine the paths that matter can take to flow onto the star. These paths are different in stars with different magnetospheres and periods of rotation. External field lines of the magnetosphere may inflate and produce favorable conditions for outflows from the disk-magnetosphere boundary. Outflows can be particularly strong in the propeller regime, wherein a star rotates more rapidly than the inner disk. Outflows may also form at the disk-magnetosphere boundary of slowly rotating stars, if the magnetosphere is compressed by the accreting matter. In isolated, strongly magnetized stars, the magnetic field can influence formation and/or propagation of stellar wind outflows. Winds from low-mass, solar-type stars may be either thermally or magnetically driven, while winds from massive, luminous O and B type stars are radiatively driven. In all of these cases, the magnetic field influences matter flow from the stars and determines many observational properties. In this chapter we review recent studies of accretion, outflows, and winds of magnetized stars with a focus on three main topics: (1) accretion onto magnetized stars; (2) outflows from the disk-magnetosphere boundary; and (3) winds from isolated massive magnetized stars. We show results obtained from global magnetohydrodynamic simulations and, in a number of cases compare global simulations with observations.Comment: 60 pages, 44 figure

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

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    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
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