Questioning ten common assumptions about peatlands

Peatlands have been widely studied in terms of their ecohydrology, carbon dynamics, ecosystem services and palaeoenvironmental archives. However, several assumptions are frequently made about peatlands in the academic literature, practitioner reports and the popular media which are either ambiguous or in some cases incorrect. Here we discuss the following ten common assumptions about peatlands: 1. the northern peatland carbon store will shrink under a warming climate; 2. peatlands are fragile ecosystems; 3. wet peatlands have greater rates of net carbon accumulation; 4. different rules apply to tropical peatlands; 5. peat is a single soil type; 6. peatlands behave like sponges; 7. Sphagnum is the main ‘ecosystem engineer’ in peatlands; 8. a single core provides a representative palaeo-archive from a peatland; 9. water-table reconstructions from peatlands provide direct records of past climate change; and 10. restoration of peatlands results in the re-establishment of their carbon sink function. In each case we consider the evidence supporting the assumption and, where appropriate, identify its shortcomings or ways in which it may be misleading

Whole genome analysis of a schistosomiasis-transmitting freshwater snail

Biomphalaria snails are instrumental in transmission of the human blood fluke Schistosoma mansoni. With the World Health Organization's goal to eliminate schistosomiasis as a global health problem by 2025, there is now renewed emphasis on snail control. Here, we characterize the genome of Biomphalaria glabrata, a lophotrochozoan protostome, and provide timely and important information on snail biology. We describe aspects of phero-perception, stress responses, immune function and regulation of gene expression that support the persistence of B. glabrata in the field and may define this species as a suitable snail host for S. mansoni. We identify several potential targets for developing novel control measures aimed at reducing snail-mediated transmission of schistosomiasis

Basic Methods for Computing Special Functions

This paper gives an overview of methods for the numerical evaluation of special functions, that is, the functions that arise in many problems from mathematical physics, engineering, probability theory, and other applied sciences. We consider in detail a selection of basic methods which are frequently used in the numerical evaluation of special functions: converging and asymptotic series, including Chebyshev expansions, linear recurrence relations, and numerical quadrature. Several other methods are available and some of these will be discussed in less detail. We give examples of recent software for special functions where these methods are used. We mention a list of new publications on computational aspects of special functions available on our website

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