Phylogenetic placement and the timing of diversification in Australia's endemic Vachellia (Caesalpinioideae, Mimosoid Clade, Fabaceae) species

The genus Vachellia Wight & Arn. has a pantropical distribution, with species being distributed through Africa, the Americas, Asia and Australia. The relationships among the lineages from Africa and America are well understood, but the phylogenetic placement and evolutionary origins of the Australian species of Vachellia are not known. We, therefore, sequenced four plastid genes from representatives of each of the nine Australian species of Vachellia, and used Bayesian inference to assess the phylogenetic placement of these lineages, and a relaxed molecular clock to assess the timing of diversification. The Australian species of Vachellia form a well-supported monophyletic clade, with molecular-dating analysis suggesting a single dispersal into Australia 6.5 million years ago (95% range 13.9-2.7 million years ago). Diversification of the Australian clade commenced more recently, c. 3.1 million years ago (95% range 9.2-1.2 million years ago), perhaps driven by the increased aridification of Australia at this time. The closest relatives to the Australian Vachellia were not from the Malesian bioregion, suggesting either a long-distance dispersal from Africa, or two separate migrations through Asia. These results not only improve our understanding of the biogeography of Vachellia species, but also have significant implications for the biological control of invasive Vachellia species in Australia. © 2020 CSIRO

The flyby anomaly: a multivariate analysis approach

[EN] The flyby anomaly is the unexpected variation of the asymptotic post-encounter velocity of a spacecraft with respect to the pre-encounter velocity as it performs a slingshot manoeuvre. This effect has been detected in, at least, six flybys of the Earth but it has not appeared in other recent flybys. In order to find a pattern in these, apparently contradictory, data several phenomenological formulas have been proposed but all have failed to predict a new result in agreement with the observations. In this paper we use a multivariate dimensional analysis approach to propose a fitting of the data in terms of the local parameters at perigee, as it would occur if this anomaly comes from an unknown fifth force with latitude dependence. Under this assumption, we estimate the range of this force around 300 km .Acedo Rodríguez, L. (2017). The flyby anomaly: a multivariate analysis approach. Astrophysics and Space Science. 362(2):1-7. doi:10.1007/s10509-017-3025-zS173622Acedo, L.: Adv. 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South African guidelines on the determination of death

Death is a medical occurrence that has social, legal, religious and cultural consequences requiring common clinical standards for its diagnosis and legal regulation. This document compiled by the Critical Care Society of Southern Africa outlines the core standards for determination of death in the hospital context. It aligns with the latest evidence-based research and international guidelines and is applicable to the South African context and legal system. The aim is to provide clear medical standards for healthcare providers to follow in the determination of death, thereby promoting safe practices and high-quality care through the use of uniform standards. Adherence to such guidelines will provide assurance to medical staff, patients, their families and the South African public that the determination of death is always undertaken with diligence, integrity, respect and compassion, and is in accordance with accepted medical standards and latest scientific evidence. The consensus guidelines were compiled using the AGREE II checklist with an 18-member expert panel participating in a three-round modified Delphi process. Checklists and advice sheets were created to assist with application of these guidelines in the clinical environmenAlso published as: Thomson, D., Joubert, I., De Vasconcellos, K. et al. South African guidelines on the determination of death. Southern African Journal of Critical Care 2021, vol. 37, no. 1b, pp. 41-54. https://doi.org/10.7196/SAJCC.2021v37i1b.466.The Critical Care Society of Southern Africa (CCSSA)http://www.samj.org.zahttp://www.sajcc.org.zadm2022Critical CareNursing ScienceSurger

Parental origin of sequence variants associated with complex diseases

To access publisher full text version of this article. Please click on the hyperlink in Additional Links fieldEffects of susceptibility variants may depend on from which parent they are inherited. Although many associations between sequence variants and human traits have been discovered through genome-wide associations, the impact of parental origin has largely been ignored. Here we show that for 38,167 Icelanders genotyped using single nucleotide polymorphism (SNP) chips, the parental origin of most alleles can be determined. For this we used a combination of genealogy and long-range phasing. We then focused on SNPs that associate with diseases and are within 500 kilobases of known imprinted genes. Seven independent SNP associations were examined. Five-one with breast cancer, one with basal-cell carcinoma and three with type 2 diabetes-have parental-origin-specific associations. These variants are located in two genomic regions, 11p15 and 7q32, each harbouring a cluster of imprinted genes. Furthermore, we observed a novel association between the SNP rs2334499 at 11p15 and type 2 diabetes. Here the allele that confers risk when paternally inherited is protective when maternally transmitted. We identified a differentially methylated CTCF-binding site at 11p15 and demonstrated correlation of rs2334499 with decreased methylation of that site.info:eu-repo/grantAgreement/EC/FP7/21807

Meta-analysis of type 2 Diabetes in African Americans Consortium

Type 2 diabetes (T2D) is more prevalent in African Americans than in Europeans. However, little is known about the genetic risk in African Americans despite the recent identification of more than 70 T2D loci primarily by genome-wide association studies (GWAS) in individuals of European ancestry. In order to investigate the genetic architecture of T2D in African Americans, the MEta-analysis of type 2 DIabetes in African Americans (MEDIA) Consortium examined 17 GWAS on T2D comprising 8,284 cases and 15,543 controls in African Americans in stage 1 analysis. Single nucleotide polymorphisms (SNPs) association analysis was conducted in each study under the additive model after adjustment for age, sex, study site, and principal components. Meta-analysis of approximately 2.6 million genotyped and imputed SNPs in all studies was conducted using an inverse variance-weighted fixed effect model. Replications were performed to follow up 21 loci in up to 6,061 cases and 5,483 controls in African Americans, and 8,130 cases and 38,987 controls of European ancestry. We identified three known loci (TCF7L2, HMGA2 and KCNQ1) and two novel loci (HLA-B and INS-IGF2) at genome-wide significance (4.15 × 10(-94)<P<5 × 10(-8), odds ratio (OR)  = 1.09 to 1.36). Fine-mapping revealed that 88 of 158 previously identified T2D or glucose homeostasis loci demonstrated nominal to highly significant association (2.2 × 10(-23) < locus-wide P<0.05). These novel and previously identified loci yielded a sibling relative risk of 1.19, explaining 17.5% of the phenotypic variance of T2D on the liability scale in African Americans. Overall, this study identified two novel susceptibility loci for T2D in African Americans. A substantial number of previously reported loci are transferable to African Americans after accounting for linkage disequilibrium, enabling fine mapping of causal variants in trans-ethnic meta-analysis studies.Peer reviewe

Novel Loci for Adiponectin Levels and Their Influence on Type 2 Diabetes and Metabolic Traits : A Multi-Ethnic Meta-Analysis of 45,891 Individuals

J. Kaprio, S. Ripatti ja M.-L. Lokki työryhmien jäseniä.Peer reviewe

Measurement of the lifetime of the Bc+B_c^+ meson using the Bc+→J/ψπ+B_c^+\rightarrow J/\psi\pi^+ decay mode

The difference in total widths between the $B_c^+$ and $B^+$ mesons is measured using 3.0fb$^{-1}$ of data collected by the LHCb experiment in 7 and 8 TeV centre-of-mass energy proton-proton collisions at the LHC. Through the study of the time evolution of $B_c^+ \rightarrow J/\psi \pi^+$ and $B^+\rightarrow J/\psi K^+$ decays, the width difference is measured to be $$\Delta\Gamma \equiv \Gamma_{B_c^+} - \Gamma_{B^+} = 4.46 \pm 0.14 \pm 0.07mm^{-1}c,$$ where the first uncertainty is statistical and the second systematic. The known lifetime of the $B^+$ meson is used to convert this to a precise measurement of the $B_c^+$ lifetime, $$\tau_{B_c^+} = 513.4 \pm 11.0 \pm 5.7fs,$$ where the first uncertainty is statistical and the second systematic.Comment: 19 pagers, 3 figure

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