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Burnett, A.

Publications and source records attributed to Burnett, A..

5 recordsLinked to original sources

A single freshwater invasion gave rise to the world's dominant freshwater fish group

The ultraspeciose clade Otophysa - catfishes, carps, minnows, tetras, and their kin - accounts for most vertebrate diversity in modern freshwater ecosystems. However, a controversial assemblage of largely-fragmentary marine fossils has led some authors, most recently Liu et al., to advocate parallel freshwater invasions for this otherwise inland lineage. Here, we test this hypothesis under multiple sources of uncertainty. We provide the first phylogenetic analysis of the recently-named marine fossil genus Sooinichthys, resolving it as sister to all modern otophysans. We also find that Santanichthys, long treated as an early marine otophysan, lacks a Weberian apparatus and plausibly belongs outside Ostariophysi entirely. When increasing the taxon and marker sampling of Liu et al.'s genomic dataset, standardizing their ecological coding, accounting for alternative interpretations of important morphological characters, and applying a suite of biogeographic models, we find a marine origin in only 6 of 132 analyses, and only when enforcing fossil placements inconsistent with our own phylogenetic results. We contend that the parallel freshwater invasion hypothesis of otophysan diversification is an artifact of sparse taxon sampling, taphonomic biases, model selection errors, and fossil overinterpretation. The result is a cautionary case for inferences about the cradle of any ancient freshwater clade.

evolutionary biology↗

Palaeoproteomic deconvolution of physical and genetic collagen mixtures

Species identification in palaeoproteomics relies on genome-derived protein sequences which are often poor-quality, and lacks tools to cope with multi-species samples. Here, we address both challenges through the analysis of physical and genetic mixtures. Species that are absent from our database are considered a genetic mixture, i.e. a patchwork of peptides from closely related species. Inversely, various overlapping peptide stretches allow us to resolve complex physical mixtures. This is benchmarked by analysing physical mixtures of modern bone fragments, including genetic mixtures. We illustrate the impact of our approach via a rapid and high-throughput analysis of >2500 bone fragments, revealing the Eemian-era faunal environment around Scladina Cave, including the first Palaeoloxodon antiquus identified at this site. O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=182 SRC="FIGDIR/small/732552v1_ufig1.gif" ALT="Figure 1"> View larger version (67K): org.highwire.dtl.DTLVardef@a33296org.highwire.dtl.DTLVardef@4e4b85org.highwire.dtl.DTLVardef@402290org.highwire.dtl.DTLVardef@9d35b6_HPS_FORMAT_FIGEXP M_FIG C_FIG

biochemistry↗

Palaeoproteomics reveals bovine carcass processing with 6,000-year-old flint tools

Lithic tools are the most abundant cultural artefacts found at prehistoric archaeological sites. Through their study, we can understand essential activities such as hunting, processing of animal carcasses and plant materials, and working of resources such as ochre and bone, as well as broader technological and cultural practices. For the first time, proteomics was applied alongside use-wear and optical microscopy residue analyses, enabling the identification of bovine, plant, and human proteins on faceted tools from the Mesolithic-Neolithic site of Bazel-Sluis, Belgium. This retrieval of identifiable protein from an area with poor organic preservation demonstrates wide-reaching potential for archaeological research, opening a new avenue of investigation into prehistoric lifeways and adding to the growing corpus of evidence accessible through palaeoproteomics. A workflow for future analyses is suggested, based on our integrated sampling strategy requiring no additional tool manipulations.

paleontology↗

Serum Flt3 ligand is a biomarker of progenitor cell mass and prognosis in acute myeloid leukemia

Fms-like tyrosine kinase 3 (Flt3) is a hematopoietic growth factor receptor expressed on lymphomyeloid progenitors and frequently, by AML blasts. Its ligand, Flt3L, has non-hematopoietic and lymphoid origins, is detectable during homeostasis and increases to high levels in states of hypoplasia due to genetic defects or treatment with cytoreductive agents. Measurement of Flt3L by ELISA reveals that Flt3+AML, is associated with depletion of Flt3L to undetectable levels. After induction chemotherapy, Flt3L is restored in patients entering CR, but remains depressed in those with refractory disease. Weekly sampling reveals marked differences in the kinetics of Flt3L response during the first 6 weeks of treatment, proportionate to the clearance of blasts and cellularity of the BM. In the UK NCRI AML17 trial, Flt3L was measured at day 26 in a subgroup of 135 patients with Flt3 mutation randomized to the tyrosine kinase inhibitor lestaurtinib. In these patients, attainment of CR was associated with higher Flt3L at day 26 (Mann-Whitney p < 0.0001). Day 26 Flt3L was also associated with survival: Flt3L [&le;] 291pg/ml was associated with inferior event-free survival; and, Flt3L >1185pg/ml was associated with higher overall survival (p = 0.0119). Serial measurement of Flt3L in patients who had received a hematopoietic stem cell transplant for AML further illustrated the potential value of declining Flt3L to identify relapse. Together these observations suggest that measurement of Flt3L provides a non-invasive estimate of progenitor cell mass in most patients with AML, with the potential to inform clinical decisions.\n\nGraphical abstract\n\nO_FIG O_LINKSMALLFIG WIDTH=151 HEIGHT=200 SRC=\"FIGDIR/small/588319_ufig1.gif\" ALT=\"Figure 1\">\nView larger version (21K):\norg.highwire.dtl.DTLVardef@132f3f3org.highwire.dtl.DTLVardef@2e033eorg.highwire.dtl.DTLVardef@d70598org.highwire.dtl.DTLVardef@b0648a_HPS_FORMAT_FIGEXP M_FIG C_FIG

cancer biology↗

Neutrophil microvesicles drive atherosclerosis by delivering miR-155 to atheroprone endothelium.

Neutrophils have been implicated in the pathogenesis of atherosclerosis, a lipid-driven disease of arteries, but they are seldom found in atherosclerotic plaques. To resolve this longstanding paradox, we investigated whether neutrophil-derived microvesicles may influence arterial pathophysiology. Clinical and pre-clinical studies revealed that levels of circulating neutrophil microvesicles were enhanced by exposure to a high fat diet, a known risk factor for atherosclerosis. Neutrophil microvesicles accumulated at disease-prone regions of arteries that are exposed to complex flow patterns, and they promoted vascular inflammation and atherosclerosis in a murine model. Using cultured endothelial cells exposed to disturbed flow, it was demonstrated that neutrophil microvesicles promoted inflammatory gene expression by delivering a microRNA (miR-155) that enhanced NF-{kappa}B activation. Similary, neutrophil microvesicles increased miR-155 and enhanced NF-{kappa}B at disease-prone sites of disturbed flow in arteries of mice. We conclude that delivery of microvesicles carrying miR-155 to disease-prone regions of arteries provides a novel mechanism by which neutrophils contribute to vascular inflammation and atherogenesis.

cell biology↗