Placing Joseph Banks in the North Pacific

The South Pacific was a fulcrum of Joseph Banks's maritime world and global networks. The North Pacific was a distance and intangible fringe. This article is concerned with how Banks should be ‘placed’ in the North Pacific. It tracks how Banks's activities have been delineated in terms of languages and categories of global and local, and centre and margin, and then considers the historical and geographical specifics apposite to his connection to the North Pacific. In this setting, ideas of place (as location and assignment) and capital (as a circulatory and everyday practice of exchange and opportunism) come into view and question the distinction between science and commerce in Banks historiography. The article considers a diverse group of non-Indigenous figures – explorers, traders, cartographers, scientists, collectors – operating in the North Pacific in the 1780s and 1790s whose initiatives and missives passed across Banks's desk, and assesses their place in Banks's archive by drawing on Peter Sloterdijk's ideas about the interiorising and exteriorising logic of capital.PostprintPeer reviewe

The Hominin Sites and Paleolakes Drilling Project:High-Resolution Paleoclimate Records from the East African Rift System and Their Implications for Understanding the Environmental Context of Hominin Evolution

The possibility of a causal relationship between Earth history processes and hominin evolution in Africa has been the subject of intensive paleoanthropological research for the last 25 years. One fundamental question is: can any geohistorical processes, in particular, climatic ones, be characterized with sufficient precision to enable temporal correlation with events in hominin evolution and provide support for a possible causal mechanism for evolutionary changes? Previous attempts to link paleoclimate and hominin evolution have centered on evidence from the outcrops where the hominin fossils are found, as understanding whether and how hominin populations responded to habitat change must be examined at the local basinal scale. However, these outcrop records typically provide incomplete, low-resolution climate and environmental histories, and surface weathering often precludes the application of highly sensitive, state-of-the-art paleoenvironmental methods. Continuous and well-preserved deep-sea drill core records have provided an alternative approach to reconstructing the context of hominin evolution, but have been collected at great distances from hominin sites and typically integrate information over vast spatial scales. The goal of the Hominin Sites and Paleolakes Drilling Project (HSPDP) is to analyze climate and other Earth system dynamics using detailed paleoenvironmental data acquired through scientific drilling of lacustrine depocenters at or near six key paleoanthropological sites in Kenya and Ethiopia. This review provides an overview of a unique collaboration of paleoanthropologists and earth scientists who have joined together to explicitly explore key hypotheses linking environmental history and mammalian (including hominin) evolution and potentially develop new testable hypotheses. With a focus on continuous, high-resolution proxies at timescales relevant to both biological and cultural evolution, the HSPDP aims to dramatically expand our understanding of the environmental history of eastern Africa during a significant portion of the Late Neogene and Quaternary, and to generate useful models of long-term environmental dynamics in the regionpublishersversionPeer reviewe

Asteroseismology and Interferometry

Asteroseismology provides us with a unique opportunity to improve our understanding of stellar structure and evolution. Recent developments, including the first systematic studies of solar-like pulsators, have boosted the impact of this field of research within Astrophysics and have led to a significant increase in the size of the research community. In the present paper we start by reviewing the basic observational and theoretical properties of classical and solar-like pulsators and present results from some of the most recent and outstanding studies of these stars. We centre our review on those classes of pulsators for which interferometric studies are expected to provide a significant input. We discuss current limitations to asteroseismic studies, including difficulties in mode identification and in the accurate determination of global parameters of pulsating stars, and, after a brief review of those aspects of interferometry that are most relevant in this context, anticipate how interferometric observations may contribute to overcome these limitations. Moreover, we present results of recent pilot studies of pulsating stars involving both asteroseismic and interferometric constraints and look into the future, summarizing ongoing efforts concerning the development of future instruments and satellite missions which are expected to have an impact in this field of research.Comment: Version as published in The Astronomy and Astrophysics Review, Volume 14, Issue 3-4, pp. 217-36

Tegumentary leishmaniasis and coinfections other than HIV

<div><p>Background</p><p>Tegumentary leishmaniasis (TL) is a disease of skin and/or mucosal tissues caused by <i>Leishmania</i> parasites. TL patients may concurrently carry other pathogens, which may influence the clinical outcome of TL.</p><p>Methodology and principal findings</p><p>This review focuses on the frequency of TL coinfections in human populations, interactions between <i>Leishmania</i> and other pathogens in animal models and human subjects, and implications of TL coinfections for clinical practice. For the purpose of this review, TL is defined as all forms of cutaneous (localised, disseminated, or diffuse) and mucocutaneous leishmaniasis. Human immunodeficiency virus (HIV) coinfection, superinfection with skin bacteria, and skin manifestations of visceral leishmaniasis are not included. We searched MEDLINE and other databases and included 73 records: 21 experimental studies in animals and 52 studies about human subjects (mainly cross-sectional and case studies). Several reports describe the frequency of <i>Trypanosoma cruzi</i> coinfection in TL patients in Argentina (about 41%) and the frequency of helminthiasis in TL patients in Brazil (15% to 88%). Different hypotheses have been explored about mechanisms of interaction between different microorganisms, but no clear answers emerge. Such interactions may involve innate immunity coupled with regulatory networks that affect quality and quantity of acquired immune responses. Diagnostic problems may occur when concurrent infections cause similar lesions (e.g., TL and leprosy), when different pathogens are present in the same lesions (e.g., <i>Leishmania</i> and <i>Sporothrix schenckii</i>), or when similarities between phylogenetically close pathogens affect accuracy of diagnostic tests (e.g., serology for leishmaniasis and Chagas disease). Some coinfections (e.g., helminthiasis) appear to reduce the effectiveness of antileishmanial treatment, and drug combinations may cause cumulative adverse effects.</p><p>Conclusions and significance</p><p>In patients with TL, coinfection is frequent, it can lead to diagnostic errors and delays, and it can influence the effectiveness and safety of treatment. More research is needed to unravel how coinfections interfere with the pathogenesis of TL.</p></div

Comprehensive analysis of epigenetic clocks reveals associations between disproportionate biological ageing and hippocampal volume

The concept of age acceleration, the difference between biological age and chronological age, is of growing interest, particularly with respect to age-related disorders, such as Alzheimer’s Disease (AD). Whilst studies have reported associations with AD risk and related phenotypes, there remains a lack of consensus on these associations. Here we aimed to comprehensively investigate the relationship between five recognised measures of age acceleration, based on DNA methylation patterns (DNAm age), and cross-sectional and longitudinal cognition and AD-related neuroimaging phenotypes (volumetric MRI and Amyloid-β PET) in the Australian Imaging, Biomarkers and Lifestyle (AIBL) and the Alzheimer’s Disease Neuroimaging Initiative (ADNI). Significant associations were observed between age acceleration using the Hannum epigenetic clock and cross-sectional hippocampal volume in AIBL and replicated in ADNI. In AIBL, several other findings were observed cross-sectionally, including a significant association between hippocampal volume and the Hannum and Phenoage epigenetic clocks. Further, significant associations were also observed between hippocampal volume and the Zhang and Phenoage epigenetic clocks within Amyloid-β positive individuals. However, these were not validated within the ADNI cohort. No associations between age acceleration and other Alzheimer’s disease-related phenotypes, including measures of cognition or brain Amyloid-β burden, were observed, and there was no association with longitudinal change in any phenotype. This study presents a link between age acceleration, as determined using DNA methylation, and hippocampal volume that was statistically significant across two highly characterised cohorts. The results presented in this study contribute to a growing literature that supports the role of epigenetic modifications in ageing and AD-related phenotypes

The genetic architecture of the human cerebral cortex

The cerebral cortex underlies our complex cognitive capabilities, yet little is known about the specific genetic loci that influence human cortical structure. To identify genetic variants that affect cortical structure, we conducted a genome-wide association meta-analysis of brain magnetic resonance imaging data from 51,665 individuals. We analyzed the surface area and average thickness of the whole cortex and 34 regions with known functional specializations. We identified 199 significant loci and found significant enrichment for loci influencing total surface area within regulatory elements that are active during prenatal cortical development, supporting the radial unit hypothesis. Loci that affect regional surface area cluster near genes in Wnt signaling pathways, which influence progenitor expansion and areal identity. Variation in cortical structure is genetically correlated with cognitive function, Parkinson's disease, insomnia, depression, neuroticism, and attention deficit hyperactivity disorder

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

Mapping and linking supply- and demand-side measures in climate-smart agriculture. A review

Climate change and food security are two of humanity’s greatest challenges and are highly interlinked. On the one hand, climate change puts pressure on food security. On the other hand, farming significantly contributes to anthropogenic greenhouse gas emissions. This calls for climate-smart agriculture—agriculture that helps to mitigate and adapt to climate change. Climate-smart agriculture measures are diverse and include emission reductions, sink enhancements, and fossil fuel offsets for mitigation. Adaptation measures include technological advancements, adaptive farming practices, and financial management. Here, we review the potentials and trade-offs of climate-smart agricultural measures by producers and consumers. Our two main findings are as follows: (1) The benefits of measures are often site-dependent and differ according to agricultural practices (e.g., fertilizer use), environmental conditions (e.g., carbon sequestration potential), or the production and consumption of specific products (e.g., rice and meat). (2) Climate-smart agricultural measures on the supply side are likely to be insufficient or ineffective if not accompanied by changes in consumer behavior, as climate-smart agriculture will affect the supply of agricultural commodities and require changes on the demand side in response. Such linkages between demand and supply require simultaneous policy and market incentives. It, therefore, requires interdisciplinary cooperation to meet the twin challenge of climate change and food security. The link to consumer behavior is often neglected in research but regarded as an essential component of climate-smart agriculture. We argue for not solely focusing research and implementation on one-sided measures but designing good, site-specific combinations of both demand- and supply-side measures to use the potential of agriculture more effectively to mitigate and adapt to climate change

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