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Johnson, K. M.

Publications and source records attributed to Johnson, K. M..

17 recordsLinked to original sources

Chromosome-level genome assembly of the Olympia oyster (Ostrea lurida), the only oyster species native to the West Coast of North America

The Olympia oyster (Ostrea lurida) was once a major food source and a key component of coastal marine ecosystems and culture on the US West Coast. Overfishing and habitat contamination in the early to mid-20th century severely depleted populations of Olympia oysters, and the species is currently considered a species of concern. Although multiple restoration efforts are underway, progress understanding the species biology and recovery potential has been limited by the historical lack of genomic resources. Here, we report a chromosome-level assembly of the Olympia oyster. The assembly was built using Oxford Nanopore reads and Hi-C to obtain a highly contiguous 1.03 Gb-assembly consisting of 10 chromosomes. RNA from gills, mantle, adductor muscle, and a mix of brooding eggs and larvae were also sequenced as 150 nt long paired-end reads which were used to guide the genome annotation. Over 52 K genes were predicted in the genome, of which 34K were protein-coding. A BUSCO analysis on the assembly showed 98.9% of the mollusca_odb12 gene set were complete (with 2.1% duplicated, and 0.8% missing). The short RNA reads were also used to identify tissue-level gene expression signatures in adductor muscles, egg and brooding larvae, and mantle. Development-related genes were highly expressed in eggs and brooding larvae whereas many xenobiotic metabolism genes were present in mantle tissues, highlighting mantles role in the interaction of the oyster with external environments. This new genomic resource will greatly advance our understanding of this keystone mollusk and provide a critical tool for guiding restoration efforts and the development of sustainable commercial production.

genomics↗

Ferumoxytol dynamic contrast-enhanced MRI for in vivo longitudinal cotyledon perfusion assessment with pathology correlation in a rhesus macaque thrombotic injury model

IntroductionWhile placental perfusion and pathology jointly affect pregnancy outcomes, cotyledon-specific perfusion across gestation and its correlation with local injury is not yet well understood. Ferumoxytol dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI) offers a promising way to noninvasively identify cotyledons across gestation and quantify longitudinal cotyledon-specific perfusion changes. Additionally, intraplacental injection of bioactive fibrin sealant allows us to model thrombotic placental injury and further assess cotyledon-level relationships between perfusion and significant injury. MethodsPregnant rhesus macaques (N=13) received intrauterine saline or fibrin sealant injections at gestational day (GD) [~]101 and underwent ferumoxytol DCE-MRI at GDs [~]100, 115, and 145. Placental perfusion domains derived from contrast arrival time were segmented at each imaging time point and matched to cotyledons identified following tissue collection by cesarean section, with cotyledon perfusion quantified longitudinally and correlated with cotyledon-specific quantitative histopathology. ResultsAll pregnancies were successfully carried to term. Fibrin sealant injections induced significantly higher levels of placental pathology compared to saline controls. MRI-derived perfusion domains were largely consistent across gestation and showed predominantly one-to-one correspondence with term cotyledons, with successful perfusion-pathology pairing achieved in 153 cotyledons. Longitudinal cotyledon perfusion changes showed significant positive correlations with villous agglutination injuries. ConclusionsFeasibility of noninvasively tracking placental cotyledon perfusion using ferumoxytol DCE-MRI was demonstrated, and the efficacy of the rhesus macaque thrombotic injury model was confirmed. The positive perfusion-pathology correlations suggested intrinsic placental regulatory mechanisms and functional plasticity. This new framework is promising for future translational studies and validation of ex vivo cotyledon perfusion models. HighlightsO_LILongitudinal tracking of placental perfusion domains with ferumoxytol MRI C_LIO_LISuccessful matching of cotyledons and MRI-derived perfusion domains C_LIO_LIConfirmed thrombotic injury-model induced cotyledon pathology C_LIO_LIMaternal perfusion compensation in presence of villous pathology C_LI

pathology↗

A data-driven approach to automate embolism detection in leaves

1O_LIEmbolism, the formation of air bubbles in the plant water transport system, is a mechanistic driver of plant death. The Optical Vulnerability Technique (OVT) is an imaging method for non-invasive quantification of embolism (including P50, a common metric for drought vulnerability), which can also provide detailed spatial and temporal information. Its major cost lies in the post-processing of thousands of images. C_LIO_LIHere we designed, tested, trained, and make publicly available a neural network model to automate post-processing of OVT images. Using a dataset of 65 leaves from Senecio pterophorous, we compared our model predictions to results obtained via traditional post-processing by an expert. C_LIO_LIOur model resolved P50 to within 0.027 MPa of the expert-processed data with training taking 30 minutes to 2.5 hours and model-runtime in the order of seconds to minutes, demonstrating its promise for increasing the efficiency and throughput of P50 calculation. The models performance in replicating the pixels that constitute embolism events was lower (mean event-frame IoU of 0.38). C_LIO_LIWe invite the community to utilise our model but emphasise that it does not replace the expert-processing pipeline and that care must be taken when considering applying this and similar approaches to OVT data. C_LI

plant biology↗

Lysosomal lipid metabolism promotes tumor cell invasion through local energetics and membrane lipid remodeling

Metabolic vulnerabilities in cancer have been targeted primarily to suppress tumor growth, but less is known about the metabolic requirements for tumor cell invasion. Here we report that lipid catabolism by cytosolic and lysosomal lipases supports pancreatic cancer cell invasion through both overlapping and distinct functional and metabolic mechanisms. Lysosomal acid lipase (LAL)-dependent lipid droplet catabolism promotes invadopodia formation and stabilization, enabling extracellular matrix degradation. In addition to modulating cellular energetics, lipidomics revealed that lipid droplet catabolism regulates cholesterol and membrane phospholipid levels. Using spatially resolved biosensors and cholesterol imaging, we found that lysosomal lipid catabolism occurs at invadopodia and sustains local ATP and membrane cholesterol. These findings identify spatially organized lipid catabolism as a mechanism that couples local energetics and membrane remodeling during the earliest steps of pancreatic cancer cell invasion.

cell biology↗

Nitroxoline-O-protected derivatives inhibit MetAP2 and activate ATF4 through mTORC1 to inhibit cancer cell growth

Reprogrammed cancer cell proliferation requires high levels of protein synthesis and concomitant folding and processing. N-terminal methionine amino peptidases (MetAP) are a class of enzymes that cleave the initiator methionine amino acids to allow for peptide maturation and co-translational processing. Specifically, based on its role in protein synthesis, MetAP2 has been found to be upregulated in cancer cells and has been explored as a potential anticancer target. Cellular perturbations that impinge on protein synthesis activate cellular stress pathways, including the integrated stress response and mTORC1. Nitroxoline, a MetAP2 inhibitor has been explored as an anticancer agent but is hampered by poor pharmacokinetic properties. Here, we synthesize a few O-substituted silyl and nonsilyl nitroxoline analogs to diversify the nitroxoline template to reduce metabolic vulnerability. In vitro MetAP2 and cancer cell proliferation inhibition assays demonstrate that synthesized analogs retain potency when compared to the parent nitroxoline. Mechanistically, we show that the lead candidate compound 3 and nitroxoline activate ATF4 mediated stress responses through non-canonical mTORC1. These results further implicate MetAP2 protein processing in mTORC1 nutrient sensing pathways and provide novel synthetic analogs of nitroxoline for potential cancer treatment.

cancer biology↗

Ice and air: Visualisation of freeze-thaw embolism and freezing spread in young L. tulipifera leaves

Spring freezing is an unforgiving stress for young leaves, often leading to death, with consequences for tree productivity and survival. While both the plant water transport system and living tissues are vulnerable to freezing, we do not know whether damage to one or both of these systems causes death in leaves exposed to freezing. Whole saplings of Liriodendron tulipifera were exposed to freezing and thawing trajectories designed to mimic natural spring freezes. We monitored the formation of freeze-thaw xylem embolism and damage to photosynthetic tissues to reveal a predictable progression of ice formation across the leaf surface that is strongly influenced by leaf vein architecture, notably the presence or absence of bundle sheath extensions. Our data also show that freeze-thaw embolism occurs only in the largest vein orders where mean vessel diameter exceeds 30{micro}m. With evidence of both freeze-thaw embolism and damage to photosynthetic tissue, we conclude that this dual-mode lethality may be common among other wide-vesseled angiosperm-leaves, potentially playing a role in limiting geographic distributions, and show that bundle sheath extensions may stall or even prevent freezing spread. HighlightBoth ice and air lead likely lead to death in young L.tulipfera leaves exposed to freezing, with the spread of both governed by physical characteristics of these leaves.

physiology↗

Constitutive gene expression differs in three brain regions important for cognition in neophobic and non-neophobic house sparrows (Passer domesticus)

Neophobia (aversion to new objects, food, and environments) is a personality trait that affects the ability of wildlife to adapt to new challenges and opportunities. Despite the ubiquity and importance of this trait, the molecular mechanisms underlying repeatable individual differences in neophobia in wild animals are poorly understood. We evaluated wild-caught house sparrows (Passer domesticus) for neophobia in the lab using novel object tests. We then selected the most and least neophobic individuals (n=3 of each) and extracted RNA from four brain regions involved in learning, memory, threat perception, and executive function: striatum, dorsomedial hippocampus, medial ventral arcopallium, and caudolateral nidopallium (NCL). Our analysis of differentially expressed genes (DEGs) used 11,889 gene regions annotated in the house sparrow reference genome for which we had an average of 25.7 million mapped reads/sample. PERMANOVA identified significant effects of brain region, phenotype (neophobic vs. non-neophobic), and a brain region by phenotype interaction. Comparing neophobic and non-neophobic birds revealed constitutive differences in DEGs in three of the four brain regions examined: hippocampus (12% of the transcriptome significantly differentially expressed), striatum (4%) and NCL (3%). DEGs included important known neuroendocrine mediators of learning, memory, executive function, and anxiety behavior, including serotonin receptor 5A, dopamine receptors 1, 2 and 5 (downregulated in neophobic birds), and estrogen receptor beta (upregulated in neophobic birds). These results suggest that some of the behavioral differences between phenotypes may be due to underlying gene expression differences in the brain. The large number of DEGs in neophobic and non-neophobic birds also implies that there are major differences in neural function between the two phenotypes that could affect a wide variety of behavioral traits beyond neophobia.

animal behavior and cognition↗

Invertebrate methylomes provide insight into mechanisms of environmental tolerance and reveal methodological biases

There is a growing focus on the role of DNA methylation in the ability of marine invertebrates to rapidly respond to changing environmental factors and anthropogenic impacts. However, genome-wide DNA methylation studies in non-model organisms are currently hampered by limited understanding of methodological biases. Here we compare three methods for quantifying DNA methylation at single base-pair resolution -- Whole Genome Bisulfite Sequencing (WGBS), Reduced Representation Bisulfite Sequencing (RRBS), and Methyl-CpG Binding Domain Bisulfite Sequencing (MBDBS) -- using multiple individuals from two reef-building coral species with contrasting environmental sensitivity. All methods reveal substantially greater methylation in Montipora capitata (11.4%) than the more sensitive Pocillopora acuta (2.9%). The majority of CpG methylation in both species occurs in gene bodies and flanking regions. In both species, MBDBS has the greatest capacity for detecting CpGs in coding regions at our sequencing depth, however MBDBS may be influenced by intra-sample methylation heterogeneity. RRBS yields robust information for specific loci albeit without enrichment of any particular genome feature and with significantly reduced genome coverage. Relative genome size strongly influences the number and location of CpGs detected by each method when sequencing depth is limited, illuminating nuances in cross-species comparisons. As genome-wide methylation differences, supported by data across bisulfite sequencing methods, may contribute to environmental sensitivity phenotypes in critical marine invertebrate taxa, these data provide a genomic resource for investigating the functional role of DNA methylation in environmental tolerance.

genomics↗

Development and External Validation of the Acute COPD Exacerbation Prediction Tool (ACCEPT)

BackgroundAccurate prediction of exacerbation risk enables personalised chronic obstructive pulmonary disease (COPD) care. We developed and validated a generalisable model to predict the individualised rate and severity of COPD exacerbations. MethodsWe pooled data from three COPD trials on patients with a history of exacerbations. We developed a mixed-effect model to predict exacerbations over one-year. Severe exacerbations were those requiring inpatient care. Predictors were a history of exacerbations, age, sex, body mass index, smoking status, domiciliary oxygen therapy, lung function, symptom burden, and current medication use. ECLIPSE, a multicentre cohort study, was used for external validation. ResultsThe development dataset included 2,380 patients (mean 64{middle dot}7 years, 1373 [57{middle dot}7%] men, mean exacerbation rate 1{middle dot}42/year, 0{middle dot}29/year [20{middle dot}5%] severe). When validated against all COPD patients in ECLIPSE (n=1819, mean 63{middle dot}3 years, 1186 [65{middle dot}2%] men, mean exacerbation rate 1{middle dot}20/year, 0{middle dot}27/year [22{middle dot}2%] severe), the area-under-curve was 0{middle dot}81 (95%CI 0{middle dot}79-0{middle dot}83) for [≥]2 exacerbations and 0{middle dot}77 (95%CI 0{middle dot}74-0{middle dot}80) for [≥]1 severe exacerbation. Predicted rates were 0{middle dot}25/year for severe and 1{middle dot}31/year for all exacerbations, close to the observed rates (0{middle dot}27/year and 1{middle dot}20/year, respectively). In ECLIPSE patients with a prior exacerbation history (n=996, mean 63{middle dot}6 years, 611 (61{middle dot}3%) men, mean exacerbation rate 1{middle dot}82/year, 0{middle dot}40/year [22{middle dot}0%] severe), the area-under-curve was 0{middle dot}73 (95%CI 0{middle dot}70-0{middle dot}76) for [≥]2 exacerbations and 0{middle dot}74 (95%CI 0{middle dot}70-0{middle dot}78) for [≥]1 severe exacerbation. Calibration was accurate for severe exacerbations (predicted=0{middle dot}37/year, observed=0{middle dot}40/year) and all exacerbations (predicted=1{middle dot}80/year, observed=1{middle dot}82/year). The model is accessible at http://resp.core.ubc.ca/ipress/accept. InterpretationThis model can be used as a decision tool to personalise COPD treatment and prevent exacerbations. Research in contextO_ST_ABSEvidence before this studyC_ST_ABSPreventing future exacerbations is a major goal in COPD care. Because of adverse effects, preventative treatments should be reserved for those at a higher risk of future exacerbations. Predicting exacerbation risk in individual patients can guide these clinical decisions. A 2017 systematic review reported that of the 27 identified COPD exacerbation prediction tools, only two had reported external validation and none was ready for clinical implementation. To find the studies that were published afterwards, we searched PubMed for articles on development and validation of COPD exacerbation prediction since 2015, using the search terms "COPD", "exacerbation", "model", and "validation". We included studies that reported prediction of either the risk or the rate of exacerbations and excluded studies that did not report external validation. Our literature search revealed two more prediction models neither of which was deemed generalisable due to lack of methodological rigour, or local and limited nature of the data available to investigators. Added value of this studyWe used data from three randomised trials to develop ACCEPT, a clinical prediction tool based on routinely available predictors for COPD exacerbations. We externally validated ACCEPT in a large, multinational prospective cohort. To our knowledge, ACCEPT is the first COPD exacerbation prediction tool that jointly estimates the individualised rate and severity of exacerbations. Successful external validation of ACCEPT showed that its generalisability can be expanded across geography and beyond the setting of therapeutic trials. ACCEPT is designed to be easily applicable in clinical practice and is readily accessible as a web application. Implications of all the available evidenceCurrent guidelines rely on a history of exacerbations as the sole predictor of future exacerbations. Simple clinical and demographic variables, in aggregate, can be used to predict COPD exacerbations with improved accuracy. ACCEPT enables a more personalised approach to treatment based on routinely collected clinical data by allowing clinicians to objectively differentiate risk profiles of patients with similar exacerbation history. Care providers and patients can use individualised exacerbation risk estimates to decide on preventive therapies based on objectively-established or patient-specific thresholds for treatment benefit and harm. COPD clinical researchers can use this tool to target enriched populations for enrolment in clinical trials.

epidemiology↗

Sensory lesioning induces microglial synapse elimination via ADAM10 and fractalkine signaling

Microglia rapidly respond to changes in neural activity and inflammation to regulate synaptic connectivity. The extracellular signals, particularly neuron-derived molecules, that drive these microglial functions at synapses remains a key open question. Here, whisker lesioning, known to dampen cortical activity, induces microglia-mediated synapse elimination. We show that this synapse elimination is dependent on the microglial fractalkine receptor, CX3CR1, but not complement receptor 3, signaling. Further, mice deficient in the CX3CR1 ligand (CX3CL1) also have profound defects in synapse elimination. Single-cell RNAseq then revealed that Cx3cl1 is cortical neuron-derived and ADAM10, a metalloprotease that cleaves CX3CL1 into a secreted form, is upregulated specifically in layer IV neurons and microglia following whisker lesioning. Finally, inhibition of ADAM10 phenocopies Cx3cr1-/- and Cx3cl1-/- synapse elimination defects. Together, these results identify novel neuron-to-microglia signaling necessary for cortical synaptic remodeling and reveal context-dependent immune mechanisms are utilized to remodel synapses in the mammalian brain.

neuroscience↗

The costs of misdiagnosed asthma in a longitudinal study of the general population

ObjectivesA current diagnosis of asthma cannot be objectively confirmed in many patients with physician-diagnosed asthma. Estimates of resource use in overdiagnosed cases of asthma are necessary to measure the burden of overdiagnosis and evaluate strategies to reduce this burden. We assessed the difference in asthma-related healthcare resource use between patients with a confirmed asthma diagnosis and those with asthma ruled out.\n\nDesignPopulation-based prospective cohort study.\n\nSettingParticipants were recruited through random-digit dialling of both landlines and mobile phones in BC, Canada.\n\nParticipantsWe included 345 individuals [≥]12 years of age with a self-reported physician diagnosis of asthma which was confirmed by a bronchodilator reversibility or methacholine challenge test at the end of the 12-month follow-up.\n\nPrimary and secondary outcome measuresSelf-reported annual asthma-related direct healthcare costs (2017 Canadian dollars), outpatient physician visits, and medication use from the Canadian healthcare system perspective.\n\nResultsAsthma was ruled out in 86 (24.9%) participants. Average annual asthma-related direct healthcare costs for participants with confirmed asthma were $497.9 (SD $677.9), and $307.7 (SD $424.1) for participants with asthma ruled out. In the adjusted analyses, a confirmed diagnosis was associated with higher direct healthcare costs (Relative Ratio [RR]=1.60, 95%CI 1.14-2.22), increased rate of specialist visits (RR=2.41, 95%CI 1.05-5.40) and reliever medication use (RR=1.62, 95%CI 1.09-2.35), but not primary care physician visits (p=0.10) or controller medication use (p=0.11).\n\nConclusionsA quarter of individuals with a physician diagnosis of asthma did not have asthma after objective re-evaluation. These participants still consumed a significant amount of asthma-related healthcare resources. The population-level economic burden of asthma overdiagnosis could be substantial.\n\nStrengths and limitations of this studyO_LIParticipants were recruited through random sampling of the general population in the province of British Columbia.\nC_LIO_LIAsthma diagnosis was confirmed or ruled out using sequential guideline-recommended objective airway tests.\nC_LIO_LIHealthcare resource use was self-reported, potential recall bias may have led to reduced accuracy.\nC_LIO_LIThe study was unable to evaluate the indirect costs of overdiagnosis or the cost-savings from correcting the diagnosis.\nC_LIO_LIThe generalizability of the results may be limited by regional differences in medical costs and practices.\nC_LI

epidemiology↗

Heterogeneity in the respiratory symptoms of patients with mild-moderate COPD

BackgroundThe burden of symptoms varies markedly between patients with Chronic Obstructive Pulmonary Disease (COPD) and is only weakly correlated with lung function impairment. While heterogeneity in lung function decline and exacerbations have been previously studied, the extent of heterogeneity in symptoms and the factors associated with this heterogeneity are not well understood.\n\nMethodsA sample of the general Canadian population [&ge;]40 years with persistent airflow limitation was followed for up to 3 years. Participants reported whether they experienced chronic coughing, phlegm, wheezing, or dyspnea during visits at 18-month intervals. We used mixed-effect logistic regression models (separately for each symptom) to assess overall heterogeneity in the occurrence of symptoms between individuals, and the proportion of variation in symptom burden explained by lung function versus all other clinical characteristics of participants.\n\nResults548 participants (54% male, mean age 67 years) contributed 1,086 visits in total, and 82% of patients reported at least one symptom during follow-up. There was substantial heterogeneity in the individual-specific probabilities for the occurrence of symptoms. This heterogeneity was highest for dyspnea and lowest for phlegm (interquartile range of probabilities: 0.15-0.77 and <0.01-0.53, respectively). FEV1 explained 82% of the variation between individuals in the occurrence of phlegm, 26% for dyspnea, 3% for cough, and <0.1% for wheeze. All clinical characteristics of participants (including FEV1) explained between 86% of heterogeneity in the occurrence of phlegm to <1% for wheeze.\n\nConclusionThere is marked heterogeneity in the burden of respiratory symptoms between COPD patients. The ability of lung function and other commonly measured clinical characteristics to explain this heterogeneity differs between symptoms.

epidemiology↗

Development and validation of the Evaluation Platform In COPD (EPIC): a population-based outcomes model of COPD for Canada

BackgroundWe report the development, validation, and implementation of an open-source population-based outcomes model of Chronic Obstructive Pulmonary Disease (COPD) for Canada.\n\nMethodsEvaluation Platform in COPD (EPIC) is a discrete event simulation model of Canadians 40 years of age or older. Three core features of EPIC are its open-population design (incorporating projections of future population growth, aging, and smoking trends), its incorporation of heterogeneity in lung function decline and burden of exacerbations, and its modeling of the natural history of COPD from inception. Multiple original data analyses, as well as values reported in the literature, were used to populate the model. Extensive face validity as well as internal and external validity evaluations were performed.\n\nResultsThe model was internally validated on demographic projections, mortality rates, lung function trajectories, COPD exacerbations, and stability of COPD prevalence over time within strata of risk factors. In external validation, it moderately overestimated rate of overall exacerbations in two independent trials, but generated consistent estimates of rate of severe exacerbations and mortality.\n\nLimitationsIn its current version, EPIC does not consider uncertainty in the evidence. Several components such as additional (e.g., environmental and occupational) risk factors, treatment, symptoms, and comorbidity will have to be added in future iterations.\n\nConclusionsEPIC is the first multi-purpose outcome- and policy-focused model of COPD for Canada. By modeling the natural history of COPD from its inception, it is capable of modeling the outcomes of decisions across the entire care pathway of COPD. Platforms of this type have the capacity to be iteratively updated to incorporate the latest evidence and to project the outcomes of many different scenarios within a consistent framework.

epidemiology↗

Dose-dependent effects of inhaled corticosteroids on bone mineral density in postmenopausal women with asthma or COPD: A registry-based cohort study

BackgroundThe effect of long-term inhaled corticosteroid (ICS) therapy on the bone health of older adults remains unclear due to its possible impact on bone mineral density (BMD).\n\nObjectiveTo evaluate, cross-sectionally and longitudinally, the impact of ICS use on BMD in postmenopausal women with asthma or chronic obstructive pulmonary disease (COPD).\n\nMethodsWe used a population-based bone densitometry registry linked with administrative health data of the province of Manitoba, Canada (1999-2013), to identify women with diagnosed asthma or COPD. ICS use was defined as cumulative dispensed days prior to baseline BMD (cross-sectional analysis), and medication possession ratio (MPR) between two BMD measurements (longitudinal analysis). Results were adjusted for multiple covariates including the underlying respiratory diagnosis and its severity.\n\nResultsIn the cross sectional analysis, compared with non-users, women with the highest tertile of prior ICS exposure had lower baseline BMD at the femoral neck (-0.09 standard deviations [SD] below a healthy young adult, 95% CI: -0.16, -0.02) and total hip (-0.14 SD, 95% CI: -0.22, -0.05), but not at the lumbar spine. Longitudinally, the highest tertile of ICS exposure was associated with a slight decline in total hip BMD relative to non-users (-0.02 SD/year, 95% CI: -0.04, -0.01), with no significant effect at the femoral neck and lumbar spine. Middle and lower tertiles of ICS use had no significant effects.\n\nConclusionHigh exposure to ICS was associated with a small adverse effect on baseline hip BMD and total hip BMD loss in post-menopausal women with asthma or COPD.

epidemiology↗

Characterising undiagnosed chronic obstructive pulmonary disease: a systematic review and meta-analysis

BackgroundA significant proportion of patients with chronic obstructive pulmonary disease (COPD) remain undiagnosed. Characterising these patients can increase our understanding of the hidden burden of COPD and the effectiveness of case detection interventions.\n\nMethodsWe conducted a systematic review and meta-analysis to compare patient and disease risk factors between patients with undiagnosed persistent airflow limitation and those with diagnosed COPD. We searched MEDLINE and EMBASE for observational studies of adult patients meeting accepted spirometric definitions of COPD. We extracted and pooled summary data on the proportion or mean of each risk factor among diagnosed and undiagnosed patients (unadjusted analysis), and coefficients for the adjusted association between risk factors and diagnosis status (adjusted analysis). This protocol is registered with PROSPERO (CRD42017058235).\n\nFindings2,083 records were identified through database searching and 16 articles were used in the meta-analyses. Diagnosed patients were less likely to have mild (v. moderate to very severe) COPD (odds ratio [OR] 0{middle dot}30, 95% CI 0{middle dot}24-0{middle dot}37, 6 studies) in unadjusted analysis. This association remained significant but its strength was attenuated in the adjusted analysis (OR 0{middle dot}72, 95% CI 0{middle dot}58-0{middle dot}89, 2 studies). Diagnosed patients were more likely to report respiratory symptoms such as wheezing (OR 3{middle dot}51, 95% CI 2{middle dot}19-5{middle dot}63, 3 studies) and phlegm (OR 2{middle dot}16, 95% CI 1{middle dot}38-3{middle dot}38, 3 studies), had more severe dyspnoea (modified Medical Research Council scale mean difference 0{middle dot}52, 95% CI 0{middle dot}40-0{middle dot}64, 3 studies) and slightly greater smoking history than undiagnosed patients. Patient age, sex, current smoking status, and the presence of coughing were not associated with a previous diagnosis.\n\nInterpretationPatients with undiagnosed persistent airflow limitation had less severe airflow obstruction and fewer respiratory symptoms than diagnosed patients. This indicates that there is lower disease burden among undiagnosed patients compared to those with diagnosed COPD, which may significantly delay the diagnosis of COPD.\n\nFundingCanadian Institutes of Health Research.\n\nDeclaration of interestsWe declare no competing interests.\n\nAuthor ContributionsMS, SB, and KJ formulated the study idea and designed the study. KJ and SG performed all data analyses and MS, SB and DS contributed to interpretation of findings. KJ wrote the first draft of the manuscript. All authors critically commented on the manuscript and approved the final version. MS is the guarantor of the manuscript.

epidemiology↗

Demographic consequences of invasion by a native, controphic competitor to an insular bird population

Species invasions and range shifts can lead to novel competitive interactions between historically resident and colonizing species, but the demographic consequences of such interactions remain controversial. We present results from field experiments and 45 yrs of demographic monitoring to test the hypothesis that the colonization of Mandarte Is., BC, Canada, by fox sparrows (Passerella iliaca) caused the long-term decline of the song sparrow (Melospiza melodia) population resident there. Several lines of evidence indicate that competition with fox sparrows for winter food reduced over-winter survival in juvenile song sparrows, enforcing population decline despite an increase in annual reproductive rate in song sparrows over the same period. In contrast, we found no evidence of interspecific competition for resources during the breeding season. Our results indicate that in the absence of a sufficient ecological or evolutionary shift in niche dimension, range expansions by dominant competitors have the potential to cause the extirpation of historically resident species when competitive interactions between them are strong and resources not equitably partitioned.

ecology↗

Highly efficient maternal-fetal Zika virus transmission in pregnant rhesus macaques

Infection with Zika virus (ZIKV) is associated with human congenital fetal anomalies. To model fetal outcomes in nonhuman primates, we administered Asian-lineage ZIKV subcutaneously to four pregnant rhesus macaques. While non-pregnant animals clear viremia within 10-12 days, maternal viremia was prolonged in 3 of 4 pregnancies. Fetal head growth velocity in the last month of gestation determined by ultrasound assessment of head circumference was decreased in comparison with biparietal diameter and femur length within each fetus, both within normal range. ZIKV RNA was detected in tissues from all four fetuses at term cesarean section. In all pregnancies, neutrophilic infiltration was present at the maternal-fetal interface (decidua, placenta, fetal membranes), in various fetal tissues, and in fetal retina, choroid, and optic nerve (first trimester infection only). Consistent vertical transmission in this primate model may provide a platform to assess risk factors and test therapeutic interventions for interruption of fetal infection.

pathology↗