Diversity of plant DNA in stool is linked to dietary quality, age, and household income

Eating a varied diet is a central tenet of good nutrition. Here, we develop a molecular tool to quantify human dietary plant diversity by applying DNA metabarcoding with the chloroplast trnL-P6 marker to 1,029 fecal samples from 324 participants across two interventional feeding studies and three observational cohorts. The number of plant taxa per sample (plant metabarcoding richness or pMR) correlated with recorded intakes in interventional diets and with indices calculated from a food frequency questionnaire in typical diets (δ = 0.40 to 0.63). In adolescents unable to collect validated dietary survey data, trnL metabarcoding detected 111 plant taxa, with 86 consumed by more than one individual and four (wheat, chocolate, corn, and potato family) consumed by <70% of individuals. Adolescent pMR was associated with age and household income, replicating prior epidemiologic findings. Overall, trnL metabarcoding promises an objective and accurate measure of the number and types of plants consumed that is applicable to diverse human populations

The Canadian Urban Environmental Health Research Consortium - A protocol for building a national environmental exposure data platform for integrated analyses of urban form and health

Background: Multiple external environmental exposures related to residential location and urban form including, air pollutants, noise, greenness, and walkability have been linked to health impacts or benefits. The Canadian Urban Environmental Health Research Consortium (CANUE) was established to facilitate the linkage of extensive geospatial exposure data to existing Canadian cohorts and administrative health data holdings. We hypothesize that this linkage will enable investigators to test a variety of their own hypotheses related to the interdependent associations of built environment features with diverse health outcomes encompassed by the cohorts and administrative data. Methods: We developed a protocol for compiling measures of built environment features that quantify exposure; vary spatially on the urban and suburban scale; and can be modified through changes in policy or individual behaviour to benefit health. These measures fall into six domains: air quality, noise, greenness, weather/climate, and transportation and neighbourhood factors; and will be indexed to six-digit postal codes to facilitate merging with health databases. Initial efforts focus on existing data and include estimates of air pollutants, greenness, temperature extremes, and neighbourhood walkability and socioeconomic characteristics. Key gaps will be addressed for noise exposure, with a new national model being developed, and for transportation-related exposures, with detailed estimates of truck volumes and diesel emissions now underway in selected cities. Improvements to existing exposure estimates are planned, primarily by increasing temporal and/or spatial resolution given new satellite-based sensors and more detailed national air quality modelling. Novel metrics are also planned for walkability and food environments, green space access and function and life-long climate-related exposures based on local climate zones. Critical challenges exist, for example, the quantity and quality of input data to many of the models and metrics has changed over time, making it difficult to develop and validate historical exposures. Discussion: CANUE represents a unique effort to coordinate and leverage substantial research investments and will enable a more focused effort on filling gaps in exposure information, improving the range of exposures quantified, their precision and mechanistic relevance to health. Epidemiological studies may be better able to explore the common theme of urban form and health in an integrated manner, ultimately contributing new knowledge informing policies that enhance healthy urban living

Para-infectious brain injury in COVID-19 persists at follow-up despite attenuated cytokine and autoantibody responses

To understand neurological complications of COVID-19 better both acutely and for recovery, we measured markers of brain injury, inflammatory mediators, and autoantibodies in 203 hospitalised participants; 111 with acute sera (1–11 days post-admission) and 92 convalescent sera (56 with COVID-19-associated neurological diagnoses). Here we show that compared to 60 uninfected controls, tTau, GFAP, NfL, and UCH-L1 are increased with COVID-19 infection at acute timepoints and NfL and GFAP are significantly higher in participants with neurological complications. Inflammatory mediators (IL-6, IL-12p40, HGF, M-CSF, CCL2, and IL-1RA) are associated with both altered consciousness and markers of brain injury. Autoantibodies are more common in COVID-19 than controls and some (including against MYL7, UCH-L1, and GRIN3B) are more frequent with altered consciousness. Additionally, convalescent participants with neurological complications show elevated GFAP and NfL, unrelated to attenuated systemic inflammatory mediators and to autoantibody responses. Overall, neurological complications of COVID-19 are associated with evidence of neuroglial injury in both acute and late disease and these correlate with dysregulated innate and adaptive immune responses acutely

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

Innate and acquired resistance to African trypanosomiasis

The review discusses the current field status of human and bovine trypanosomiases, and focuses on the molecular basis of innate and acquired control of African trypanosomes in people, cattle and Cape buffal

Nineteenth annual seed catalog : farm, field and garden seeds /

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