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120 results for “Disease exposure”
Fig. 3 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 3. Pesticide research bias across bee genera depending on pesticide type based on Web of Science searches. The number of studies per search term is indicated for each genus with at least 10 studies across search terms; Understudied is a cumulative group including genera which contain less than 10 studies; Unexplored is a cumulative group including genera which have no published papers for any pesticide exposure category. Warmer colours are used to indicate a higher number of studies related to a genus for the corresponding pesticide search term, while colder colours indicate a lower number of studies found. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 4 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 4. Brood pathogens studies per bee genera found from Web of Science searches using search terms "brood disease", "brood pathogen", "brood virus", "larvae disease", "larvae pathogen" and "larvae virus" across bee genera. Red squares indicate that a pathogen on the x-axis has been found to infect at least one species in the bee genus corresponding to its position in the phylogeny shown on the y-axis; yellow squares indicate that the pathogen on the x-axis has been found in individuals from at least one species in the genus on the y-axis but no symptoms were reported in the studies; dark grey squares indicate that the pathogen on the x-axis has been tested for in at least one species in the genus corresponding on the yaxis, however has not been found; white squares indicate that the searches found no studies where any bee species of the genus on the y-axis were tested for in the corresponding pathogens on the x-axis. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 2 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 2. Proportion of results per search term across bee genera on the Web of Science search engine (n = the total number of studies corresponding to each search term). Search terms related to brood disease (A) and pesticide exposure (B) are both compared to species diversity at the genus level. Genera with less than 5 studies in any brood disease search term (A) and less than 10 studies across any pesticide exposure search term (B) have been classified as 'Understudied' (brown) and grouped. Genera with no studies related to any brood disease search term (A) and no studies related to any pesticide exposure search term (B) have been classified as 'Unexplored' (grey) and grouped. (For interpretation of the references to colour in this figure legend, the reader is referred to the Web version of this article.)
Fig. 1 in The threat of pesticide and disease co-exposure to managed and wild bee larvae
Fig. 1. Flowers contaminated with brood pathogens and pesticides can lead to simultaneous exposure to pesticides and brood pathogens from flowers in adult foraging bees (A). This leads to brood being co-exposed to the stressors via food provisioning (B). Pesticides may increase larval mortality from brood infections directly through compromised immunocompetence (C), and/or indirectly through manipulating microbial communities and compromising food provisions from adult bees (D) (Icons8, 2022).
All data for the preprint Population genetics of Glossina palpalis gambiensis in the sleeping sickness focus of Boffa (Guinea) before and after eight years of vector control: no effect of control despite a significant decrease of human exposure to the disease
<p>Data set for the paper titled "Population genetics of <em>Glossina palpalis gambiensis</em> in the sleeping sickness focus of Boffa (Guinea) before and after eight years of vector control: no effect of control despite a significant decrease of human exposure to the disease"</p>
Assessing the Drug Exposure Risk of Infants Breastfed by Women With Inflammatory Bowel Disease
ClinicalTrials.gov study NCT03397108. IPD Sharing: YES. Countries: 1. Publications: 2.
Exposure to sugar rationing in the first 1000 days of life protected against chronic disease
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Data for: Developmental origins of Parkinson’s disease risk: perinatal exposure to the organochlorine pesticide dieldrin leads to sex-specific DNA modifications in critical neurodevelopmental pathways in the mouse midbrain
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Data from: Developmental Dieldrin exposure alters DNA methylation at genes related to dopaminergic neuron development and Parkinson's disease in mouse midbrain
Human and animal studies have shown that exposure to the organochlorine pesticide dieldrin is associated with increased risk of Parkinson's disease (PD). Despite previous work showing a link between developmental dieldrin exposure and increased neuronal susceptibility to MPTP toxicity in male C57BL/6 mice, the mechanism mediating this effect has not been identified. Here, we tested the hypothesis that developmental exposure to dieldrin increases neuronal susceptibility via genome-wide changes in DNA methylation. Starting at 8 weeks of age and prior to mating, female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin by feeding (every 3 days) throughout breeding, gestation, and lactation. At 12 weeks of age, pups were sacrificed and ventral mesencephalon, containing primarily substantia nigra, were microdissected. DNA was isolated and dieldrin-related changes in DNA methylation were assessed via reduced representation bisulfite sequencing (RRBS). We identified significant, sex-specific differentially methylated CpGs (DMCs) and regions (DMRs) by developmental dieldrin exposure (FDRNr4a2 and Lmx1b genes, which are involved in dopaminergic neuron development and maintenance. Developmental dieldrin exposure had distinct effects on the male and female epigenome. Together, our data suggest that developmental dieldrin exposure establishes sex-specific poised epigenetic states early in life. These poised epigenomes may mediate sensitivity to subsequent toxic stimuli and contribute to the development of late-life neurodegenerative disease, including PD.
Occupational exposure to silica and risk of heart disease: a systematic review with meta-analysis
<p><b><span>Objective</span></b> To search for evidence of the relationship between occupational silica exposure and heart disease.</p> <p><b><span>Design</span></b> A systematic review and meta-analysis.</p> <p><b><span>Background</span></b> Growing evidences suggest a connection between occupational silica exposure and heart disease; however, the link between them is less clear.</p> <p><b><span>Data sources </span></b>PubMed, ScienceDirect, Springer and EMBASE were searched for articles published between 1 January 1995 and 20 June 2019. Articles that investigated the effects of occupational silica exposure on heart disease risk were considered.</p> <p><b><span>Study selection </span></b><span>We included c</span><span>ohort stud</span><span>ies</span>, including prospective, retrospective and retro-prospective studies.</p> <p><b><span>Data extraction and synthesis</span></b> We extracted data by using a piloted data collection form and conducted random-effects meta-analysis and exposure-response analyses. The meta-relative risk (meta-RR), a measure of the average ratio of heart disease rates for those with and without silica exposure, was used as an inverse variance-weighted average of relative risks from the individual studies. The Newcastle-Ottawa Quality assessment Scale about cohort studies was used for study quality assessment.</p> <p><b><span>Outcome measure</span></b> We calculated heart disease risks of pulmonary heart disease, ischaemic heart disease and other heart diseases.</p> <p><span><b><span>Results</span></b> Twenty cohort articles were included. Results suggest a significant increase of overall heart disease risk (meta-RR = 1.08, 95% CI = 1.03, 1.13). Stronger evidences of association with pulmonary heart disease were found through both categories of heart disease risk estimate (meta-RR = 1.24, 95% CI = 1.08, 1.43) and exposure-response analyses (meta-RR = 1.39, 95% CI = 1.19, 1.62). Moreover, our subgroup analyses revealed that the statistical heterogeneity among studies could be attributed mainly to the diversities of reference group, occupation and study quality score.</span></p> <p><b><span>Conclusions</span></b> Silica-exposed workers have increased risk of overall heart disease, especially pulmonary heart disease. While further research is needed to better clarify the relationship between occupational silica exposure and ischaemic heart disease.</p>
Costs of attributable burden disease to PM2.5 ambient air pollution exposure in Medellín, Colombia, 2010-2016
<pre>The repository includes the consolidated databases design to analyze the economic cost of local attributable burden disease to PM2.5 ambient air pollution in Medellín from 2010-2016.</pre>
Data from: Developmental exposure to the Parkinson's disease-associated organochlorine pesticide dieldrin alters dopamine neurotransmission in α-synuclein pre-formed fibril (PFF)-injected mice
<p>Parkinson's disease (PD) is the fastest-growing neurological diseases worldwide, with increases outpacing aging and most rapid in recently industrialized areas, suggesting the role of environmental factors. Together, epidemiological studies, post-mortem analysis and mechanistic studies suggest that exposure to persistent organic pollutants, including the organochlorine pesticide dieldrin, increases PD risk. In mouse models, developmental dieldrin exposure causes male-specific exacerbation of neuronal susceptibility to MPTP and synucleinopathy. Specifically, developmental dieldrin exposure induces male-specific exacerbation of toxicity in the α-synuclein (α-syn) pre-formed fibril (PFF) model with increased deficits in striatal dopamine (DA) turnover and motor deficits on the challenging beam. Here, we hypothesized that alterations in DA handling contribute to the observed changes and assessed vesicular monoamine transporter 2 (VMAT2) function and DA release in this dieldrin/PFF two-hit model. Female C57BL/6 mice were exposed to 0.3 mg/kg dieldrin or vehicle every 3 days by feeding, starting at 8 weeks of age by ingestion and continuing throughout breeding, gestation, and lactation. Male offspring from independent litters underwent unilateral, intrastriatal injections of α-syn PFFs at 12 weeks of age and vesicular <sup>3</sup>H-DA uptake assays and fast-scan cyclic voltammetry (FSCV) were performed at 4 months post-PFF injection. We observed a dieldrin-induced increase in DA release in striatal slices in PFF-injected animals, but no change in VMAT2 activity. These results suggest that developmental dieldrin exposure increases a compensatory response to synucleinopathy-triggered striatal DA loss and supports our hypothesis that alterations in DA handling may underly the observed exacerbation of PFF-induced deficits in motor behavior and DA turnover.</p>
Hydroxychloroquine Post Exposure Prophylaxis for Coronavirus Disease (COVID-19)
ClinicalTrials.gov study NCT04318444. IPD Sharing: NO. Countries: 1. Publications: 1.
Melanoma of the Skin and Exposure to Solar Ultraviolet Radiation at Work in Modena Territory: a Case-control Study to Promote an Active Search and Prevention of Occupational Diseases Based on Recent I
ClinicalTrials.gov study NCT07251335. IPD Sharing: NO. Countries: 1. Publications: 7.
Assessment of Pre-Exposure Prophylaxis (PrEP) Administered at Sexually Transmitted Disease (STD) Clinics
ClinicalTrials.gov study NCT01632995. IPD Sharing: Not stated. Countries: 1. Publications: 1.
Occupational exposure to silica and risk of heart disease: a systematic review with meta-analysis
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Data from: Developmental exposure to the Parkinson’s disease-associated organochlorine pesticide dieldrin alters dopamine neurotransmission in α-synuclein pre-formed fibril (PFF)-injected mice
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Developmental dieldrin exposure alters DNA methylation at genes related to dopaminergic neuron development and Parkinson’s disease in mouse midbrain
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Data from: Early-life disease exposure and associations with adult survival, cause of death, and reproductive success in preindustrial humans
A leading hypothesis proposes that increased human life span since 1850 has resulted from decreased exposure to childhood infections, which has reduced chronic inflammation and later-life mortality rates, particularly from cardiovascular disease, stroke, and cancer. Early-life cohort mortality rate often predicts later-life survival in humans, but such associations could arise from factors other than disease exposure. Additionally, the impact of early-life disease exposure on reproduction remains unknown, and thus previous work ignores a major component of fitness through which selection acts upon life-history strategy. We collected data from seven 18th- and 19th-century Finnish populations experiencing naturally varying mortality and fertility levels. We quantified early-life disease exposure as the detrended child mortality rate from infectious diseases during an individual's first 5 y, controlling for important social factors. We found no support for an association between early-life disease exposure and all-cause mortality risk after age 15 or 50. We also found no link between early-life disease exposure and probability of death specifically from cardiovascular disease, stroke, or cancer. Independent of survival, there was no evidence to support associations between early-life disease exposure and any of several aspects of reproductive performance, including lifetime reproductive success and age at first birth, in either males or females. Our results do not support the prevailing assertion that exposure to infectious diseases in early life has long-lasting associations with later-life all-cause mortality risk or mortality putatively linked to chronic inflammation. Variation in adulthood conditions could therefore be the most likely source of recent increases in adult life span.
Data from: Use of environmental sites by mule deer: a proxy for relative risk of chronic wasting disease exposure and transmission
Prions that cause chronic wasting disease (CWD) in cervids can remain infective for years outside the host. Infectious cervids shed prions for a long time, consequently depositing prions in frequently used areas. These environmental prions are important in CWD epidemiology. Unfortunately, effective tools for quantifying CWD prions in soil, water, and other environmental sources are not currently available. Our goal was to investigate relative differences in visits by mule deer (Odocoileus hemionus hemionus) to various environmental site types as an indicator of the relative risk of prion contamination and disease transmission. For this, we deployed a system of triggered-by-movement cameras at eight site types in a CWD-endemic area in Saskatchewan, Canada. We first assessed whether the relative differences among site types in the frequency of visits by mule deer of any sex-and-age class, males, and females varied by season and site type. We then assessed whether the rate of behaviors with a high risk of environmental prion transmission (either contamination or acquisition) differed by season and site type. Finally, we assessed whether the intensity of visitation, based on the number of animals per picture, differed by season and site type. We found that grain sources and beds were key attractants for mule deer: (1) The greatest number of pictures with mule deer per camera-day occurred at grain sources across all seasons, except in fawning, when beds were the most visited sites; (2) during pre-rut and early gestation, mule deer visited grain sources at least twice as often as most other sites; (3) females were more likely to visit beds and grain sources, but there was no significant site preferences for males after accounting for season; (4) mule deer were most likely to be pictured contacting the environment at grain sources in early gestation; and (5) beds and grain sources were the most intensively visited sites. We also found that environmental contacts at waterholes were more frequent during spring. We discuss the potential importance of various sites in the transmission of CWD and how their modification could potentially reduce the risk of prion environmental exposure among mule deer.
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Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.