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17 results for “Co-exposure”

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zenodo44/100

Increased uptake of silica nanoparticles in inflamed macrophages but not upon co-exposure to micron-sized particles

<p>Silica nanoparticles (NPs) are widely used in various industrial and biomedical applications. Little is known about the cellular uptake of co-exposed silica particles, as can be expected in our daily life. In addition, an inflamed microenvironment might affect a NP&rsquo;s uptake and a cell&rsquo;s physiological response. Herein, prestimulated mouse J774A.1 macrophages with bacterial lipopolysaccharide were post-exposed to micron- and nanosized silica particles, either alone or together, i.e., simultaneously or sequentially, for different time points. The results indicated a morphological change and increased expression of tumor necrosis factor alpha in lipopolysaccharide prestimulated cells, suggesting a M1-polarization phenotype. Confocal laser scanning microscopy revealed the intracellular accumulation and uptake of both particle types for all exposure conditions. A flow cytometry analysis showed an increased particle uptake in lipopolysaccharide prestimulated macrophages. However, no differences were observed in particle uptakes between single- and co-exposure conditions. We did not observe any colocalization between the two silica (SiO<sub>2</sub>) particles. However, there was a positive colocalization between lysosomes and nanosized silica but only a few colocalized events with micro-sized silica particles. This suggests differential intracellular localizations of silica particles in macrophages and a possible activation of distinct endocytic pathways. The results demonstrate that the cellular uptake of NPs is modulated in inflamed macrophages but not in the presence of micron-sized particles.</p>

opencc-by-4.0Jul 2020View details →
zenodo40/100

Understanding the risks of co-exposures in a changing world: A case study of dual monitoring of the biotoxin domoic acid and Vibrio spp. in Pacific oyster

<div> <p><span>Assessing the co-occurrence of multiple health risk factors in coastal ecosystems is challenging due to the complexity of multi-factor interactions and limited availability simultaneously collected data. Understanding co-occurrence is particularly important for risk factors that may be associated with or occur in similar environmental conditions. In marine ecosystems, the co-occurrence of harmful algal bloom toxins and bacterial pathogens within the genus <em>Vibrio </em>may impact both ecosystem and human health. This study examined the co-occurrence of <em>Vibrio</em> spp. and domoic acid (DA) produced by the harmful algae <em>Pseudonitzschia</em> by 1) analyzing existing California Department of Public Health monitoring data for <em>V. parahaemolyticus</em> and DA in oysters; 2) and conducting a one-year seasonal monitoring of these risk factors across two Southern California embayments. Existing public health monitoring efforts in the state were robust for individual risk factors; however, it was difficult to evaluate the co-occurrence of these risk factors in oysters due to low number of co-monitoring instances between 2015 and 2020. Seasonal co-monitoring of that DA and <em>Vibrio</em> spp. (<em>V. vulnificus</em> or <em>V. parahaemolyticus</em>) at two embayments revealed the co-occurrence of these health risk factors in 35% of sampled oysters in most seasons. Interestingly, both the overall detection frequency and co-occurrence of these risk factors was considerably less frequent in water samples. These findings may in part suggest the slow depuration of <em>Vibrio </em>spp. and DA in oysters as residual levels may be retained. This study expanded our understanding of the simultaneous presence of DA and <em>Vibrio</em> spp. in bivalves and demonstrate the feasibility of co-monitoring different risk factors from the same sample. Individual programs monitoring for different risk factors from the same sample matrix may consider combining efforts to reduce cost, streamline the process, and better understand the prevalence of co-occurring health risk factors.</span></p> </div>

opencc-by-4.0Apr 2024View details →
zenodo40/100

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.)

opencc-by-4.0Apr 2022View details →
zenodo40/100

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.)

opencc-by-4.0Apr 2022View details →
zenodo40/100

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.)

opencc-by-4.0Apr 2022View details →
zenodo40/100

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).

opencc-by-4.0Apr 2022View details →
dryad40/100

Data from: Co-exposure to a honeybee pathogen and an insecticide: Synergistic effects in a new solitary bee host but not in Apis mellifera

Open the record for dataset details and reuse information.

publicFeb 2025View details →
edi40/100

Co-exposure of uranyl acetate and sodium arsenite differentially alters gene expression in CD3/CD28 activated CD4+ T-cells.

Communities in the western region of the United States experience environmental exposure to metal mixtures from living in proximity to numerous unremediated abandoned uranium mines. Metals including arsenic and uranium co-occur in and around these sites at levels higher than the United States Environmental Protection Agency maximum contaminant levels. To address the potential effect of these metals on the activation of CD4+ T-cells, we used RNA sequencing methods to determine the effect of exposure to uranyl acetate, sodium arsenite or a mixture of uranyl acetate and sodium arsenite. Oxidative stress is a mechanism proposed for metal toxicity, but findings for uranium differ across cell models. No significant changes in oxidative stress genes were detected for uranyl acetate, in contrast to sodium arsenite. Sodium arsenite induced a dose dependent effect on activation associated gene expression, targeting immune response genes at the lower dose. While uranyl acetate alone did not significantly alter activation associated gene expression, the mixture demonstrated a combined effect relative to sodium arsenite alone. The results demonstrate the need to investigate uranium alone and in metalloid mixtures at environmentally relevant concentrations to better understand the toxicological impact of these mixtures on T-cell activation, function and immune dysregulation.

openCC0Apr 2021View details →
ClinicalTrials.gov32/100

Effects of Co-Exposure to Air Pollution and Allergen

ClinicalTrials.gov study NCT01792232. IPD Sharing: Not stated. Countries: 1. Publications: 10.

restrictedIPD-UNDECIDEDFeb 2026View details →
geo24/100

ADDITIVE EFFECTS OF MILLIMETER WAVES AND 2 DEOXYGLUCOSE CO-EXPOSURE ON THE HUMAN KERATINOCYTE TRANSCRIPTOME

GEO Series GSE83829. Homo sapiens. 16 samples. Type: Expression profiling by array.

openGEO-OpenSep 2016View details →
geo24/100

Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a dosage study (study 2/2)

GEO Series GSE71520. Homo sapiens. 21 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenOct 2015View details →
geo24/100

Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters, a time course study (study 1/2)

GEO Series GSE71519. Homo sapiens. 41 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenOct 2015View details →
geo20/100

Synergistic gene expression signature observed in TK6 cells upon co-exposure to UVC-irradiation and protein kinase C-activating tumor promoters

GEO Series GSE71521. Homo sapiens. 62 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenOct 2015View details →
geo16/100

Hepatotoxicity evaluation of co-exposure of microplastics and TBBPA by 3D biofabricated multicellular organoids

GEO Series GSE212099. Homo sapiens. 27 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenAug 2025View details →
geo16/100

Next Generation Sequencing of lung homogenate mRNA from 8-12 week male C57BL/6 mice following Sham, Carbon Black, Ozone, or Carbon Black-Ozone Co-exposure.

GEO Series GSE161538. Mus musculus. 28 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenNov 2020View details →
geo16/100

Caco2 response to methotrexate, lactoferrin, and methotrexate-lactoferrin co-exposure

GEO Series GSE140066. Homo sapiens. 12 samples. Type: Expression profiling by high throughput sequencing.

openGEO-OpenJan 2020View details →
geo12/100

Synergism of Iraqi Sand/Cigarette Smoke Co-Exposure in Rats

GEO Series GSE28804. Rattus norvegicus. 24 samples. Type: Expression profiling by array.

openGEO-OpenJan 2012View details →

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International Brain Laboratory public data

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