The Experts below are selected from a list of 49122 Experts worldwide ranked by ideXlab platform
Katherine C Thompson - One of the best experts on this subject based on the ideXlab platform.
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Environmental Pollutant ozone causes damage to lung surfactant protein b sp b
Biochemistry, 2015Co-Authors: Joanna M Hemming, Brian R Hughes, Arwel V Hughes, Salvador Tomas, A. R. Rennie, Stanley W Botchway, Richard A. Campbell, Thomas Arnold, Katherine C ThompsonAbstract:Lung surfactant protein B (SP-B) is an essential protein found in the surfactant fluid at the air–water interface of the lung. Exposure to the air Pollutant ozone could potentially damage SP-B and lead to respiratory distress. We have studied two peptides, one consisting of the N-terminus of SP-B [SP-B(1–25)] and the other a construct of the N- and C-termini of SP-B [SP-B(1–25,63–78)], called SMB. Exposure to dilute levels of ozone (∼2 ppm) of monolayers of each peptide at the air–water interface leads to a rapid reaction, which is evident from an increase in the surface tension. Fluorescence experiments revealed that this increase in surface tension is accompanied by a loss of fluorescence from the tryptophan residue at the interface. Neutron and X-ray reflectivity experiments show that, in contrast to suggestions in the literature, the peptides are not solubilized upon oxidation but rather remain at the interface with little change in their hydration. Analysis of the product material reveals that no cle...
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Environmental Pollutant ozone causes damage to lung surfactant protein b sp b
Biochemistry, 2015Co-Authors: Joanna M Hemming, Brian R Hughes, Arwel V Hughes, Salvador Tomas, A. R. Rennie, Stanley W Botchway, Richard A. Campbell, Thomas Arnold, Katherine C ThompsonAbstract:Lung surfactant protein B (SP-B) is an essential protein found in the surfactant fluid at the air-water interface of the lung. Exposure to the air Pollutant ozone could potentially damage SP-B and lead to respiratory distress. We have studied two peptides, one consisting of the N-terminus of SP-B [SP-B(1-25)] and the other a construct of the N- and C-termini of SP-B [SP-B(1-25,63-78)], called SMB. Exposure to dilute levels of ozone (~2 ppm) of monolayers of each peptide at the air-water interface leads to a rapid reaction, which is evident from an increase in the surface tension. Fluorescence experiments revealed that this increase in surface tension is accompanied by a loss of fluorescence from the tryptophan residue at the interface. Neutron and X-ray reflectivity experiments show that, in contrast to suggestions in the literature, the peptides are not solubilized upon oxidation but rather remain at the interface with little change in their hydration. Analysis of the product material reveals that no cleavage of the peptides occurs, but a more hydrophobic product is slowly formed together with an increased level of oligomerization. We attributed this to partial unfolding of the peptides. Experiments conducted in the presence of phospholipids reveal that the presence of the lipids does not prevent oxidation of the peptides. Our results strongly suggest that exposure to low levels of ozone gas will damage SP-B, leading to a change in its structure. The implication is that the oxidized protein will be impaired in its ability to interact at the air-water interface with negatively charged phosphoglycerol lipids, thus compromising what is thought to be its main biological function.
Sebhat Erqou - One of the best experts on this subject based on the ideXlab platform.
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association between cumulative social risk particulate matter Environmental Pollutant exposure and cardiovascular disease risk
BMC Cardiovascular Disorders, 2020Co-Authors: Ann Canterbury, Justin B Echouffotcheugui, Daniel Shpilsky, Aryan Aiyer, Steven E Reis, Sebhat ErqouAbstract:Background Long-term exposure to pollution has been shown to increase risk of cardiovascular disease (CVD) and mortality, and may contribute to the increased risk of CVD among individuals with higher social risk. Methods Data from the community-based Heart Strategies Concentrating on Risk Evaluation (HeartSCORE) study were used to quantify Cumulative Social Risk (CSR) by assigning a score of 1 for the presence of each of 4 social risk factors: racial minority, single living, low income, and low educational status. 1-year average air pollution exposure to PM2.5 was estimated using land-use regression models. Associations with clinical outcomes were assessed using Cox models, adjusting for traditional CVD risk factors. The primary clinical outcome was combined all-cause mortality and nonfatal CVD events. Results Data were available on 1933 participants (mean age 59 years, 66% female, 44% Black). In a median follow up time of 8.3 years, 137 primary clinical outcome events occurred. PM2.5 exposure increased with higher CSR score. PM2.5 was independently associated with clinical outcome (adjusted hazard ratio [HR]: 1.19 [95% CI: 1.00, 1.41]). Participants with ≥2 CSR factors had an adjusted HR of 2.34 (1.48-3.68) compared to those with CSR = 0. The association was attenuated after accounting for PM2.5 (HR: 2.16; [1.34, 3.49]). Mediation analyses indicate that PM2.5 explained 13% of the risk of clinical outcome in individuals with CSR score ≥ 2. Conclusion In a community-based cohort study, we found that the association of increasing CSR with higher CVD and mortality risks is partially accounted for by exposure to PM2.5 Environmental Pollutants.
Agneta Akesson - One of the best experts on this subject based on the ideXlab platform.
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relation between dietary cadmium intake and biomarkers of cadmium exposure in premenopausal women accounting for body iron stores
Environmental Health, 2011Co-Authors: Bettina Julin, Billy Amzal, Marie Vahter, Alicja Wolk, Marika Berglund, Agneta AkessonAbstract:Background Cadmium is a widespread Environmental Pollutant with adverse effects on kidneys and bone, but with insufficiently elucidated public health consequences such as risk of end-stage renal diseases, fractures and cancer. Urinary cadmium is considered a valid biomarker of lifetime kidney accumulation from overall cadmium exposure and thus used in the assessment of cadmium-induced health effects. We aimed to assess the relationship between dietary cadmium intake assessed by analyses of duplicate food portions and cadmium concentrations in urine and blood, taking the toxicokinetics of cadmium into consideration.
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population toxicokinetic modeling of cadmium for health risk assessment
Environmental Health Perspectives, 2009Co-Authors: Billy Amzal, Bettina Julin, Marie Vahter, Alicja Wolk, Agneta AkessonAbstract:Background Cadmium is a widespread Environmental Pollutant that has been shown to exert toxic effects on kidney and bones in humans after long-term exposure. Urinary cadmium concentration is considered a good biomarker of accumulated cadmium in kidney, and diet is the main source of cadmium among nonsmokers.
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population toxicokinetic modeling of cadmium for health risk assessment
Environmental Health Perspectives, 2009Co-Authors: Billy Amzal, Bettina Julin, Marie Vahter, Alicja Wolk, Agneta AkessonAbstract:BackgroundCadmium is a widespread Environmental Pollutant that has been shown to exert toxic effects on kidney and bones in humans after long-term exposure. Urinary cadmium concentration is conside...
Joanna M Hemming - One of the best experts on this subject based on the ideXlab platform.
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Environmental Pollutant ozone causes damage to lung surfactant protein b sp b
Biochemistry, 2015Co-Authors: Joanna M Hemming, Brian R Hughes, Arwel V Hughes, Salvador Tomas, A. R. Rennie, Stanley W Botchway, Richard A. Campbell, Thomas Arnold, Katherine C ThompsonAbstract:Lung surfactant protein B (SP-B) is an essential protein found in the surfactant fluid at the air–water interface of the lung. Exposure to the air Pollutant ozone could potentially damage SP-B and lead to respiratory distress. We have studied two peptides, one consisting of the N-terminus of SP-B [SP-B(1–25)] and the other a construct of the N- and C-termini of SP-B [SP-B(1–25,63–78)], called SMB. Exposure to dilute levels of ozone (∼2 ppm) of monolayers of each peptide at the air–water interface leads to a rapid reaction, which is evident from an increase in the surface tension. Fluorescence experiments revealed that this increase in surface tension is accompanied by a loss of fluorescence from the tryptophan residue at the interface. Neutron and X-ray reflectivity experiments show that, in contrast to suggestions in the literature, the peptides are not solubilized upon oxidation but rather remain at the interface with little change in their hydration. Analysis of the product material reveals that no cle...
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Environmental Pollutant ozone causes damage to lung surfactant protein b sp b
Biochemistry, 2015Co-Authors: Joanna M Hemming, Brian R Hughes, Arwel V Hughes, Salvador Tomas, A. R. Rennie, Stanley W Botchway, Richard A. Campbell, Thomas Arnold, Katherine C ThompsonAbstract:Lung surfactant protein B (SP-B) is an essential protein found in the surfactant fluid at the air-water interface of the lung. Exposure to the air Pollutant ozone could potentially damage SP-B and lead to respiratory distress. We have studied two peptides, one consisting of the N-terminus of SP-B [SP-B(1-25)] and the other a construct of the N- and C-termini of SP-B [SP-B(1-25,63-78)], called SMB. Exposure to dilute levels of ozone (~2 ppm) of monolayers of each peptide at the air-water interface leads to a rapid reaction, which is evident from an increase in the surface tension. Fluorescence experiments revealed that this increase in surface tension is accompanied by a loss of fluorescence from the tryptophan residue at the interface. Neutron and X-ray reflectivity experiments show that, in contrast to suggestions in the literature, the peptides are not solubilized upon oxidation but rather remain at the interface with little change in their hydration. Analysis of the product material reveals that no cleavage of the peptides occurs, but a more hydrophobic product is slowly formed together with an increased level of oligomerization. We attributed this to partial unfolding of the peptides. Experiments conducted in the presence of phospholipids reveal that the presence of the lipids does not prevent oxidation of the peptides. Our results strongly suggest that exposure to low levels of ozone gas will damage SP-B, leading to a change in its structure. The implication is that the oxidized protein will be impaired in its ability to interact at the air-water interface with negatively charged phosphoglycerol lipids, thus compromising what is thought to be its main biological function.
Shau Ku Huang - One of the best experts on this subject based on the ideXlab platform.
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a common Environmental Pollutant 4 nonylphenol promotes allergic lung inflammation in a murine model of asthma
Allergy, 2013Co-Authors: Jauling Suen, Shihhsien Hsu, Chihhsing Hung, Y S Chao, C L Lee, C Y Lin, T H Weng, Shau Ku HuangAbstract:Background Exposure to Environmental hormones, such as alkylphenols, has been suggested to be associated with the development of asthma, but the mechanism of action remains unclear. Objective This study examined the effect of 4-nonylphenol (NP), one of the most important alkylphenols, on conventional dendritic cells (cDCs) and adaptive T-cell responses. It also explored the role of aryl hydrocarbon receptor (AhR) in NP's effect. Methods NP-conditioned bone marrow-derived DCs (BM-DCs) and splenic CD11c+ cDCs were assessed regarding function in a murine model under conditions relevant to route and level of exposure in humans. Results Our results showed that splenic cDCs from NP-exposed mice have potent Th2-skewing ability and secrete increased levels of IL-6 and TNF-α, but not IL-10 and IL-12, at baseline and after stimulation with LPS. Further, bone marrow-derived DCs were cultured in the presence of NP and showed similar cytokine pattern and influenced the antigen-specific T cells secreting significantly less IFN-γ. Importantly, NP-exposed mice developed more severe OVA-induced allergic lung inflammation compared with control group. Interestingly, in a congenic strain of mice carrying low-affinity, ligand-binding mutant AhR (AhRd), NP's effect on DC functions and lung inflammation was not observed in vitro and in vivo. Conclusion These results suggested that NP may disturb physiologic function of DCs through, in part, AhR-dependent mechanisms, supporting the importance of NP exposure on the regulation of DC functions and allergic inflammation.