8,688 research outputs found

    Asian Dust Storm Elevates Childrenâs Respiratory Health Risks: A Spatiotemporal Analysis of Childrenâs Clinic Visits across Taipei (Taiwan)

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    [[abstract]]Concerns have been raised about the adverse impact of Asian dust storms (ADS) on human health; however, few studies have examined the effect of these events on childrenâs health. Using databases from the Taiwan National Health Insurance and Taiwan Environmental Protection Agency, this study investigates the documented daily visits of children to respiratory clinics during and after ADS that occurred from 1997 to 2007 among 12 districts across Taipei City by applying a Bayesian structural additive regressive model controlled for spatial and temporal patterns. This study finds that the significantly impact of elevated childrenâs respiratory clinic visits happened after ADS. Five of the seven lagged days had increasing percentages of relative rate, which was consecutively elevated from a 2-day to a 5-day lag by 0.63%,2.19% for preschool children (i.e., 0,6 years of age) and 0.72%,3.17% for school children (i.e., 7,14 years of age). The spatial pattern of clinic visits indicated that geographical heterogeneity was possibly associated with the clinicâs location and accessibility. Moreover, day-of-week effects were elevated on Monday, Friday, and Saturday. We concluded that ADS may significantly increase the risks of respiratory diseases consecutively in the week after exposure, especially in school children

    Supplementary Catechins Attenuate Cooking-Oil-Fumes-Induced Oxidative Stress in Rat Lung

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    Cooking-oil-fumes containing toxic components may induce reactive oxygen species (ROS) to oxidize macromolecules and lead to acute lung injury. Our previous study showed that a decaffineated green tea extract containing ( +)-catechin, (-) -epicatechin, (+)-gallocatechin, (-)-epigallocatechin, (- )- epicatechin gallate, and (-)-epigallocatechin gallate can inhibit oxidation,, inflammation, and apoptosis. We determined whether the catechins supplement may reduce cooking-oil-fumes-induced acute lung injury in rat. In the urethane-anesthetized Wistar rat subjected to 30-120 min of cooking-oil-fumes exposure, blood ROS significantly, increased in the recovery stage. After 30-min cooking-oil- fumes exposure, the enhanced blood ROS level further increased in a time-dependent manner during the recovery stage (321 +/- 69 counts/10 s after 1 h, 540 +/- 89 counts/ 10 s after 2 h. and 873 +/- 112 counts/10 s after 4 h). Four hours after 30-min cooking-oil-fumes exposure, lung lavage neutrophils and ROS its well as lung tissue dityrosine and 4 -hydroxy-2-nonenal increased significantly. Two weeks of catechins supplement significantly reduced the enhanced lavage ROS, lung dityrosine and 4-hydroxy-2-nonenal level. Cooking-oil- fumes-induced oxidative stress decreased lung Bcl-2/Bax ratio and HSP70 expression, but catechins treatment preserved the downregulation of Bcl-2/ Bax ratio and HSP70 expression. We conclude that catechins supplement attenuates cooking-oil-fumes-induced acute lung injury via the preservation of oil-smoke induced downregulation of antioxidant, antiapoptosis, and chaperone protein expression

    Nrf2 deficiency influences susceptibility to steroid resistance via HDAC2 reduction

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    Abnormal lung inflammation and oxidant burden are associated with a significant reduction in histone deacetylase 2 (HDAC2) abundance and steroid resistance. We hypothesized that Nrf2 regulates steroid sensitivity via HDAC2 in response to inflammation in mouse lung. Furthermore, HDAC2 deficiency leads to steroid resistance in attenuating lung inflammatory response, which may be due to oxidant/antioxidant imbalance. Loss of antioxidant transcription factor Nrf2 resulted in decreased HDAC2 level in lung, and increased inflammatory lung response which was not reversed by steroid. Thus, steroid resistance or inability of steroids to control lung inflammatory response is dependent on Nrf2-HDAC2 axis. These findings have implications in steroid resistance, particularly during the conditions of oxidative stress when the lungs are more susceptible to inflammatory response, which is seen in patients with chronic obstructive pulmonary disease, asthma, rheumatoid arthritis, and inflammatory bowel disease

    Deletion of vitamin D receptor leads to premature emphysema/COPD by increased matrix metalloproteinases and lymphoid aggregates formation

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    Deficiency of vitamin D is associated with accelerated decline in lung function. Vitamin D is a ligand for nuclear hormone vitamin D receptor (VDR), and upon binding it modulates various cellular functions. The level of VDR is reduced in lungs of patients with chronic obstructive pulmonary disease (COPD) which led us to hypothesize that deficiency of VDR leads to significant alterations in lung phenotype that are characteristics of COPD/emphysema associated with increased inflammatory response. We found that VDR knock-out (VDR(-/-)) mice had increased influx of inflammatory cells, phospho-acetylation of nuclear factor-kappaB (NF-κB) associated with increased proinflammatory mediators, and up-regulation of matrix metalloproteinases (MMPs) MMP-2, MMP-9, and MMP-12 in the lung. This was associated with emphysema and decline in lung function associated with lymphoid aggregates formation compared to WT mice. These findings suggest that deficiency of VDR in mouse lung can lead to an early onset of emphysema/COPD because of chronic inflammation, immune dysregulation, and lung destruction
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