Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung
Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury respon...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Schiffers, Caspar [verfasserIn] |
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| Format: |
E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2017transfer abstract |
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| Umfang: |
2 |
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| Übergeordnetes Werk: |
Enthalten in: New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells - Wu, Zhi-Sheng ELSEVIER, 2020, the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research, New York, NY [u.a.] |
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| Übergeordnetes Werk: |
volume:112 ; year:2017 ; pages:56-57 ; extent:2 |
| Links: |
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| DOI / URN: |
10.1016/j.freeradbiomed.2017.10.077 |
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| 245 | 1 | 0 | |a Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung |
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| 520 | |a Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. | ||
| 520 | |a Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. | ||
| 700 | 1 | |a Dustin, Christopher M. |4 oth | |
| 700 | 1 | |a Lundblad, Lennart |4 oth | |
| 700 | 1 | |a Hristova, Milena |4 oth | |
| 700 | 1 | |a Habibovic, Aida |4 oth | |
| 700 | 1 | |a van der Vliet, Albert |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier |a Wu, Zhi-Sheng ELSEVIER |t New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells |d 2020 |d the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research |g New York, NY [u.a.] |w (DE-627)ELV003689417 |
| 773 | 1 | 8 | |g volume:112 |g year:2017 |g pages:56-57 |g extent:2 |
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10.1016/j.freeradbiomed.2017.10.077 doi GBV00000000000059A.pica (DE-627)ELV04111096X (ELSEVIER)S0891-5849(17)30861-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Schiffers, Caspar verfasserin aut Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Dustin, Christopher M. oth Lundblad, Lennart oth Hristova, Milena oth Habibovic, Aida oth van der Vliet, Albert oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:112 year:2017 pages:56-57 extent:2 https://doi.org/10.1016/j.freeradbiomed.2017.10.077 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 112 2017 56-57 2 045F 570 |
| spelling |
10.1016/j.freeradbiomed.2017.10.077 doi GBV00000000000059A.pica (DE-627)ELV04111096X (ELSEVIER)S0891-5849(17)30861-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Schiffers, Caspar verfasserin aut Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Dustin, Christopher M. oth Lundblad, Lennart oth Hristova, Milena oth Habibovic, Aida oth van der Vliet, Albert oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:112 year:2017 pages:56-57 extent:2 https://doi.org/10.1016/j.freeradbiomed.2017.10.077 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 112 2017 56-57 2 045F 570 |
| allfields_unstemmed |
10.1016/j.freeradbiomed.2017.10.077 doi GBV00000000000059A.pica (DE-627)ELV04111096X (ELSEVIER)S0891-5849(17)30861-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Schiffers, Caspar verfasserin aut Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Dustin, Christopher M. oth Lundblad, Lennart oth Hristova, Milena oth Habibovic, Aida oth van der Vliet, Albert oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:112 year:2017 pages:56-57 extent:2 https://doi.org/10.1016/j.freeradbiomed.2017.10.077 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 112 2017 56-57 2 045F 570 |
| allfieldsGer |
10.1016/j.freeradbiomed.2017.10.077 doi GBV00000000000059A.pica (DE-627)ELV04111096X (ELSEVIER)S0891-5849(17)30861-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Schiffers, Caspar verfasserin aut Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Dustin, Christopher M. oth Lundblad, Lennart oth Hristova, Milena oth Habibovic, Aida oth van der Vliet, Albert oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:112 year:2017 pages:56-57 extent:2 https://doi.org/10.1016/j.freeradbiomed.2017.10.077 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 112 2017 56-57 2 045F 570 |
| allfieldsSound |
10.1016/j.freeradbiomed.2017.10.077 doi GBV00000000000059A.pica (DE-627)ELV04111096X (ELSEVIER)S0891-5849(17)30861-4 DE-627 ger DE-627 rakwb eng 570 610 570 DE-600 610 DE-600 620 VZ 52.57 bkl 53.36 bkl Schiffers, Caspar verfasserin aut Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung 2017transfer abstract 2 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. Dustin, Christopher M. oth Lundblad, Lennart oth Hristova, Milena oth Habibovic, Aida oth van der Vliet, Albert oth Enthalten in Elsevier Wu, Zhi-Sheng ELSEVIER New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells 2020 the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research New York, NY [u.a.] (DE-627)ELV003689417 volume:112 year:2017 pages:56-57 extent:2 https://doi.org/10.1016/j.freeradbiomed.2017.10.077 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U 52.57 Energiespeicherung VZ 53.36 Energiedirektumwandler elektrische Energiespeicher VZ AR 112 2017 56-57 2 045F 570 |
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Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung |
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Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. |
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Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. |
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Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement. |
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<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV04111096X</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230625233726.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">180725s2017 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.freeradbiomed.2017.10.077</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">GBV00000000000059A.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV04111096X</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0891-5849(17)30861-4</subfield></datafield><datafield tag="040" ind1=" " ind2=" "><subfield code="a">DE-627</subfield><subfield code="b">ger</subfield><subfield code="c">DE-627</subfield><subfield code="e">rakwb</subfield></datafield><datafield tag="041" ind1=" " ind2=" "><subfield code="a">eng</subfield></datafield><datafield tag="082" ind1="0" ind2=" "><subfield code="a">570</subfield><subfield code="a">610</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">570</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">610</subfield><subfield code="q">DE-600</subfield></datafield><datafield tag="082" ind1="0" ind2="4"><subfield code="a">620</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">52.57</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="084" ind1=" " ind2=" "><subfield code="a">53.36</subfield><subfield code="2">bkl</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Schiffers, Caspar</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Progressive loss of dual oxidase 1 (DUOX1) contributes to impaired airway epithelial wound responses in the aging lung</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2017transfer abstract</subfield></datafield><datafield tag="300" ind1=" " ind2=" "><subfield code="a">2</subfield></datafield><datafield tag="336" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zzz</subfield><subfield code="2">rdacontent</subfield></datafield><datafield tag="337" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">z</subfield><subfield code="2">rdamedia</subfield></datafield><datafield tag="338" ind1=" " ind2=" "><subfield code="a">nicht spezifiziert</subfield><subfield code="b">zu</subfield><subfield code="2">rdacarrier</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Age-related chronic diseases, including chronic respiratory diseases such as COPD, are associated with organ function decline, impaired regenerative capacity, and immuno-senescence. Our recent studies indicate that such reparative processes in the lung are mediated by innate epithelial injury responses and production of reactive oxygen species (ROS) by the NADPH oxidase dual oxidase 1 (DUOX1), which were found to be associated with oxidation and activation of epithelial tyrosine kinases, such as epidermal growth factor receptor (EGFR) and the non-receptor tyrosine kinase Src, and also with epithelial secretion of alarmins such as IL-33, which promote epithelial regeneration by activating type 2 immune responses. Contrasting the common belief that aging is associated with increased ROS production, we observed that DUOX1 expression in mouse lungs markedly decreases with age. Moreover, we noticed that DUOX1-deficient mice display accelerated age-related decline in lung function and features of emphysema, as shown by airspace enlargement and increased lung compliance. We hypothesized that loss of DUOX1 may contribute to other features of lung aging, but aged-related lung changes such as increased parenchymal collagen deposition, molecular indices of senescence, or tissue levels of pro-inflammatory cytokines, were all largely unaltered in DUOX1-deficient mice. However, we observed that aged mice display markedly attenuated innate airway responses to inhaled allergens, as illustrated by diminished secretion of IL-33 and other related cytokines. Similar findings were observed in vitro using cultured mouse tracheal epithelial cells (MTEC), in which MTECs from older mice showed dramatically reduced innate responses to injury, which was associated with reduced oxidation and activation of Src and EGFR. Consistent with a potential age-related suppression of DUOX1 by epigenetic mechanisms such as promoter hypermethylation, allergen-induced IL-33 secretion in MTECs from aged mice could be rescued by treatment with the DNA methyltransferase inhibitor AzdC. Overall, these results underline the importance of DUOX1 in airway host defense and regenerative capacity, and indicate that age-related loss of DUOX1 contributes to accelerated impairment of epithelial regenerative capacity and air-space enlargement.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Dustin, Christopher M.</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Lundblad, Lennart</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Hristova, Milena</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Habibovic, Aida</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">van der Vliet, Albert</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier</subfield><subfield code="a">Wu, Zhi-Sheng ELSEVIER</subfield><subfield code="t">New organic dyes with varied arylamine donors as effective co-sensitizers for ruthenium complex N719 in dye sensitized solar cells</subfield><subfield code="d">2020</subfield><subfield code="d">the official journal of the Oxygen Society, a constituent member of the International Society for Free Radical Research</subfield><subfield code="g">New York, NY [u.a.]</subfield><subfield code="w">(DE-627)ELV003689417</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:112</subfield><subfield code="g">year:2017</subfield><subfield code="g">pages:56-57</subfield><subfield code="g">extent:2</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.freeradbiomed.2017.10.077</subfield><subfield code="3">Volltext</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_USEFLAG_U</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">GBV_ELV</subfield></datafield><datafield tag="912" ind1=" " ind2=" "><subfield code="a">SYSFLAG_U</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">52.57</subfield><subfield code="j">Energiespeicherung</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="936" ind1="b" ind2="k"><subfield code="a">53.36</subfield><subfield code="j">Energiedirektumwandler</subfield><subfield code="j">elektrische Energiespeicher</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">112</subfield><subfield code="j">2017</subfield><subfield code="h">56-57</subfield><subfield code="g">2</subfield></datafield><datafield tag="953" ind1=" " ind2=" "><subfield code="2">045F</subfield><subfield code="a">570</subfield></datafield></record></collection>
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