Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats
Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environm...
Ausführliche Beschreibung
Gespeichert in:
| Autor*in: |
Chen, Mingyue [verfasserIn] |
|---|
| Format: |
E-Artikel |
|---|---|
| Sprache: |
Englisch |
| Erschienen: |
2020transfer abstract |
|---|
| Übergeordnetes Werk: |
Enthalten in: SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota - Wang, Meimei ELSEVIER, 2018, an international journal for scientific research into the environment and its relationship with man, Amsterdam [u.a.] |
|---|---|
| Übergeordnetes Werk: |
volume:720 ; year:2020 ; day:10 ; month:06 ; pages:0 |
| Links: |
|---|
| DOI / URN: |
10.1016/j.scitotenv.2020.137615 |
|---|
| Katalog-ID: |
ELV049994247 |
|---|
| LEADER | 01000caa a22002652 4500 | ||
|---|---|---|---|
| 001 | ELV049994247 | ||
| 003 | DE-627 | ||
| 005 | 20230626025603.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 200518s2020 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1016/j.scitotenv.2020.137615 |2 doi | |
| 028 | 5 | 2 | |a /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica |
| 035 | |a (DE-627)ELV049994247 | ||
| 035 | |a (ELSEVIER)S0048-9697(20)31126-8 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 082 | 0 | 4 | |a 630 |a 640 |a 610 |q VZ |
| 100 | 1 | |a Chen, Mingyue |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| 264 | 1 | |c 2020transfer abstract | |
| 336 | |a nicht spezifiziert |b zzz |2 rdacontent | ||
| 337 | |a nicht spezifiziert |b z |2 rdamedia | ||
| 338 | |a nicht spezifiziert |b zu |2 rdacarrier | ||
| 520 | |a Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. | ||
| 520 | |a Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. | ||
| 700 | 1 | |a Guo, Jiaojiao |4 oth | |
| 700 | 1 | |a Ruan, Jinpeng |4 oth | |
| 700 | 1 | |a Yang, Zhibing |4 oth | |
| 700 | 1 | |a He, Chengyong |4 oth | |
| 700 | 1 | |a Zuo, Zhenghong |4 oth | |
| 773 | 0 | 8 | |i Enthalten in |n Elsevier Science |a Wang, Meimei ELSEVIER |t SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |d 2018 |d an international journal for scientific research into the environment and its relationship with man |g Amsterdam [u.a.] |w (DE-627)ELV001360035 |
| 773 | 1 | 8 | |g volume:720 |g year:2020 |g day:10 |g month:06 |g pages:0 |
| 856 | 4 | 0 | |u https://doi.org/10.1016/j.scitotenv.2020.137615 |3 Volltext |
| 912 | |a GBV_USEFLAG_U | ||
| 912 | |a GBV_ELV | ||
| 912 | |a SYSFLAG_U | ||
| 912 | |a SSG-OLC-PHA | ||
| 951 | |a AR | ||
| 952 | |d 720 |j 2020 |b 10 |c 0610 |h 0 | ||
| author_variant |
m c mc |
|---|---|
| matchkey_str |
chenmingyueguojiaojiaoruanjinpengyangzhi:2020----:entlxoueoniomnrlvnlvlotiuytnedt |
| hierarchy_sort_str |
2020transfer abstract |
| publishDate |
2020 |
| allfields |
10.1016/j.scitotenv.2020.137615 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica (DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 DE-627 ger DE-627 rakwb eng 630 640 610 VZ Chen, Mingyue verfasserin aut Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Guo, Jiaojiao oth Ruan, Jinpeng oth Yang, Zhibing oth He, Chengyong oth Zuo, Zhenghong oth Enthalten in Elsevier Science Wang, Meimei ELSEVIER SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota 2018 an international journal for scientific research into the environment and its relationship with man Amsterdam [u.a.] (DE-627)ELV001360035 volume:720 year:2020 day:10 month:06 pages:0 https://doi.org/10.1016/j.scitotenv.2020.137615 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 720 2020 10 0610 0 |
| spelling |
10.1016/j.scitotenv.2020.137615 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica (DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 DE-627 ger DE-627 rakwb eng 630 640 610 VZ Chen, Mingyue verfasserin aut Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Guo, Jiaojiao oth Ruan, Jinpeng oth Yang, Zhibing oth He, Chengyong oth Zuo, Zhenghong oth Enthalten in Elsevier Science Wang, Meimei ELSEVIER SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota 2018 an international journal for scientific research into the environment and its relationship with man Amsterdam [u.a.] (DE-627)ELV001360035 volume:720 year:2020 day:10 month:06 pages:0 https://doi.org/10.1016/j.scitotenv.2020.137615 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 720 2020 10 0610 0 |
| allfields_unstemmed |
10.1016/j.scitotenv.2020.137615 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica (DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 DE-627 ger DE-627 rakwb eng 630 640 610 VZ Chen, Mingyue verfasserin aut Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Guo, Jiaojiao oth Ruan, Jinpeng oth Yang, Zhibing oth He, Chengyong oth Zuo, Zhenghong oth Enthalten in Elsevier Science Wang, Meimei ELSEVIER SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota 2018 an international journal for scientific research into the environment and its relationship with man Amsterdam [u.a.] (DE-627)ELV001360035 volume:720 year:2020 day:10 month:06 pages:0 https://doi.org/10.1016/j.scitotenv.2020.137615 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 720 2020 10 0610 0 |
| allfieldsGer |
10.1016/j.scitotenv.2020.137615 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica (DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 DE-627 ger DE-627 rakwb eng 630 640 610 VZ Chen, Mingyue verfasserin aut Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Guo, Jiaojiao oth Ruan, Jinpeng oth Yang, Zhibing oth He, Chengyong oth Zuo, Zhenghong oth Enthalten in Elsevier Science Wang, Meimei ELSEVIER SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota 2018 an international journal for scientific research into the environment and its relationship with man Amsterdam [u.a.] (DE-627)ELV001360035 volume:720 year:2020 day:10 month:06 pages:0 https://doi.org/10.1016/j.scitotenv.2020.137615 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 720 2020 10 0610 0 |
| allfieldsSound |
10.1016/j.scitotenv.2020.137615 doi /cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica (DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 DE-627 ger DE-627 rakwb eng 630 640 610 VZ Chen, Mingyue verfasserin aut Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats 2020transfer abstract nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. Guo, Jiaojiao oth Ruan, Jinpeng oth Yang, Zhibing oth He, Chengyong oth Zuo, Zhenghong oth Enthalten in Elsevier Science Wang, Meimei ELSEVIER SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota 2018 an international journal for scientific research into the environment and its relationship with man Amsterdam [u.a.] (DE-627)ELV001360035 volume:720 year:2020 day:10 month:06 pages:0 https://doi.org/10.1016/j.scitotenv.2020.137615 Volltext GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA AR 720 2020 10 0610 0 |
| language |
English |
| source |
Enthalten in SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota Amsterdam [u.a.] volume:720 year:2020 day:10 month:06 pages:0 |
| sourceStr |
Enthalten in SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota Amsterdam [u.a.] volume:720 year:2020 day:10 month:06 pages:0 |
| format_phy_str_mv |
Article |
| institution |
findex.gbv.de |
| dewey-raw |
630 |
| isfreeaccess_bool |
false |
| container_title |
SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |
| authorswithroles_txt_mv |
Chen, Mingyue @@aut@@ Guo, Jiaojiao @@oth@@ Ruan, Jinpeng @@oth@@ Yang, Zhibing @@oth@@ He, Chengyong @@oth@@ Zuo, Zhenghong @@oth@@ |
| publishDateDaySort_date |
2020-01-10T00:00:00Z |
| hierarchy_top_id |
ELV001360035 |
| dewey-sort |
3630 |
| id |
ELV049994247 |
| language_de |
englisch |
| fullrecord |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV049994247</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626025603.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">200518s2020 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.scitotenv.2020.137615</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV049994247</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0048-9697(20)31126-8</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="4"><subfield code="a">630</subfield><subfield code="a">640</subfield><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Chen, Mingyue</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020transfer abstract</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">Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Guo, Jiaojiao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ruan, Jinpeng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Zhibing</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Chengyong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zuo, Zhenghong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Wang, Meimei ELSEVIER</subfield><subfield code="t">SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota</subfield><subfield code="d">2018</subfield><subfield code="d">an international journal for scientific research into the environment and its relationship with man</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV001360035</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:720</subfield><subfield code="g">year:2020</subfield><subfield code="g">day:10</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.scitotenv.2020.137615</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="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">720</subfield><subfield code="j">2020</subfield><subfield code="b">10</subfield><subfield code="c">0610</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| author |
Chen, Mingyue |
| spellingShingle |
Chen, Mingyue ddc 630 Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| authorStr |
Chen, Mingyue |
| ppnlink_with_tag_str_mv |
@@773@@(DE-627)ELV001360035 |
| format |
electronic Article |
| dewey-ones |
630 - Agriculture & related technologies 640 - Home & family management 610 - Medicine & health |
| delete_txt_mv |
keep |
| author_role |
aut |
| collection |
elsevier |
| remote_str |
true |
| illustrated |
Not Illustrated |
| topic_title |
630 640 610 VZ Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| topic |
ddc 630 |
| topic_unstemmed |
ddc 630 |
| topic_browse |
ddc 630 |
| format_facet |
Elektronische Aufsätze Aufsätze Elektronische Ressource |
| format_main_str_mv |
Text Zeitschrift/Artikel |
| carriertype_str_mv |
zu |
| author2_variant |
j g jg j r jr z y zy c h ch z z zz |
| hierarchy_parent_title |
SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |
| hierarchy_parent_id |
ELV001360035 |
| dewey-tens |
630 - Agriculture 640 - Home & family management 610 - Medicine & health |
| hierarchy_top_title |
SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |
| isfreeaccess_txt |
false |
| familylinks_str_mv |
(DE-627)ELV001360035 |
| title |
Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| ctrlnum |
(DE-627)ELV049994247 (ELSEVIER)S0048-9697(20)31126-8 |
| title_full |
Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| author_sort |
Chen, Mingyue |
| journal |
SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |
| journalStr |
SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota |
| lang_code |
eng |
| isOA_bool |
false |
| dewey-hundreds |
600 - Technology |
| recordtype |
marc |
| publishDateSort |
2020 |
| contenttype_str_mv |
zzz |
| container_start_page |
0 |
| author_browse |
Chen, Mingyue |
| container_volume |
720 |
| class |
630 640 610 VZ |
| format_se |
Elektronische Aufsätze |
| author-letter |
Chen, Mingyue |
| doi_str_mv |
10.1016/j.scitotenv.2020.137615 |
| dewey-full |
630 640 610 |
| title_sort |
neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| title_auth |
Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| abstract |
Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. |
| abstractGer |
Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. |
| abstract_unstemmed |
Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system. |
| collection_details |
GBV_USEFLAG_U GBV_ELV SYSFLAG_U SSG-OLC-PHA |
| title_short |
Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats |
| url |
https://doi.org/10.1016/j.scitotenv.2020.137615 |
| remote_bool |
true |
| author2 |
Guo, Jiaojiao Ruan, Jinpeng Yang, Zhibing He, Chengyong Zuo, Zhenghong |
| author2Str |
Guo, Jiaojiao Ruan, Jinpeng Yang, Zhibing He, Chengyong Zuo, Zhenghong |
| ppnlink |
ELV001360035 |
| mediatype_str_mv |
z |
| isOA_txt |
false |
| hochschulschrift_bool |
false |
| author2_role |
oth oth oth oth oth |
| doi_str |
10.1016/j.scitotenv.2020.137615 |
| up_date |
2024-07-06T23:06:33.211Z |
| _version_ |
1803872835429466112 |
| fullrecord_marcxml |
<?xml version="1.0" encoding="UTF-8"?><collection xmlns="http://www.loc.gov/MARC21/slim"><record><leader>01000caa a22002652 4500</leader><controlfield tag="001">ELV049994247</controlfield><controlfield tag="003">DE-627</controlfield><controlfield tag="005">20230626025603.0</controlfield><controlfield tag="007">cr uuu---uuuuu</controlfield><controlfield tag="008">200518s2020 xx |||||o 00| ||eng c</controlfield><datafield tag="024" ind1="7" ind2=" "><subfield code="a">10.1016/j.scitotenv.2020.137615</subfield><subfield code="2">doi</subfield></datafield><datafield tag="028" ind1="5" ind2="2"><subfield code="a">/cbs_pica/cbs_olc/import_discovery/elsevier/einzuspielen/GBV00000000001586.pica</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(DE-627)ELV049994247</subfield></datafield><datafield tag="035" ind1=" " ind2=" "><subfield code="a">(ELSEVIER)S0048-9697(20)31126-8</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="4"><subfield code="a">630</subfield><subfield code="a">640</subfield><subfield code="a">610</subfield><subfield code="q">VZ</subfield></datafield><datafield tag="100" ind1="1" ind2=" "><subfield code="a">Chen, Mingyue</subfield><subfield code="e">verfasserin</subfield><subfield code="4">aut</subfield></datafield><datafield tag="245" ind1="1" ind2="0"><subfield code="a">Neonatal exposure to environment-relevant levels of tributyltin leads to uterine dysplasia in rats</subfield></datafield><datafield tag="264" ind1=" " ind2="1"><subfield code="c">2020transfer abstract</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">Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system.</subfield></datafield><datafield tag="520" ind1=" " ind2=" "><subfield code="a">Endocrine-disrupting chemicals (EDCs) are natural/synthetic compounds that mimic or inhibit the biological actions of endogenous hormones. Studies have revealed that environmental estrogen, such as bisphenol A (BPA), causes developmental defects in the uterus. Tributyltin (TBT) is a typical environmental androgen. In this study, we aimed to explore the effect and mechanism of TBT on uterine development. Neonatal female rats were exposed to TBT (10 and 100 ng/kg bw) from postnatal days 1 to 16. BPA (50 μg/kg bw) was used as a positive control. Neonatal exposure to environmental concentrations of TBT resulted in pathological changes in the uterus, including thickening of the uterine luminal epithelium, a low density of glands, endometrial inflammation and fibrosis. Further, TBT affected the Wnt signaling pathway, which might mediate developmental disorders of the endometrial epithelial cells and glands in the uterus. TBT exposure also activated the NF-κB signaling pathway, which triggered inflammation. Moreover, TBT exposure upregulated the TGF-β/Smads signaling pathway, possibly leading to endometrial fibrosis. In summary, our results demonstrate that neonatal exposure to an environment-relevant level of TBT leads to uterine dysplasia and provide potential molecular mechanisms. Our study is helpful for clarifying the effects of environmental androgens on the female reproduction system.</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Guo, Jiaojiao</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Ruan, Jinpeng</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Yang, Zhibing</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">He, Chengyong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="700" ind1="1" ind2=" "><subfield code="a">Zuo, Zhenghong</subfield><subfield code="4">oth</subfield></datafield><datafield tag="773" ind1="0" ind2="8"><subfield code="i">Enthalten in</subfield><subfield code="n">Elsevier Science</subfield><subfield code="a">Wang, Meimei ELSEVIER</subfield><subfield code="t">SPG-56 from Sweet potato Zhongshu-1 delayed growth of tumor xenografts in nude mice by modulating gut microbiota</subfield><subfield code="d">2018</subfield><subfield code="d">an international journal for scientific research into the environment and its relationship with man</subfield><subfield code="g">Amsterdam [u.a.]</subfield><subfield code="w">(DE-627)ELV001360035</subfield></datafield><datafield tag="773" ind1="1" ind2="8"><subfield code="g">volume:720</subfield><subfield code="g">year:2020</subfield><subfield code="g">day:10</subfield><subfield code="g">month:06</subfield><subfield code="g">pages:0</subfield></datafield><datafield tag="856" ind1="4" ind2="0"><subfield code="u">https://doi.org/10.1016/j.scitotenv.2020.137615</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="912" ind1=" " ind2=" "><subfield code="a">SSG-OLC-PHA</subfield></datafield><datafield tag="951" ind1=" " ind2=" "><subfield code="a">AR</subfield></datafield><datafield tag="952" ind1=" " ind2=" "><subfield code="d">720</subfield><subfield code="j">2020</subfield><subfield code="b">10</subfield><subfield code="c">0610</subfield><subfield code="h">0</subfield></datafield></record></collection>
|
| score |
7.3988447 |