Automated Author ProfileYang, Chunyan
Yang, Chunyan
Current S-Index
Sum of Dataset Indices for all datasets
Average Dataset Index per Dataset
Average Dataset Index per dataset
Total Datasets
Total datasets for this author
Average FAIR Score
Average FAIR Score per dataset
Total Citations
Total citations to the author's datasets
Total Mentions
Total mentions of the author's datasets
S-Index Interpretation
The S-Index (Sharing Index) is a comprehensive metric that represents the cumulative impact of all your datasets. It is calculated as the sum of Dataset Index scores across all your claimed datasets.
What it means:
- A higher S-index indicates greater overall impact of your datasets relative to typical datasets in their fields of research
- The S-Index grows as you add more datasets or as existing datasets gain more citations and mentions
- It provides a single number to track your research data impact over time
Current S-Index: 6.6 (sum of 10 datasets Dataset Index scores)
More information here.
S-Index Over Time
Cumulative Citations Over Time
Cumulative Mentions Over Time
Datasets
Supplementary Material 4.
Authors
- Chen, HuiJuan ;
- Zhang, YiRan ;
- Wang, Bing ;
- Liao, Rui ;
- Duan, XiaoHong ;
- Yang, ChunYan ;
- Chen, Jing ;
- Hao, YanTong ;
- Shu, YingShuang ;
- Cai, LiLi ;
- Leng, Xue ;
- Qian, Nian-Song ;
- Sun, DaWei ;
- Niu, Beifang ;
- Zhou, Qiming
Supplementary Material 4.
Authors
- Chen, HuiJuan ;
- Zhang, YiRan ;
- Wang, Bing ;
- Liao, Rui ;
- Duan, XiaoHong ;
- Yang, ChunYan ;
- Chen, Jing ;
- Hao, YanTong ;
- Shu, YingShuang ;
- Cai, LiLi ;
- Leng, Xue ;
- Qian, Nian-Song ;
- Sun, DaWei ;
- Niu, Beifang ;
- Zhou, Qiming
JD17 reference genome assembly results and genome annotation data
Authors
- Yi, Xinxin ;
- Liu, Jing ;
- Chen, Shengcai ;
- Wu, Hao ;
- Liu, Min ;
- Xu, Qing ;
- Lei, Lingshan ;
- Lee, Seunghee ;
- Zhang, Bao ;
- Kudrna, Dave ;
- Fan, Wei ;
- A. Wing, Rod ;
- Wang, Xuelu ;
- Zhang, Mengchen ;
- Zhang, Jianwei ;
- Yang, Chunyan ;
- Chen, Nansheng
JD17 reference genome assembly results and genome annotation data
Authors
- Yi, Xinxin ;
- Liu, Jing ;
- Chen, Shengcai ;
- Wu, Hao ;
- Liu, Min ;
- Xu, Qing ;
- Lei, Lingshan ;
- Lee, Seunghee ;
- Zhang, Bao ;
- Kudrna, Dave ;
- Fan, Wei ;
- A. Wing, Rod ;
- Wang, Xuelu ;
- Zhang, Mengchen ;
- Zhang, Jianwei ;
- Yang, Chunyan ;
- Chen, Nansheng
No description available
Authors
- Huang, Tianle ;
- Yang, Chunyan ;
- Shi, Yuesen ;
- Chen, Jian ;
- Wang, Ting ;
- Guo, Xiaoyu ;
- Liu, Xuexin ;
- Ding, Haosheng ;
- Wu, Zhouping ;
- Hai, Li ;
- Wu, Yong
No description available
Authors
- Huang, Tianle ;
- Yang, Chunyan ;
- Shi, Yuesen ;
- Chen, Jian ;
- Wang, Ting ;
- Guo, Xiaoyu ;
- Liu, Xuexin ;
- Ding, Haosheng ;
- Wu, Zhouping ;
- Hai, Li ;
- Wu, Yong
Figure S1. SEM images of (a) ITO, (b) CdS thin films on ITO, and (c) Sb2S3 thin films on ITO. Figure S2 SEM images of (a) P3HT:PC61BM, (b) P3HT:PC61BM:3 wt.% CdS, and (c) P3HT:PC61BM:3 wt.% Sb2S3 films on ITO substrates. (ZIP 3399 kb)
Authors
- Yang, Chunyan ;
- Sun, Yingying ;
- Li, Xinjie ;
- Li, Cheng ;
- Tong, Junfeng ;
- Li, Jianfeng ;
- Zhang, Peng ;
- Xia, Yangjun
Figure S1. SEM images of (a) ITO, (b) CdS thin films on ITO, and (c) Sb2S3 thin films on ITO. Figure S2 SEM images of (a) P3HT:PC61BM, (b) P3HT:PC61BM:3 wt.% CdS, and (c) P3HT:PC61BM:3 wt.% Sb2S3 films on ITO substrates. (ZIP 3399 kb)
Authors
- Yang, Chunyan ;
- Sun, Yingying ;
- Li, Xinjie ;
- Li, Cheng ;
- Tong, Junfeng ;
- Li, Jianfeng ;
- Zhang, Peng ;
- Xia, Yangjun
Aim of the Study: Idiopathic pulmonary fibrosis (IPF) is a lethal human disease with short survival time and few treatment options. In this study, we aim to demonstrate that cyclic nucleotide phosphodiesterase 1A (PDE1A), a Ca2+/calmodulin-stimulating PDE family member, plays a critical role in the induction of fibrosis and angiogenesis in the lung. Materials and Methods: To induce pulmonary damage, adult male SD rats were treated with bleomycin in a dose of 6 mg/kg body weight by a single intratracheal instillation. For in vivo silencing of PDE1A in rat lung, a nonspecific control siRNA or PDE1A-specific siRNA was used to treat rat through nasal instillation. Human normal pulmonary fibroblasts MRC-5 and hFL1 and rat lung fibroblasts were used as in vitro model. Immunohistochemistry and immunoflurescence staining were performed to detect PDE1A and α-SMA expression. Reverse transcription-qPCR was performed to detect microRNA and mRNA expression. In vitro wound healing assay was performed to detect pulmonary fibroblasts'mortality ability. Results: In vitro studies showed that PDE1A can stimulate lung fibroblasts to undergo myofibroblastic changes. This led to the identification of miR-541-5p as one of the miRNA candidates associated with bleomycin response. We found that miR-541-5p expression is downregulated in TGF-β-treated lung fibroblasts and the rat pulmonary fibrosis model. Overexpression of miR-541-5p in lung fibroblasts inhibited mortality of human lung fibroblasts. Conclusions: MiR-541-5p is a key effector in lung fibroblastsby by regulating PDE1A expression at protein translation level and its overexpression is protective against bleomycin-induced lung fibrosis.
Authors
- Ren, Liqin ;
- Yang, Chunyan ;
- Dou, Yongfeng ;
- Zhan, Renhui ;
- Sun, Yi ;
- Yu, Yan
Aim of the Study: Idiopathic pulmonary fibrosis (IPF) is a lethal human disease with short survival time and few treatment options. In this study, we aim to demonstrate that cyclic nucleotide phosphodiesterase 1A (PDE1A), a Ca2+/calmodulin-stimulating PDE family member, plays a critical role in the induction of fibrosis and angiogenesis in the lung. Materials and Methods: To induce pulmonary damage, adult male SD rats were treated with bleomycin in a dose of 6 mg/kg body weight by a single intratracheal instillation. For in vivo silencing of PDE1A in rat lung, a nonspecific control siRNA or PDE1A-specific siRNA was used to treat rat through nasal instillation. Human normal pulmonary fibroblasts MRC-5 and hFL1 and rat lung fibroblasts were used as in vitro model. Immunohistochemistry and immunoflurescence staining were performed to detect PDE1A and α-SMA expression. Reverse transcription-qPCR was performed to detect microRNA and mRNA expression. In vitro wound healing assay was performed to detect pulmonary fibroblasts'mortality ability. Results: In vitro studies showed that PDE1A can stimulate lung fibroblasts to undergo myofibroblastic changes. This led to the identification of miR-541-5p as one of the miRNA candidates associated with bleomycin response. We found that miR-541-5p expression is downregulated in TGF-β-treated lung fibroblasts and the rat pulmonary fibrosis model. Overexpression of miR-541-5p in lung fibroblasts inhibited mortality of human lung fibroblasts. Conclusions: MiR-541-5p is a key effector in lung fibroblastsby by regulating PDE1A expression at protein translation level and its overexpression is protective against bleomycin-induced lung fibrosis.
Authors
- Ren, Liqin ;
- Yang, Chunyan ;
- Dou, Yongfeng ;
- Zhan, Renhui ;
- Sun, Yi ;
- Yu, Yan