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8,076 results on '"Luo, Dan"'

216. Disclosure of Bank-Specific Information and the Stability of Financial Systems.

Author

Dai, Liang, Luo, Dan, and Yang, Ming

Subjects
BANKING industry, BANK runs, DISCLOSURE, RISK exposure, SYSTEMIC risk (Finance)
Abstract

We find that disclosing bank-specific information reallocates systemic risk, but whether it mitigates systemic bank runs depends on the nature of information disclosed. Disclosure reveals banks' resilience to adverse shocks and shifts systemic risk from weak to strong banks. Yet, only disclosure of banks' exposure to systemic risk can mitigate systemic bank runs because it shifts systemic risk from more vulnerable banks to those less vulnerable. Disclosure of banks' idiosyncratic shortfalls of funds does not differentiate such exposure, rendering the resultant reallocation of systemic risk ineffective in mitigating systemic runs. [ABSTRACT FROM AUTHOR]

Published
2024
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219. Pangenomic analysis identifies structural variation associated with heat tolerance in pearl millet

Author

Yan, Haidong, Sun, Min, Zhang, Zhongren, Jin, Yarong, Zhang, Ailing, Lin, Chuang, Wu, Bingchao, He, Min, Xu, Bin, Wang, Jing, Qin, Peng, Mendieta, John Pablo, Nie, Gang, Wang, Jianping, Jones, Chris S., Feng, Guangyan, Srivastava, Rakesh K., Zhang, Xinquan, Bombarely, Aureliano, Luo, Dan, Jin, Long, Peng, Yuanying, Wang, Xiaoshan, Ji, Yang, Tian, Shilin, and Huang, Linkai

Published
2023
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225. Triboelectric performances of biodegradable polymers

Author

Meng, Hongyu, Yu, Qiao, Liu, Zhuo, Gai, Yansong, Xue, Jiangtao, Bai, Yuan, Qu, Xuecheng, Tan, Puchuan, Luo, Dan, Huang, Wenwen, Nie, Kexin, Bai, Wei, Hou, Zhaosheng, Tang, Rupei, Xu, Hangxun, Zhang, Ying, Cai, Qing, Yang, Xianzhu, Wang, Zhong Lin, and Li, Zhou

Published
2023
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248. Creatine transporter content and localisation in human skeletal muscle : the effect of ageing and disuse

Author

Luo, Dan

Subjects
Q Science (General), QP Physiology
Abstract

The maintenance of intramuscular creatine (Cr) is important for sustainability of skeletal muscle mass across the life-course. Creatine transporter (CreaT) is the only known specific Cr transporter which embedded in the cell membrane as a gate-keeper that transports Cr from blood into skeletal muscle. The impairments of structure and functions in CreaT will lead to insufficient intracellular Cr concentration, resulting in the disturbance of cellular energy homeostasis, metabolic disorders, muscle atrophy and neurological disorders. Impaired energy homeostasis could also have implications for dysregulated proteostasis, and muscle atrophy. Maintenance of proteostasis is essential to sustain skeletal muscle mass and therefore vital to health across the life-course. This is especially important to populations in the context of musculoskeletal ageing and scenarios of disease/injury. In this regard, detections of tissue CreaT content may aid the clinical diagnosis of diseases. As such, to understand the CreaT regulation mechanisms and its role in Cr metabolism can help the development of therapeutic interventions to improve intramuscular Cr levels and support muscle mass in health and disease. However, the role of CreaT in modulating Cr metabolism in skeletal muscle remains largely unexplored. The existing measurement techniques lack precision to fully explain the regulatory role of CreaT in different physiological scenarios of muscle deterioration. Accordingly, Chapter 2 of this thesis validated and optimized an immunofluorescence microscopy technique and provided a more precise approach to identify CreaT protein expression and distribution in human skeletal muscle. A new method of calculation was designed and developed to identify CreaT protein intensity in specific sub-cellular regions. By using these developed methods, Chapter 3 of this thesis investigated whether CreaT distribution and sub-cellular expression is altered in older age. A sub-set of quadriceps muscle biopsy samples from 6 young and 6 older healthy individuals were involved in study to identify CreaT content and distribution, Creatine kinase (CK) and high-energy phosphagens. No significantly difference of CreaT content was observed between young and older individuals but with a declined concentration of phosphocreatine (PCr) (P<0.05) in older muscles. CreaT protein localisation was determined to predominantly distribute at the cell peripheral in both young and old individuals (P<0.05) but with fibre type specific difference in old individuals. These results demonstrated that Cr metabolism did alter by ageing, however, CreaT content remains relatively unaffected. Chapter 4 of this thesis investigated the effect of immobilization on CreaT protein expression and distribution in human skeletal muscle. The 7-days leg immobilization trial was undertaken in which 15 healthy young individuals. The results elucidated that 7 days immobilization lead to a declined muscle isometric strength and fat free mass (P<0.01), in addition with a reduced type II muscle fibre cross-section area (CSA) (P<0.05). CreaT protein content was greater in immobilised leg compared control leg (P<0.01). CreaT was mainly distribute at the cell peripheral in both immobilised and control legs with fibre type specific difference (P<0.01). These outcomes determined that the greater muscle fibre CreaT expression with immobilization may have important implications for skeletal muscle energy production during disuse-induced atrophy and in the recovery of muscle mass upon re-loading. In conclusion, this thesis provides a novel immunofluorescence approach to investigate CreaT activities in human skeletal muscle. This developed method provides valuable insight into the role of CreaT in alteration in intramuscular Cr metabolism across the spectrum of health and disease. In addition, this thesis enhances our understanding of CreaT protein expression and sub-cellular localisation in the role of Cr in skeletal muscle physiology.

Published
2020

249. Trophoblast H2S Maintains Early Pregnancy via Regulating Maternal-Fetal Interface Immune Hemostasis.

Author

Wang, Banqin, Xu, Tonghui, Li, Yan, Wang, Wenfu, Lyu, Chunzi, Luo, Dan, Yang, Qiuhong, Ning, Nannan, Chen, Zi-Jiang, Yan, Junhao, Chen, Dong-bao, and Li, Jingxin

Subjects
Reproductive Medicine, Biomedical and Clinical Sciences, Contraception/Reproduction, Pediatric, Aetiology, 2.1 Biological and endogenous factors, Reproductive health and childbirth, Good Health and Well Being, Abortion, Habitual, Animals, Cells, Cultured, Cystathionine beta-Synthase, Cystathionine gamma-Lyase, Female, Homeostasis, Humans, Hydrogen Sulfide, Male, Maternal-Fetal Exchange, Mice, Knockout, Pregnancy, Signal Transduction, Trophoblasts, hydrogen sulfide, cystathionine beta-synthase, immune hemostasis, maternal-fetal interface, unexplained recurrent spontaneous abortion, cystathionine β-synthase, Clinical Sciences, Paediatrics and Reproductive Medicine, Endocrinology & Metabolism, Clinical sciences
Abstract

Dysregulated immune hemostasis occurs in unexplained recurrent spontaneous abortion (URSA). Synthesized by cystathionine β-synthase (CBS) and cystathionine γ-lyase (CSE), hydrogen sulfide (H2S) promotes regulatory T-cell differentiation and regulates immune hemostasis; yet, its role in URSA is elusive. To determine if H2S plays a role in early pregnancy and if dysregulated H2S signaling results in recurrent spontaneous abortion. First trimester placenta villi and decidua were collected from normal and URSA pregnancies. Protein expression was examined by immunohistochemistry and immunoblotting. Human trophoblast HTR8/SVneo and JEG3 cells were treated with H2S donors; HTR8/SVneo cells were transfected with CBS ribonucleic acid interference (RNAi) or complementary deoxyribonucleic acid. Cell migration and invasion were determined by transwell assays; trophoblast transcriptomes were determined by RNA sequencing (RNA-seq). Wild-type, CBS-deficient, and CBA/J × DBA/2 mice were treated with CBS and CSE inhibitors or H2S donors to determine the role of H2S in early pregnancy in vivo. CBS and CSE proteins showed cell-specific expressions, but only CBS decreased in the villous cytotrophoblast in URSA versus normal participants. H2S donors promoted migration and invasion and MMP-2 and VEGF expression in human placenta trophoblast cells that contain SV40 viral deoxyribonucleic acid sequences (HTR8/SVneo) and human placenta trophoblast cells (JEG3 cells), similar to forced CBS expression in HTR8/SVneo cells. The CBS-responsive transcriptomes in HTR8/SVneo cells contained differentially regulated genes (ie, interleukin-1 receptor and prostaglandin-endoperoxide synthase 2) that are associated with nuclear factor-κB-mediated inflammatory response. In vivo, dysregulated CBS/H2S signaling significantly increased embryonic resorption and decidual T-helper 1/T-helper 2 imbalance in mice, which was partially rescued by H2S donors. CBS/H2S signaling maintains early pregnancy, possibly via regulating maternal-fetal interface immune hemostasis, offering opportunities for H2S-based immunotherapies for URSA.

Published
2020

250. Integrin-Src-YAP1 signaling mediates the melanoma acquired resistance to MAPK and PI3K/mTOR dual targeted therapy

Author

Yu, Chune, Zhang, Min, Song, Jinen, Zheng, Xiaobo, Xu, Guangchao, Bao, Yu, Lan, Jiang, Luo, Dan, Hu, Jianping, Li, Jingyi Jessica, and Shi, Hubing

Subjects
Biochemistry and Cell Biology, Biomedical and Clinical Sciences, Biological Sciences, Clinical Research, Cancer, Development of treatments and therapeutic interventions, 5.1 Pharmaceuticals, Melanoma, Targeted therapy, Resistance, MAPK, PI3K, mTOR, Integrin-Src-YAP1 axis, PI3K/mTOR
Abstract

Activation of PI3K/AKT pathway is one of the most recurrent resistant mechanisms for BRAF-targeted therapy, and the combination of MAPK and PI3K/AKT inhibitors becomes one of the most promising regimens for BRAF-targeted relapsed melanoma patients. Although the potent drug efficacy was observed in preclinical experiments and early clinical trials, the dual-drug resistance is inevitable observed. In this study, we systematically explored the mechanisms of dual-drug resistance to MAPKi and PI3K/mTORi in melanoma. With transcriptomic dissection of dual-drug resistant models, we identified that the drug tolerance was mediated by ECM-integrins α3β1 and α11β1 signaling. Upon binding ECM, the integrins activated downstream kinase Src rather than FAK, WNT, or TGFβ. Knockdown of integrins α3, α11, and β1 significantly inhibited the proliferation of dual-drug resistant sublines while with trivial effects on parental cells. Although Src inhibition suppressed the phosphorylation of AKT, c-JUN, and p38, none of inhibitors targeting these kinases reversed the dual-drug resistance in model cells. Notably, Src inhibitor promoted the phosphorylations of LATS1 and YAP1, subsequently, re-localized YAP1 from nucleus to cytosol facilitating further degradation. Both small molecule inhibitors and shRNAs targeting YAP1 or Src overcame the MAPKi and PI3K/mTORi dual-drug resistance. In conclusion, our data not only illuminated an integrin-Src-YAP1 pathway mediated MAPKi and PI3K/mTORi dual-drug resistant mechanism but also provided a potential combinatorial regimen for the drug-relapsed melanoma patients.

Published
2020

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