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612 results on '"Liao, Duan-Fang"'

101. PVAT targets VSMCs to regulate vascular remodelling: angel or demon.

Author

Zhang, Yin-Yu, Shi, Ya-Ning, Zhu, Neng, Zhao, Tan-Jun, Guo, Yi-Jie, Liao, Duan-Fang, Dai, Ai-Guo, and Qin, Li

Subjects
VASCULAR remodeling, LEPTIN, VASCULAR smooth muscle, ADIPOKINES, CARDIOVASCULAR diseases, PULMONARY hypertension, ADIPOSE tissues, VASCULAR diseases, HYPERTENSION
Abstract

Vascular remodelling refers to abnormal changes in the structure and function of blood vessel walls caused by injury, and is the main pathological basis of cardiovascular diseases such as atherosclerosis, hypertension, and pulmonary hypertension. Among them, the neointimal hyperplasia caused by abnormal proliferation of vascular smooth muscle cells (VSMCs) plays a key role in the pathogenesis of vascular remodelling. Perivascular adipose tissue (PVAT) can release vasoactive substances to target VSMCs and regulate the pathological process of vascular remodelling. Specifically, PVAT can promote the conversion of VSMCs phenotype from contraction to synthesis by secreting visfatin, leptin, and resistin, and participate in the development of vascular remodelling-related diseases. Conversely, it can also inhibit the growth of VSMCs by secreting adiponectin and omentin to prevent neointimal hyperplasia and alleviate vascular remodelling. Therefore, exploring and developing new drugs or other treatments that facilitate the beneficial effects of PVAT on VSMCs is a potential strategy for prevention or treatment of vascular remodelling-related cardiovascular diseases. [ABSTRACT FROM AUTHOR]

Published
2021
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102. Human torpor: translating insights from nature into manned deep space expedition.

Author

Shi, Zhe, Qin, Meng, Huang, Lu, Xu, Tao, Chen, Ying, Hu, Qin, Peng, Sha, Peng, Zhuang, Qu, Li‐Na, Chen, Shan‐Guang, Tuo, Qin‐Hui, Liao, Duan‐Fang, Wang, Xiao‐Ping, Wu, Ren‐Rong, Yuan, Ti‐Fei, Li, Ying‐Hui, and Liu, Xin‐Min

Subjects
BODY temperature, HUMAN space flight, CENTRAL nervous system, ENERGY metabolism, SPACE flight, DIGITAL divide
Abstract

During a long‐duration manned spaceflight mission, such as flying to Mars and beyond, all crew members will spend a long period in an independent spacecraft with closed‐loop bioregenerative life‐support systems. Saving resources and reducing medical risks, particularly in mental heath, are key technology gaps hampering human expedition into deep space. In the 1960s, several scientists proposed that an induced state of suppressed metabolism in humans, which mimics 'hibernation', could be an ideal solution to cope with many issues during spaceflight. In recent years, with the introduction of specific methods, it is becoming more feasible to induce an artificial hibernation‐like state (synthetic torpor) in non‐hibernating species. Natural torpor is a fascinating, yet enigmatic, physiological process in which metabolic rate (MR), body core temperature (Tb) and behavioural activity are reduced to save energy during harsh seasonal conditions. It employs a complex central neural network to orchestrate a homeostatic state of hypometabolism, hypothermia and hypoactivity in response to environmental challenges. The anatomical and functional connections within the central nervous system (CNS) lie at the heart of controlling synthetic torpor. Although progress has been made, the precise mechanisms underlying the active regulation of the torpor–arousal transition, and their profound influence on neural function and behaviour, which are critical concerns for safe and reversible human torpor, remain poorly understood. In this review, we place particular emphasis on elaborating the central nervous mechanism orchestrating the torpor–arousal transition in both non‐flying hibernating mammals and non‐hibernating species, and aim to provide translational insights into long‐duration manned spaceflight. In addition, identifying difficulties and challenges ahead will underscore important concerns in engineering synthetic torpor in humans. We believe that synthetic torpor may not be the only option for manned long‐duration spaceflight, but it is the most achievable solution in the foreseeable future. Translating the available knowledge from natural torpor research will not only benefit manned spaceflight, but also many clinical settings attempting to manipulate energy metabolism and neurobehavioural functions. [ABSTRACT FROM AUTHOR]

Published
2021
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105. Primerless Amplification for Circulating Tumor DNA Assays

Author

Xiao, Li, primary, Luo, Di-Xian, additional, Pu, Wangyang, additional, Luo, Weihao, additional, Pan, Yunzhi, additional, Xu, Huifen, additional, Li, Wen, additional, Zhang, Rong, additional, Wang, Han, additional, Wang, Fengjiao, additional, Liu, Xuan, additional, Sun, Yi, additional, Liao, Duan-Fang, additional, Feng, Yan, additional, Xing, Chungen, additional, Sirois, Pierre, additional, Zhang, Jia, additional, He, Nongyue, additional, and Li, Kai, additional

Published
2019
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107. A Large‐Scale Multicenter Study Validates Aldo‐Keto Reductase Family 1 Member B10 as a Prevalent Serum Marker for Detection of Hepatocellular Carcinoma

Author

Ye, Xu, primary, Li, Cunyan, additional, Zu, Xuyu, additional, Lin, Minglin, additional, Liu, Qiang, additional, Liu, Jianghua, additional, Xu, Guoguo, additional, Chen, Zhiyong, additional, Xu, Yongliang, additional, Liu, Long, additional, Luo, Diteng, additional, Cao, Zhe, additional, Shi, Guiyuan, additional, Feng, Zirui, additional, Deng, Hongyu, additional, Liao, Qianjin, additional, Cai, Chuan, additional, Liao, Duan‐Fang, additional, Wang, Jing, additional, Jin, Junfei, additional, and Cao, Deliang, additional

Published
2019
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116. Direct Interaction of Daxx and Androgen Receptor Is Required for Their Regulatory Activity in Cholesterol Biosynthesis.

Author

Li, Tian-Ping, Sun, Shao-Wei, Xiong, Guo-Zuo, Qiu, Fei, Yang, Dong-Mei, Sun, Si-Yu, Xie, Xue-Jiao, Liao, Duan-Fang, Chen, Jian-Xiong, and Tuo, Qin-Hui

Subjects
CHOLESTEROL, ANDROGEN receptors, BIOSYNTHESIS, ATHEROSCLEROSIS
Abstract

Introduction: Homeostasis of cholesterol is crucial for cellular function, and dysregulated cholesterol biosynthesis is a metabolic event that can lead to hepatic and cardiovascular abnormalities. Objective: The aim of this study was to investigate the effects and mechanisms of domain-associated protein (Daxx) and androgen receptor (AR) on intracellular cholesterol synthesis. Methods: HepG2 cells were transfected with pCDNA3.1(+)/Daxx plasmid or treated with testosterone propionate to observe the effects of Daxx and AR on intracellular cholesterol levels. Co-immunoprecipitation experiments were performed to identify the interaction between Daxx and AR and to explore the regulatory effects of this interaction on cholesterol synthesis. Results: Our experiments showed that AR promoted cholesterol synthesis and accumulation by activating sterol-regulatory element-binding protein isoform 2. AR-induced cholesterol synthesis was inhibited by Daxx; however, the expression of AR was not affected. Further studies demonstrated the existence of direct binding between Daxx and AR and this interaction was required to suppress AR activity. Conclusions: The Daxx-mediated antagonism of AR depicts a more complete picture as to how Daxx regulates intracellular cholesterol level and provides a new target for treatment of atherosclerosis. [ABSTRACT FROM AUTHOR]

Published
2021
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126. Nonpeptide somatostatin analogs: recent advances in its application and research

Author

Liang Qing-mo, Liao Duan-fang, and Wang Song

Subjects
endocrine system, Broad spectrum, Somatostatin, Clinical value, General Medicine, Clinical efficacy, Computational biology, Biology, Pharmacology, Medical science, Clinical treatment, hormones, hormone substitutes, and hormone antagonists
Abstract

Along with its wide anatomical distribution, somatostatin (SST) acts on multiple targets via a family of 5 receptors to produce a broad spectrum of biological effects. Therefore, a variety of peptide analogs have been produced and are widely used in clinical treatment. However, because of their flaws in the structure of peptide, the clinical efficacy is limited. In this review, we summarize the structure, pharmacological effects and the potential clinical value of non-peptide SST analogs. We focus on the research and development of non-peptide SST analogs since 1998, and discuss the problems and potential prospects for non-peptide SST analogs. We believe that as more non-peptide somatostatin analogs are successfully developed, the extensive clinical application of SSTs will contribute a great deal to medical science.

Published
2008

131. High glucose induces formation of tau hyperphosphorylation via Cav-1-mTOR pathway: A potential molecular mechanism for diabetes-induced cognitive dysfunction

Author

Wu, Jing, primary, Zhou, Shan-Lei, additional, Pi, Lin-Hua, additional, Shi, Xia-Jie, additional, Ma, Ling-Ran, additional, Chen, Zi, additional, Qu, Min-Li, additional, Li, Xin, additional, Nie, Sheng-Dan, additional, Liao, Duan-Fang, additional, Pei, Jin-Jing, additional, and Wang, Shan, additional

Published
2017
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133. Nicotinate‐curcumin ameliorates cognitive impairment in diabetic rats by rescuing autophagic flux in CA1 hippocampus.

Author

Gu, Hong‐Feng, Li, Na, Tang, Ya‐Ling, Yan, Can‐Qun, Shi, Zhe, Yi, Si‐Ni, Zhou, Hao‐Ling, Liao, Duan‐Fang, and OuYang, Xin‐Ping

Subjects
RIBOSOMAL proteins, FLUX (Energy), BCL-2 proteins, RATS, PROTEIN kinases
Abstract

Introduction: Our previous study has confirmed that a novel curcumin derivate nicotinate‐curcumin (NC) can facilitate autophagic flux in THP‐1 cells induced by oxidized low‐density lipoprotein. Aims: Given that autophagy plays critical roles in neurodegenerative diseases, the present study was carried out to investigate whether NC can improve cognitive function of rats with diabetes mellitus (DM) via restoring autophagic flux in CA1 hippocampus. Results: Our results showed that NC treatment improved cognitive deficit and attenuated neuronal loss as well as cellular ultrastructure impairment in the CA1 region of DM rats induced by streptozotocin. Moreover, NC lowered the expressions of the apoptosis‐related proteins Bcl‐2, Bax, Cyt‐c, and cleaved Caspase‐3. Notably, NC treatment reversed autophagic flux impairment as evidenced by the deceases in LC3‐II and p62 protein levels, and autophagosome accumulation in the hippocampal CA1 region of DM rats. However, these protective effects of NC were abolished by cotreatment with 3‐methyladenine (an autophagy inhibitor) and chloroquine (an autophagic flux inhibitor), respectively. Furthermore, NC treatment decreased the expressions of phosphorylated mammalian target of rapamycin (mTOR) and p70 ribosomal protein S6 kinase (p70S6k) proteins in the CA1 region of DM rats. Conclusions: These results indicate that NC ameliorates DM‐induced cognitive function impairment via restoring autophagic flux might by inhibiting mTOR/p70S6k activation in the CA1 region, and NC may be a promising agent for diabetic cognitive dysfunction prevention and treatment. [ABSTRACT FROM AUTHOR]

Published
2019
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134. Chronic Unpredictable Mild Stress Promotes Atherosclerosis via HMGB1/TLR4-Mediated Downregulation of PPARγ/LXRα/ABCA1 in ApoE-/- Mice.

Author

Gu, Hong-Feng, Li, Na, Xu, Zhao-Qian, Hu, Lu, Li, Hui, Zhang, Rong-Jie, Chen, Ru-Meng, Zheng, Xi-Long, Tang, Ya-Ling, and Liao, Duan-Fang

Subjects
ATHEROSCLEROSIS, PSYCHOLOGICAL stress, DOWNREGULATION, TOLL-like receptors, HIGH mobility group proteins, PEROXISOME proliferator-activated receptors, ATP-binding cassette transporters
Abstract

Background: Although our previous studies have confirmed that the activation of TLR4 is implicated in the development of atherosclerosis induced by chronic unpredicted mild stress (CUMS), the underling mechanism is largely unclear. Here, we hypothesized that CUMS accelerates atherosclerotic development through lowering PPARγ/LXRα-ABCA1 expression via HMGB1/TLR4 signaling. Methods: In present study, CUMS atherosclerotic animal models were established with AopE-/- mice, and CUMS Raw 264.7 macrophage models were mimicked by high corticosterone treatment, These models were treated with Ethyl pyruvate (EP, an inhibitor of HMGB1), TLR4 inhibitor TAK-242, and PPARγ agonist RSG (Rosiglitazone) to test our hypothesis, respectively. Results: Our results indicated that the protein levels of HMGB1, TLR4, and pro-inflammatory cytokines including IL-1β, TNF-α were elevated with the development of atherosclerosis in CUMS mice, while the expressions of PPARγ, LXRα, and ABCA1 declined. Notably, HMGB1 inhibition by EP reversed CUMS-induced atherosclerotic development, pro-inflammatory cytokines upregulation, and PPARγ/LXRα-ABCA1 downregulation. The same trend was observed in the stressed mice treatment with TAK-242. Further experimental evidences indicated that EP, TAK-242, and RSG treatment notably corrected foam cell formation, HMGB1 release, and down-regulation of LXRα and ABCA1 in CUMS Raw 264.7 macrophage model. Conclusion: These results indicate that CUMS exacerbates atherosclerosis is likely via HMGB1-mediated downregulation of PPARγ/LXRα-ABCA1 through TLR4. These data reveal a novel mechanism by which CUMS aggravates atherosclerosis and may offer a potential therapeutic target for this disease. [ABSTRACT FROM AUTHOR]

Published
2019
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145. Overexpression of AKR1B10 in nasopharyngeal carcinoma as a potential biomarker

Author

He, Ying-Chun, primary, Shen, Yi, additional, Cao, Yu, additional, Tang, Fang-Qing, additional, Tian, Dao-Fa, additional, Huang, Chen-Fei, additional, Tao, Huai, additional, Zhou, Fang-Liang, additional, Zhang, Bo, additional, Song, Lan, additional, He, Lan, additional, Lin, Li-Mei, additional, Lu, Fang-Guo, additional, Liao, Duan-Fang, additional, and Cao, Deliang, additional

Published
2016
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147. A phosphomimetic mutant of RelA/p65 at Ser536 induces apoptosis and senescence: An implication for tumor‐suppressive role of Ser536 phosphorylation

Author

Bu, Yiwen, primary, Li, Xiaoning, additional, He, Yingchun, additional, Huang, Chenfei, additional, Shen, Yi, additional, Cao, Yu, additional, Huang, Dan, additional, Cai, Chuan, additional, Wang, Yuhong, additional, Wang, Ziqi, additional, Liao, Duan‐Fang, additional, and Cao, Deliang, additional

Published
2015
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148. Highly efficient and green esterification of carboxylic acids in deep eutectic solvents without any other additives.

Author

Yasmin, Sumera, Sheng, Wen-Bing, Peng, Cai-Yun, Rahman, Atta-ur, Liao, Duan-Fang, Choudhary, M. Iqbal, and Wanga, Wei

Subjects
ESTERIFICATION, CARBOXYLIC acids, EUTECTICS, SOLVENTS, ADDITIVES
Abstract

A protocol that carboxylic acids esterifies with the quaternary ammonium salt of deep eutectic solvent (DES) is presented, which opens a new access to ester using DES as alkylating agent, solvent, and catalyst. The reaction runs smoothly in DES without any other additives. Substituted cinnamic acids, aromatic acids, and aliphatic acids can be esterified in moderate to good yields. The advantages of this reaction include excellent functional group compatibility and simple reaction procedure. [ABSTRACT FROM PUBLISHER]

Published
2018
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149. MiRNA-375 promotes 3T3-L1 adipocyte differentiation via modulation of ERK signaling

Author

Ling, Hong-Yan, Wen, Ge-Bo, Feng, Shui-Dong, Tuo, Qin-Hui, Ou, He-Sheng, Yao, Chao-Hua, Zhu, Bing-Yang, Gao, Zhi-Ping, Zhang, Liang, and Liao, Duan-Fang

Subjects
Adipogenesis, MAP Kinase Signaling System, Tumor Necrosis Factor-alpha, Cell Differentiation, Fatty Acid-Binding Proteins, Article, Up-Regulation, PPAR gamma, Mice, MicroRNAs, 3T3-L1 Cells, Adipocytes, CCAAT-Enhancer-Binding Protein-alpha, Animals, RNA, Messenger, Extracellular Signal-Regulated MAP Kinases, Triglycerides
Abstract

1. Adipocyte hypertrophy and hyperplasia are important processes in the development of obesity. To understand obesity and its associated diseases, it is important to elucidate the molecular mechanisms governing adipogenesis. MicroRNA-375 has been shown to inhibit differentiation of neurites, and participate in the regulation of insulin secretion and blood homeostasis. However, it is unknown whether miR-375 plays a role in adipocyte differentiation. 2. To investigate the role of miR-375 in adipocyte differentiation, we compared the miR-375 expression level between 3T3-L1 pre-adipocytes and adipocytes using miRNA microarray and quantitative real-time reverse transcription polymerase chain reaction (qRT-PCR) analysis. Furthermore, we evaluated the effects of overexpression or inhibition of miR-375 on 3T3-L1 adipocyte differentiation. 3. In the present study, we found that miR-375 expression was increased after induction of adipogenic differentiation. Overexpression of miR-375 enhanced 3T3-L1 adipocyte differentiation, as evidenced by its ability to increase mRNA levels of both CCAAT/enhancer binding protein-α (C/EBPα) and peroxisome proliferator-activated receptor-γ (PPARγ2), and induction of adipocyte fatty acid-binding protein (aP2) and triglyceride (TG) accumulation. Furthermore, we found overexpression of miR-375 suppressed phosphorylation levels of extracellular signal-regulated kinases 1/2 (ERK1/2). In contrast, anti-miR-375 increased ERK1/2 phosphorylation levels and inhibited mRNA expression of C/EBPα, PPARγ2 and aP2 in 3T3-L1 adipocyte, accompanied by decreased adipocyte differentiation. 4. Taken together, these data suggest that miR-375 promotes 3T3-L1 adipocyte differentiation, possibly through modulating the ERK-PPARγ2-aP2 pathway.

Published
2011

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