Yunqiang Liu

Dr. Yunqiang Liu


Research Focus & Metrics

Academic Career Length

17Years (2010-Present)

(Calculated once Scilit publication data is synced: current year − year of first publication + 1)

Representative Publications

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9 April 2014 in Sustainability
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YLYunqiang Liu
Yunqiang Liu
JXJiuping Xu
Jiuping Xu
HLHuawei Luo
Huawei Luo
Urbanization has become a key part of social and economic progress in the 21st Century, but achieving healthy and safe urban development has a long way to go for many developed and developing countries. Urbanization has been recognized as a complex ecosystem which is affected by economic, social, and ecological factors. With this in mind, this paper looks at many factors to first evaluate based on the matter-element (ME) method and then model an Economy-Society-Ecology (ESE) subsystem using a hybrid method by a fuzzy analytical hierarchy process (FAHP), and then by using the entropy method (EM) to determine the relevant index weights. To avoid subjectivity when defining the model’s boundaries, the technique for order preference by similarity to an ideal solution (TOPSIS) is introduced. Then, a coupling coordination degree model focusing on the degree of coordination in the ESE subsystem is established. Panel data collected from 2003 to 2012 for Chengdu, China, is then simulated to analyze the development process. The results show that: (1) The quality of urbanization continues to improve and the phasic features are presented; (2) The sensitivity analysis of subsystem weight shown that it had less effect on the coupling coordinated system; (3) The coordination in the ESE subsystem has also improved. However, the development rate of the economic subsystem is greater than that of the societal and ecological subsystem. The approach used here therefore, is shown to provide a promising basis for policy-making to support healthy urban development.

25 April 2022 in Environmental Science and Pollution Research
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XSXiaoyu Shao
Xiaoyu Shao
SLSha Liu
Sha Liu
RRRuiping Ran
Ruiping Ran
YLYunqiang Liu
Yunqiang Liu

12 May 2017 in Human Reproduction
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YYYuanlong Yan
Yuanlong Yan
XYXiling Yang
Xiling Yang
YLYunqiang Liu
Yunqiang Liu
YSYing Shen
Ying Shen
WTWenling Tu
Wenling Tu
YYYuan Yang
Yuan Yang
What is the influence of copy number variation (CNV) in functional RNA binding motif protein Y-linked family 1 (RBMY1) on spermatogenic phenotypes? The RBMY1 functional copy dosage is positively correlated with sperm motility, and dosage insufficiency is an independent risk factor for asthenozoospermia. RBMY1, a multi-copy gene expressed exclusively in the adult testis, is one of the most important candidates for male infertility in the azoospermia factor (AZF) region of the Y-chromosome. RBMY1 encodes an RNA-binding protein that serves as a pre-mRNA splicing regulator during spermatogenesis, and male mice deficient in Rbmy are sterile. A total of 3127 adult males were recruited from 2009 to 2016; of this group, the dosage of RBMY1 functional copy were investigated in 486 fertile males. In the remaining 2641 males with known spermatogenesis status, 1070 Y-chromosome haplogroup (Y-hg) O3* or O3e carriers without chromosomal aberration or known AZF structure mutations responsible for spermatogenic impairment, including 506 men with normozoospermia and 564 men with oligozoospermia or/and asthenozoospermia, were screened, and the RBMY1 functional copy dosage and copy conversion were determined to explore their associations with sperm phenotypes. The correlation between RBMY1 dosage and its mRNA level or RBMY1 protein level and the correlation between sperm RBMY1 level and motility were analysed in 15 testis tissue samples and eight semen samples. Ten additional semen samples were used to confirm the subcellular localization of RBMY1 in individual sperm. All the Han volunteers donating whole blood, semen and testis tissue were from southwest China. RBMY1 copy number, copy conversion, mRNA/protein amount and protein location in sperm were detected using the AccuCopy® assay method, paralog ratio test, quantitative PCR, western blotting and immunofluorescence staining methods, respectively. This study identified Y-hg-independent CNV of functional RBMY1 in the enrolled population. A difference in the distribution of RBMY1 copy number was observed between the group with normal sperm motility and the group with asthenozoospermia. A positive correlation between the RBMY1 copy dosage and sperm motility was identified, and the males with fewer than six copies of RBMY1 showed an elevated risk for asthenozoospermia relative to those with six RBMY1 copies, the most common dosage in the population. The RBMY1 copy dosage was positively correlated with its mRNA and protein level in the testis. Sperm with high motility were found to carry more RBMY1 protein than those with relatively low motility. The RBMY1 protein was confirmed to predominantly localize in the neck and mid-piece region of sperm as well as the principal piece of the sperm tail. Our population study completes a chain of evidence suggesting that RBMY1 influences the susceptibility of males to asthenozoospermia by modulating sperm motility. High sequence similarity between the RBMY1 functional copies and a large number of pseudogenes potentially reduces the accuracy of the copy number detection. The mechanism underlying the CNV in RBMY1 is still unclear, and the effect of the structural variations in the RBMY1 copy cluster on the copy dosage of other protein-coding genes located in the region cannot be excluded, which may potentially bias our observations. Asthenozoospermia is a multi-factor complex disease with a limited number of proven susceptibility genes. This study identified a novel genomic candidate independently contributing to the condition, enriching our understanding of the role of AZF-linked genes in male reproduction. Our finding provides insight into the physiological and pathological characteristics of RBMY1 in terms of sperm motility, supplies persuasive evidence of the significance of RBMY1 copy number analysis in the clinical counselling of male infertility resulting from asthenozoospermia This work was funded by the National Natural Science Foundation of China (Nos. 81370748 and 30971598). The authors have no conflicts of interest.

21 February 2022 in Environmental Science and Pollution Research
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YLYunqiang Liu
Yunqiang Liu
YSYanan She
Yanan She
SLSha Liu
Sha Liu
HTHong Tang
Hong Tang

10 May 2018 in Cell Death & Disease
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YSYing Shen
Ying Shen
WTWenling Tu
Wenling Tu
YLYunqiang Liu
Yunqiang Liu
XYXiling Yang
Xiling Yang
QDQiang Dong
Qiang Dong
YYYuan Yang
Yuan Yang
Testis-specific protein Y-linked 1 (TSPY1) is expressed predominantly in adult human spermatogonia and functions in the process of spermatogenesis; however, our understanding of the underlying mechanism is limited. Here we observed that TSPY1, as an interacting partner of TSPY-like 5 (TSPYL5), enhanced the competitive binding of TSPYL5 to ubiquitin-specific peptidase 7 (USP7) in conjunction with p53. This activity, together with its promotion of TSPYL5 expression by acting as a transcription factor, resulted in increased p53 ubiquitylation. Moreover, TSPY1 could decrease the p53 level by inducing the degradation of ubiquitinated USP7. We demonstrated that the promotion of p53 degradation by TSPY1 influenced the activity of p53 target molecules (CDK1, p21, and BAX) to expedite the G2/M phase transition and decrease cell apoptosis, accelerating cell proliferation. Taken together, the observations reveal the significance of TSPY1 as a suppressor of USP7-mediated p53 function in inhibiting p53-dependent cell proliferation arrest. By simulating TSPY1 function in Tspy1-deficient spermatogonia derived from mouse testes, we found that TSPY1 could promote spermatogonial proliferation by decreasing the Usp7-modulated p53 level. The findings suggest an additional mechanism underlying the regulation of spermatogonial p53 function, indicating the significance of TSPY1 in germline homeostasis maintenance and the potential of TSPY1 in regulating human spermatogonial proliferation via the USP7-mediated p53 signaling pathway.

31 July 2023 in Humanities and Social Sciences Communications
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DYDeping Ye
Deping Ye
SZShangsong Zhen
Shangsong Zhen
WWWei Wang
Wei Wang
YLYunqiang Liu
Yunqiang Liu
Because of the reductions in China’s cultivated land area and the significant impact on the agricultural market, the main grain-producing areas (MGPA) policy has become vitally important for ensuring China’s food security. However, guaranteed food security and sustainability require ecological security, which raises the question of whether food production should come at the expense of the environment. This study used 1998–2020 panel data from 30 Chinese provinces and a spatial difference-in-differences model (SDID) to explore the MGPA policy effects and mechanism paths on agricultural total factor productivity (ATFP) and the net carbon effect (NCS). It was found that economically, the MGPA policy promoted local ATFP improvements and had positive spillover effects on surrounding provinces through factor diffusion, and environmentally, the MGPA policy had a positive effect in the MGPA policy implementation areas but inhibited the NCS in surrounding provinces. Further explorations of the environmental performances revealed that the MGPA policy promoted growth in agricultural carbon sinks and agricultural carbon emissions, with the environmental performances being primarily reflected in an increase in carbon sinks and a decline in the carbon emissions density. The mechanism test showed that the MGPA policy’s local environmental performance was achieved through economic performance. The ATFP was refined into technical innovation (TI), technology adoption (TA), and business scale (OS), with the mechanistic roles of these three refining paths being OS > TI > TA. A further mechanism test revealed that the MGPA policy effects on the ATFP were influenced by the various adjustment of production support, government support, and collaborative support. Based on the above analysis, this study gives policy recommendations to ensure food security and the realization of China’s dual carbon target.