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| 1 | Almost periodic solution of a modified Leslie-Gower predator-prey model with Holling-type II schemes and mutual interference显示文摘 | Shengbin Yu Fengde Chen | 2014 | International Journal of Biomathematics2014，7，3： | 8 |
| 2 | Combined effects of nano-hydroxyapatite and Galla chinensis on remineralisation of initial enamel lesion in vitro显示文摘 | Shengbin Huang Shanshan Gao Lei Cheng Haiyang Yu | 2010 | Journal of Dentistry2010，，10： | 1 |
| 3 | Exploring the dynamics of a Holling-Tanner model with cannibalism in both predator and prey population显示文摘 | Aladeen Al Basheer Rana D. Parshad Emmanuel Quansah Shengbin Yu Ranjit Kumar Upadhyay | 2018 | International Journal of Biomathematics2018，11，1： | 1 |
| 4 | Global Asymptotic Stability of a Predator-Prey Model with Modified Leslie-Gower and Holling-Type II Schemes显示文摘 | Shengbin Yu Zhen Jin | 2012 | Discrete Dynamics in Nature and Society2012，，： | 1 |
| 5 | X-chromosome STRs polymorphism of Han ethnic group from Northwest China显示文摘 | Bing Yu Hongbo Zhang Shengbin Li | 2005 | Forensic Sci Int2005，153，23： | 1 |
| 6 | Investigation on some Schiff bases as HCl corrosioninhibitors for copper显示文摘 | Shulan Li Shenhao Chen Shengbin Lei Houyi Ma Rui Yu Dexin Liu | 1999 | Corrosion Science1999，，7： | 1 |
| 7 | Global asymptotic stability of a predator-prey model with modified Leslie-Gower and Holling-type IIschemes显示文摘 | Yu Shengbin | 2012 | Discrete Dynamics in Nature and Society2012，12，3： | 1 |
| 8 | Inhibition of ERK-DLP1 signaling and mitochondrial division alleviates mitochondrial dysfunction in Alzheimer’s disease cybrid cell显示文摘 | Xueqi Gan Shengbin Huang Long Wu Yongfu Wang Gang Hu Guangyue Li Hongju Zhang Haiyang Yu Russell Howard Swerdlow John Xi Chen Shirley ShiDu Yan | 2014 | BBA - Molecular Basis of Disease2014，，2： | 1 |
| 9 | EXTINCTION OF A DISCRETE COMPETITIVE SYSTEM WITH BEDDINGTON-DEANGELIS FUNCTIONAL RESPONSE AND THE EFFECT OF TOXIC SUBSTANCES显示文摘In this paper, we consider a discrete competitive system with BeddingtonDe Angelis functional response and the effect of toxic substances. By constructing some suitable Lyapunov type extinction functions, sufficient conditions which guarantee the extinction of a species and global attractivity of the other one are obtained. Our results not only supplement and improve but also generalize some existing ones. Numerical simulations show the feasibility of our results. | Jiangbin Chen Shengbin Yu | 2020 | Annals of Applied Mathematics2020，36，4： | 0 |
| 10 | Melatonin protects TEGDMA-induced preodontoblast mitochondrial apoptosis via the JNK/MAPK signaling pathway显示文摘Resin monomer-induced dental pulp injury presents a pathology related to mitochondrial dysfunction.Melatonin has been regarded as a strong mitochondrial protective bioactive compound from the pineal gland.However,it remains unknown whether melatonin can prevent dental pulp from resin monomer-induced injury.The aim of this study is to investigate the effects of melatonin on apoptosis of mouse preodontoblast cells(mDPC6T)induced by triethylene glycol dimethacrylate(TEGDMA),a major component in dental resin,and to determine whether the JNK/MAPK signaling pathway mediates the protective effect of melatonin.A well-established TEGDMA-induced mDPC6T apoptosis model is adopted to investigate the preventive function of melatonin by detecting cell viability,apoptosis rate,expressions of apoptosis-related proteins,mitochondrial ROS(mtROS)production,mitochondrial membrane potential(MMP)and adenosine triphosphate(ATP)level.Inhibitors of MAPKs are used to explore which pathway is involved in TEGDMA-induced apoptosis.Finally,the role of the JNK/MAPK pathway is verified using JNK agonists and antagonists.Our results show that melatonin attenuates TEGDMA-induced mDPC6T apoptosis by reducing mtROS production and rescuing MMP and ATP levels.Furthermore,mitochondrial dysfunction and apoptosis are alleviated only by the JNK/MAPK inhibitor SP600125 but not by other MAPK inhibitors.Additionally,melatonin downregulates the expression of phosphorylated JNK and counteractes the activating effects of anisomycin on the JNK/MAPK pathway,mimicking the effects of SP600125.Our findings demonstrate that melatonin protects mDPC6T cells against TEGDMA-induced apoptosis partly through JNK/MAPK and the maintenance of mitochondrial function,offering a novel therapeutic strategy for the prevention of resin monomer-induced dental pulp injury. | Qihao Yu Ruize Hua Bingyang Zhao Dongchao Qiu Chengfei Zhang Shengbin Huang Yihuai Pan | 2024 | Acta Biochimica et Biophysica Sinica2024，56，3： | 0 |
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