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Study on the Control and Projective Synchronization of a New Fractional-order Chaos System
Shao Ke-Yong,Chen Bai-Quan,Wang Ting-Ting,Xu Xiang,Zhang Ting-Ting,Ma Di 보안공학연구지원센터 2016 International Journal of Multimedia and Ubiquitous Vol.11 No.10
In this paper, a new fractional-order chaotic system was studied, and the basic dynamic properties of the new system were analyzed. The control of the new system in unstable equilibrium point was realized by designing the reasonable nonlinear controller. Further, we investigated the projective synchronization problem about fractional order chaotic systems with different dimensions, the appropriate controller was designed to achieve the projective synchronization of a four-dimensional drive system and a three-dimensional response system by reducing the dimension. With the numerical simulation of Matlab, the feasibility of the scheme was verified.
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Shao Zifei,Xu Jinhao,Xu Xiaoyang,Wang Xiang,Zhou Yuxi,Li Yiyang,Li Kun 한국조직공학과 재생의학회 2024 조직공학과 재생의학 Vol.21 No.1
BACKGROUND: Oral submucous fibrosis (OSF) is a chronic disease with carcinogenic tendency that poses a non-negligible threat to human health. Exosomes derived from human adipose mesenchymal stem cells (ADSC-Exo) reduces visceral and cutaneous fibroses, but their role in OSF has received little attention. The aim of this study was to investigate the effects of ADSC-Exo on OSF and elucidate the mechanism. METHODS: In brief, ADSCs were extracted from adipose tissues and subjected to flow cytometry and induction culture. Fibroblasts were isolated from human buccal mucosa and subjected to immunofluorescence. Myofibroblasts were obtained from fibroblasts induced by arecoline and identified. Immunofluorescence assay confirmed that myofibroblasts could take up ADSC-Exo. The effects of ADSC-Exo on the proliferative and migratory capacities of myofibroblasts were examined using the Cell Counting Kit-8 and scratch assay. Real-time quantitative polymerase chain reaction (qPCR) was performed to evaluate mothers against decapentaplegic homolog 2 (Smad2), Smad3, Smad7, collagen type 1 (Col1), Col3, alpha smooth muscle actin (α-SMA), fibronectin, and vimentin. Western blotting was performed to detect phospho (p)-Smad2, Smad2, p-Smad2/3, Smad2/3, Smad7, Col1, Col3, α-SMA, fibronectin, and vimentin. Furthermore, the dual-luciferase reporter assay was performed to prove that miR-181a-5p in ADSC-Exo directly inhibited the expression of Smad2 mRNA to regulate the transforming growth factor beta (TGF-β) pathway. We also performed qPCR and western blotting to verify the results. RESULTS: ADSC-Exo could promote the proliferation and migration of myofibroblasts, reduce the expressions of p-smad2, Smad2, p-smad2/3, Smad2/3, Col1, αSMA, fibronectin, and vimentin and elevated the levels of Smad7 and Col3. In addition, miR-181a-5p was highly expressed in ADSC-Exo and bound to the 3'-untranslated region of Smad2. ADSC-Exo enriched with miR-181a-5p reduced collagen production in myofibroblasts and modulated the TGF-β pathway. CONCLUSIONS: ADSC-Exo promoted the proliferative and migratory capacities of myofibroblasts and inhibited collagen deposition and trans-differentiation of myofibroblasts in vitro. miR-181a-5p in exosomes targets Smad2 to regulate the TGF-β pathway in myofibroblasts. ADSC-Exo perform antifibrotic actions through the miR-181a-5p/Smad2 axis and may be a promising clinical treatment for OSF. BACKGROUND: Oral submucous fibrosis (OSF) is a chronic disease with carcinogenic tendency that poses a non-negligible threat to human health. Exosomes derived from human adipose mesenchymal stem cells (ADSC-Exo) reduces visceral and cutaneous fibroses, but their role in OSF has received little attention. The aim of this study was to investigate the effects of ADSC-Exo on OSF and elucidate the mechanism. METHODS: In brief, ADSCs were extracted from adipose tissues and subjected to flow cytometry and induction culture. Fibroblasts were isolated from human buccal mucosa and subjected to immunofluorescence. Myofibroblasts were obtained from fibroblasts induced by arecoline and identified. Immunofluorescence assay confirmed that myofibroblasts could take up ADSC-Exo. The effects of ADSC-Exo on the proliferative and migratory capacities of myofibroblasts were examined using the Cell Counting Kit-8 and scratch assay. Real-time quantitative polymerase chain reaction (qPCR) was performed to evaluate mothers against decapentaplegic homolog 2 (Smad2), Smad3, Smad7, collagen type 1 (Col1), Col3, alpha smooth muscle actin (α-SMA), fibronectin, and vimentin. Western blotting was performed to detect phospho (p)-Smad2, Smad2, p-Smad2/3, Smad2/3, Smad7, Col1, Col3, α-SMA, fibronectin, and vimentin. Furthermore, the dual-luciferase reporter assay was performed to prove that miR-181a-5p in ADSC-Exo directly inhibited the expression of Smad2 mRNA to regulate the transforming growth factor beta (TGF-β) pathway. We also performed qPCR and western blotting to verify the results. RESULTS: ADSC-Exo could promote the proliferation and migration of myofibroblasts, reduce the expressions of p-smad2, Smad2, p-smad2/3, Smad2/3, Col1, αSMA, fibronectin, and vimentin and elevated the levels of Smad7 and Col3. In addition, miR-181a-5p was highly expressed in ADSC-Exo and bound to the 3'-untranslated region of Smad2. ADSC-Exo enriched with miR-181a-5p reduced collagen production in myofibroblasts and modulated the TGF-β pathway. CONCLUSIONS: ADSC-Exo promoted the proliferative and migratory capacities of myofibroblasts and inhibited collagen deposition and trans-differentiation of myofibroblasts in vitro. miR-181a-5p in exosomes targets Smad2 to regulate the TGF-β pathway in myofibroblasts. ADSC-Exo perform antifibrotic actions through the miR-181a-5p/Smad2 axis and may be a promising clinical treatment for OSF.
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Mycotoxins Containing Diet Affects Oocyte Quality in Mouse
Shao-Chen Sun,Yan-Jun Hou,Xiang-Shun Cui,Nam-Hyung Kim 한국동물생명공학회(구 한국동물번식학회) 2013 Reproductive & Developmental Biology(Supplement) Vol.37 No.2s
Background: Mycotoxins which mainly consist of Aflatoxin (AF), Zearalenone (ZEN) and Deoxynivalenol (DON) are commonly found in many food commodities, each component has been shown to cause organ toxicity and oxidative stress in several species. Our previous study showed that mycotoxin-contaminated diet could cause oxidative stress in liver, kidney, spleen. Recently we examined its effects on oocyte quality. Materials and Methods: Mycotoxins-contaminated maize (AF 597μg/kg, ZEN 729μg/kg, DON 3.1mg/kg maize) was incorporated into the diet at three different doses (0, 5 and 20%) to feed the mice for 4 weeks. Results: Our results showed that the both the index of ovary and the number of good GV oocytes decreased in the mycotoxin-treated mice. The oocytes from mycotoxin- treated mouse displayed low developmental competence showing with lower GVBD and polar body extrusion rate; the embryo developmental competence also showed the similar pattern, most embryos could not develop to blastocyst stage. The cytoskeleton component actin expression in both oocyte cortex and cytoplasm decreased, and the expression of actin nucleation factor Profilin and mDia1 also decreased, indicating that mycotoxin may affect oocyte quality through the effects on actin. Moreover, a big proportion of oocytes with mycotoxin contaminated diet treatment showed disrupted cortical granule free domain, spindle morphology and mitochondria distribution, further confirmed the oocyte quality declination. We also used the in vitro model to confirm this, we cultured the oocytes in the medium with Zearalenone, a key component of mycotoxins, and the results were similar with the in vivo model. Conclusion: Our data indicated that the mycotoxins were toxic to mouse reproductive system and induced the oocyte quality declination.
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Involvement of microRNA-335-5p in cytoskeleton dynamics in mouse oocytes
Cui, Xiang-Shun,Sun, Shao-Chen,Kang, Yong-Kook,Kim, Nam-Hyung CSIRO Publishing 2013 Reproduction, fertility, and development Vol.25 No.4
<P> MicroRNA is a short RNA molecule expressed in eukaryotic cells that is involved in multiple processes, including translational repression, target degradation and gene silencing. However, its specific role(s) in these processes remains largely unknown, especially in terms of germ cell development. The present study identified a microRNA, namely miR-335-5p, that is involved in mouse oocyte meiosis. MiR-335-5p was highly expressed in oocytes, but levels decreased markedly shortly after fertilisation. Microinjection of miR-335-5p or its inhibitor into oocytes resulted in a higher proportion of 2-cell-like MII oocytes and oocytes at the germinal vesicle breakdown and/or MI stage, indicating failure of asymmetric oocyte division. This may be due to regulation of actin because perturbation of miR-335-5p resulted in reduced expression of actin nucleator Daam1, a member of the Formin family. Moreover, injection of miR-335-5p or its inhibitor resulted in aberrant spindle morphology, namely an elongated spindle and multiple poles spindle. After injection of oocytes, levels of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2) decreased, suggesting that miR-335-5p may regulate spindle formation via the mitogen-activated protein kinase pathway. Overexpression and inhibition of miR-335-5p had no effect on embryo development. Together, the results of the present study indicate that miR-335-5p is a novel regulator expressed in oocytes that is involved in cytoskeleton dynamics. </P>
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Zhou, Shao-Bing,Liu, Yang-Chen,Yin, Xiao-Xiang,Ding, Wen-Xiu,Guo, Xin-Wei,Gu, Liang,Huang, Xin-En Asian Pacific Journal of Cancer Prevention 2015 Asian Pacific journal of cancer prevention Vol.16 No.5
Objective: To evaluate the efficacy and adverse effects of three dimensional conformal radiotherapy (3D-CRT) with tamoxifen in treating patients with postoperative malignant glioma. Patients and Methods: 60 patients of postoperative malignant glioma were randomly assigned into two groups, 30 patients were treated with 3D-CRT plus tamoxifen (treatment group), and the other 30 patients with 3D-CRT plus temozolomide (control group). All patients were radiated by 6MV X-ray, 2.0Gy per fraction, once daily, with a total dose (DT) of 56~60Gy. Tamoxifen was delivered at $60mg/m^2/d$, temozolomide was given at $75mg/m^2/d$. All patients were treated with concurrent radiotherapy. Results: One, 2, 3 year survival rates of treatment and control group were 63.3%, 30.0%, 23.0% and 70.0%, 33.3%, 26.7%, respectively (${\chi}^2=0.01$, 0.23, 0.09, P>0.05). The rate of thromboembolism in treatment group was 6.7%. Conclusion: Therapeutic efficacy of two groups was similar, but it was more cost-effective in treatment group, and toxicity did not increase.
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Actin nucleator Arp2/3 complex is essential for mouse preimplantation embryo development
Sun, Shao-Chen,Wang, Qing-Ling,Gao, Wei-Wei,Xu, Yong-Nan,Liu, Hong-Lin,Cui, Xiang-Shun,Kim, Nam-Hyung CSIRO Publishing 2013 Reproduction, fertility, and development Vol.25 No.4
<P> The Arp2/3 complex is a critical actin nucleator, which promotes actin assembly and is widely involved in a diverse range of actin-related processes such as cell locomotion, phagocytosis and the establishment of cell polarity. Previous studies showed that the Arp2/3 complex regulates spindle migration and asymmetric division during mouse oocyte maturation; however, the role of the Arp2/3 complex in early mouse embryo development is still unknown. The results of the present study show that the Arp2/3 complex is critical for cytokinesis during mouse embryo development. The Arp2/3 complex was concentrated at the cortex of each cell at the 2- to 8-cell stage and the peripheral areas of the morula and blastocyst. Inhibition of the Arp2/3 complex by the specific inhibitor CK666 at the zygote stage caused a failure in cell division; mouse embryos failed to undergo compaction and lost apical-basal polarity. The actin level decreased in the CK666-treated group, and two or more nuclei were observed within a single cell, indicating a failure of cell division. Addition of CK666 at the 8-cell stage caused a failure of blastocyst formation, and CDX2 staining confirmed the loss of embryo polarity and the failure of trophectoderm and inner cell mass formation. Taken together, these data suggest that the Arp2/3 complex may regulate mouse embryo development via its effect on cell division. </P>
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