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Le Jian,Zhao Liangang,Liao Xiaobing,Zhou Qian,Liang Hongke 대한전기학회 2021 Journal of Electrical Engineering & Technology Vol.16 No.4
Virtual synchronous generator (VSG) control is an eff ective way to increase the equivalent inertia of grid connected inverter system and improve the stability of the power grid. However, the infl uence of this control on the stability of the whole system with time delay and parameter uncertainty should be researched further. In this paper, the state space model of the whole grid connected inverter system adopting VSG under control time-delay and parameter uncertainty is established. The Lyapunov functional with time-delay is constructed by employing time-delay dependent free weight matrix transformation. Furthermore, Lyapunov stability theorem is used to obtain the more conservative time-delay stability conditions with and without parameter uncertainty, linear matrix inequality is used to calculate the time-delay stability margin of the system under uncertainty, and the infl uence of the parameters of VSG control on the delay stability margin is analyzed. The validity of the proposed stability analysis and stability margin solution method are verifi ed by simulation examples.
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Chemical constituents from the fruiting bodies of Cryptoporus volvatus
Junchi Wang,Guangzhi Li,Na Lv,Li Gao,Liangang Shen,Jianyong Si 대한약학회 2016 Archives of Pharmacal Research Vol.39 No.6
New drimane-type sesquiterpene cryptoporol A(1), cryptoporic acid derivative 60-cryptoporic acid E methylester (2), and pseudouridine derivative cryptoporineA(3), aswell as a known ergosterol 5a,8a-epidioxy-22E-ergosta-6,22-dien-3b-ol (4), were isolated from a 90 % alcoholextract of the fruiting bodies of Cryptoporus volvatus. Thestructures of these compounds were established by spectroscopicanalysis and circular dichroism. 5a,8a-epidioxy-22Eergosta-6,22-dien-3b-ol (4) exhibited antiviral activityagainst porcine reproductive and respiratory syndrome virus,and all compounds showed weak antioxidant activities.
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Ding, Rui,Lin, Chunnan,Wei, ShanShan,Zhang, Naichong,Tang, Liangang,Lin, Yumao,Chen, Zhijun,Xie, Teng,Chen, XiaoWei,Feng, Yu,Wu, LiHua Korean Society for Molecular and Cellular Biology 2017 Molecules and cells Vol.40 No.2
Previous studies have shown that bone marrow mesenchymal stromal cell (MSC) transplantation significantly improves the recovery of neurological function in a rat model of intracerebral hemorrhage. Potential repair mechanisms involve anti-inflammation, anti-apoptosis and angiogenesis. However, few studies have focused on the effects of MSCs on inducible nitric oxide synthase (iNOS) expression and subsequent peroxynitrite formation after hypertensive intracerebral hemorrhage (HICH). In this study, MSCs were transplanted intracerebrally into rats 6 hours after HICH. The modified neurological severity score and the modified limb placing test were used to measure behavioral outcomes. Blood-brain barrier disruption and neuronal loss were measured by zonula occludens-1 (ZO-1) and neuronal nucleus (NeuN) expression, respectively. Concomitant edema formation was evaluated by H&E staining and brain water content. The effect of MSCs treatment on neuroinflammation was analyzed by immunohistochemical analysis or polymerase chain reaction of CD68, Iba1, iNOS expression and subsequent peroxynitrite formation, and by an enzyme-linked immunosorbent assay of pro-inflammatory factors (IL-$1{\beta}$ and TNF-${\alpha}$). The MSCs-treated HICH group showed better performance on behavioral scores and lower brain water content compared to controls. Moreover, the MSC injection increased NeuN and ZO-1 expression measured by immunochemistry/immunofluorescence. Furthermore, MSCs reduced not only levels of CD68, Iba1 and pro-inflammatory factors, but it also inhibited iNOS expression and peroxynitrite formation in perihematomal regions. The results suggest that intracerebral administration of MSCs accelerates neurological function recovery in HICH rats. This may result from the ability of MSCs to suppress inflammation, at least in part, by inhibiting iNOS expression and subsequent peroxynitrite formation.
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Rui Ding,Chunnan Lin,ShanShan Wei,Naichong Zhang,Liangang Tang,Yumao Lin,Zhijun Chen,Teng Xie,XiaoWei Chen,Yu Feng,LiHua Wu 한국분자세포생물학회 2017 Molecules and cells Vol.40 No.2
Previous studies have shown that bone marrow mesenchymal stromal cell (MSC) transplantation significantly improves the recovery of neurological function in a rat model of intracere-bral hemorrhage. Potential repair mechanisms involve anti-inflammation, anti-apoptosis and angiogenesis. However, few studies have focused on the effects of MSCs on inducible nitric oxide synthase (iNOS) expression and subsequent per-oxynitrite formation after hypertensive intracerebral hemorrhage (HICH). In this study, MSCs were transplanted intracerebrally into rats 6 hours after HICH. The modified neurological severity score and the modified limb placing test were used to measure behavioral outcomes. Blood–brain barrier disruption and neuronal loss were measured by zonula occludens-1 (ZO-1) and neuronal nucleus (NeuN) expression, respectively. Concomitant edema formation was evaluated by H&E staining and brain water content. The effect of MSCs treatment on neuroinflammation was analyzed by immunohistochemical analysis or polymerase chain reaction of CD68, Iba1, iNOS expression and subsequent peroxynitrite formation, and by an enzyme-linked immunosorbent assay of pro-inflammatory factors (IL-1 and TNF-). The MSCs-treated HICH group showed better performance on behavioral scores and lower brain water content compared to controls. Moreover, the MSC injection increased NeuN and ZO-1 expression measured by immunochemistry/immunofluorescence. Furthermore, MSCs reduced not only levels of CD68, Iba1 and pro-inflammatory factors, but it also inhibited iNOS expression and peroxynitrite formation in perihematomal regions. The results suggest that intracerebral administration of MSCs accelerates neurological function recovery in HICH rats. This may result from the ability of MSCs to suppress inflammation, at least in part, by inhibiting iNOS expression and subsequent peroxynitrite formation.
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